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GANGGUAN N II DAN KESEIMBANGAN PADA KELAINAN
INTRASEREBRAL
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Table 143 (2 of 12)
Optic Nerve (II)
bull Sensory nerve of vision
Filaments of olfactory nerve (I) Olfactory bulb
Olfactory tract
Optic nerve (II) Optic chiasma
Optic tract
Oculomotor nerve (III)
Trochlear nerve (IV)
Trigeminal nerve (V)
Abducens nerve (VI)
Cerebellum
Medulla
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N Optikus (N II)
bull Tajam penglihatan
ndash Normal 66
ndash Melihat jari 660
ndash Lambaian tangan 1300
ndash Melihat sinar 1~
bull Lapang pandang
ndash Tes konfrontasi dgn tangan
ndash Tes kampimeter
ndash Tes perimeter
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N Optikus (NII) contrsquod
bull Tes warna
ndash Stilling-Ishihara
bull Funduskopi
ndash Pemeriksaan papil N II
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N Optikus (NII) contrsquod
bull Gangguan N II
ndash Mata kabur = visus turun
ndash Melihat dobel (diplopia) = aksis visual terganggu
ndash Lapang penglihatan menurun
ndash Mata buta
ndash Mata menjadi gelap
ndash Papiledema
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Cerebrovascular Disease
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General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
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Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
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Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
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Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
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Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
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supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
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bull 3 Circle of Willis Blood supply of brain
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bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
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Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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Diagnosis
bull Clinical features
bull No signs between attack
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Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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BRAIN TUMOR
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INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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3
Table 143 (2 of 12)
Optic Nerve (II)
bull Sensory nerve of vision
Filaments of olfactory nerve (I) Olfactory bulb
Olfactory tract
Optic nerve (II) Optic chiasma
Optic tract
Oculomotor nerve (III)
Trochlear nerve (IV)
Trigeminal nerve (V)
Abducens nerve (VI)
Cerebellum
Medulla
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N Optikus (N II)
bull Tajam penglihatan
ndash Normal 66
ndash Melihat jari 660
ndash Lambaian tangan 1300
ndash Melihat sinar 1~
bull Lapang pandang
ndash Tes konfrontasi dgn tangan
ndash Tes kampimeter
ndash Tes perimeter
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N Optikus (NII) contrsquod
bull Tes warna
ndash Stilling-Ishihara
bull Funduskopi
ndash Pemeriksaan papil N II
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N Optikus (NII) contrsquod
bull Gangguan N II
ndash Mata kabur = visus turun
ndash Melihat dobel (diplopia) = aksis visual terganggu
ndash Lapang penglihatan menurun
ndash Mata buta
ndash Mata menjadi gelap
ndash Papiledema
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9
Cerebrovascular Disease
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10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
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11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
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Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
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Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
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Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
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supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
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16
bull 3 Circle of Willis Blood supply of brain
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17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
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19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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Diagnosis
bull Clinical features
bull No signs between attack
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Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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44
Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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57
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58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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67
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68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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69
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70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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3
Table 143 (2 of 12)
Optic Nerve (II)
bull Sensory nerve of vision
Filaments of olfactory nerve (I) Olfactory bulb
Olfactory tract
Optic nerve (II) Optic chiasma
Optic tract
Oculomotor nerve (III)
Trochlear nerve (IV)
Trigeminal nerve (V)
Abducens nerve (VI)
Cerebellum
Medulla
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N Optikus (N II)
bull Tajam penglihatan
ndash Normal 66
ndash Melihat jari 660
ndash Lambaian tangan 1300
ndash Melihat sinar 1~
bull Lapang pandang
ndash Tes konfrontasi dgn tangan
ndash Tes kampimeter
ndash Tes perimeter
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N Optikus (NII) contrsquod
bull Tes warna
ndash Stilling-Ishihara
bull Funduskopi
ndash Pemeriksaan papil N II
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6
N Optikus (NII) contrsquod
bull Gangguan N II
ndash Mata kabur = visus turun
ndash Melihat dobel (diplopia) = aksis visual terganggu
ndash Lapang penglihatan menurun
ndash Mata buta
ndash Mata menjadi gelap
ndash Papiledema
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8
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9
Cerebrovascular Disease
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10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
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11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
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Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
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Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
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Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
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supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
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16
bull 3 Circle of Willis Blood supply of brain
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17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
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19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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Diagnosis
bull Clinical features
bull No signs between attack
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25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
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40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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44
Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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57
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58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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67
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68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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69
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70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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73
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Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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N Optikus (N II)
bull Tajam penglihatan
ndash Normal 66
ndash Melihat jari 660
ndash Lambaian tangan 1300
ndash Melihat sinar 1~
bull Lapang pandang
ndash Tes konfrontasi dgn tangan
ndash Tes kampimeter
ndash Tes perimeter
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N Optikus (NII) contrsquod
bull Tes warna
ndash Stilling-Ishihara
bull Funduskopi
ndash Pemeriksaan papil N II
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6
N Optikus (NII) contrsquod
bull Gangguan N II
ndash Mata kabur = visus turun
ndash Melihat dobel (diplopia) = aksis visual terganggu
ndash Lapang penglihatan menurun
ndash Mata buta
ndash Mata menjadi gelap
ndash Papiledema
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8
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9
Cerebrovascular Disease
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10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
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11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
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Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
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Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
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Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
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15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
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16
bull 3 Circle of Willis Blood supply of brain
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17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
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19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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Diagnosis
bull Clinical features
bull No signs between attack
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25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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67
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68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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69
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70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
5
N Optikus (NII) contrsquod
bull Tes warna
ndash Stilling-Ishihara
bull Funduskopi
ndash Pemeriksaan papil N II
21032013
6
N Optikus (NII) contrsquod
bull Gangguan N II
ndash Mata kabur = visus turun
ndash Melihat dobel (diplopia) = aksis visual terganggu
ndash Lapang penglihatan menurun
ndash Mata buta
ndash Mata menjadi gelap
ndash Papiledema
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7
21032013
8
21032013
9
Cerebrovascular Disease
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10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
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11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
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12
Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
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Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
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14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
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15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
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17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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57
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58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
6
N Optikus (NII) contrsquod
bull Gangguan N II
ndash Mata kabur = visus turun
ndash Melihat dobel (diplopia) = aksis visual terganggu
ndash Lapang penglihatan menurun
ndash Mata buta
ndash Mata menjadi gelap
ndash Papiledema
21032013
7
21032013
8
21032013
9
Cerebrovascular Disease
21032013
10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
21032013
11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
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12
Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
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Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
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14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
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15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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57
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58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
7
21032013
8
21032013
9
Cerebrovascular Disease
21032013
10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
21032013
11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
21032013
12
Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
21032013
13
Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
21032013
14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
21032013
15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
21032013
18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
8
21032013
9
Cerebrovascular Disease
21032013
10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
21032013
11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
21032013
12
Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
21032013
13
Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
21032013
14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
21032013
15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
21032013
18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
21032013
21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
21032013
22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
9
Cerebrovascular Disease
21032013
10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
21032013
11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
21032013
12
Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
21032013
13
Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
21032013
14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
21032013
15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
21032013
18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
21032013
21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
21032013
22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
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21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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10
General consideration
bull Cerebrovascular disease any abnormality of the brain resulting from a pathologic process of the blood vessels
bull Cerebrovascular accident or stroke may be defined as a sudden interruption of blood supply or hemorrhage into apart of the brain
bull the third commonest cause of death
21032013
11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
21032013
12
Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
21032013
13
Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
21032013
14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
21032013
15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
21032013
18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
21032013
21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
21032013
22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
21032013
33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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11
Classification
bull Ischemic transient ischemic attack (TIA)
cerebral thrombosis
cerebral embolism cerebral infarction
lacunar infarct
bull Hemorrhagic cerebral hemorrhage
subarachnoid hemorrhage (SAH)
21032013
12
Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
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Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
21032013
14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
21032013
15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
21032013
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TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
21032013
21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
21032013
22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
21032013
33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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57
21032013
58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
12
Blood supply of brain
bull 1 Internal carotid system
Branchiocephalic trunkrarrright common carotid artery
left common carotid artery
rarrinternal carotid artery rarr carotid foramen rarr
bull Ophthalmic artery
bull Anterior choroidal artery
bull Posterior communicating artery
bull Anterior cerebral artery
bull Middle cerebral artery
21032013
13
Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
21032013
14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
21032013
15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
21032013
18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
21032013
21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
21032013
22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
21032013
33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
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21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
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21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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13
Supply eyes and anterior 35 of the brain frontal parietal part of temporal lobe basal ganglia
21032013
14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
21032013
15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
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21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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14
Blood supply of brain
bull 2 Vertebral-basilar system
bull Subclavian artery rarr vertebral artery rarr C6-C1 transverse foramen rarr great occipital foramen rarr basilar artery
bull posterior spinal arteries anterior spinal artery
bull posterior inferior cerebellar artery
bull auditory artery
bull posterior cerebral arteries
21032013
15
supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
16
bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
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Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
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Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
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95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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supply cerebellum brain stem posterior 25 of brain (occipital part of tempral lobe)
21032013
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bull 3 Circle of Willis Blood supply of brain
21032013
17
bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
21032013
19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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24
Diagnosis
bull Clinical features
bull No signs between attack
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25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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bull 3 Circle of Willis Blood supply of brain
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bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
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Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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Diagnosis
bull Clinical features
bull No signs between attack
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Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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69
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70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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bull Age family history race
bull Hypertension
bull Heart disease
bull Diabetes
bull Hyperlipemia
bull Smoking excessive drinking
bull Obesity diet contraceptive drugs
Risk factors of CVD
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TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
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Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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Diagnosis
bull Clinical features
bull No signs between attack
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Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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18
TIA
bull A transient ischemic attack is a focal disturbance of the cerebral circulation frequently repetitive resulting in a period of impaired function lasting for a short period (anything from a few minutes to twenty-four hours) Attacks can occur in the carotid andor vertebral artery territories
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19
Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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24
Diagnosis
bull Clinical features
bull No signs between attack
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25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
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40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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44
Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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57
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58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
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70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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Etiology
bull Micro embolism
bull Spasm of cerebral blood vessel
bull Hemodynamic change
bull Compression of vertebral artery steal syndrome
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Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
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2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
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(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
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Diagnosis
bull Clinical features
bull No signs between attack
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25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
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40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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44
Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
20
Clinical feature
1 50-70 MgtF
characteristics
bull Abrupt onset
bull Transient
bull Complete recovery
bull Repetitive
21032013
21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
21032013
22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
21
2 Transient carotid ischemic attacks (1)Common symptoms bull Weakness of the contralateral arm andor leg (2) Characteristic symptoms bull Transient loss of vision in the eye contralateral to
the paresis (amaurosis fugax) bull Horner sign (3) Symptoms may present bull Dysphasia bull Paraesthesia or numbness in the contralateral limbs bull hemianopia
Clinical feature
21032013
22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
21032013
33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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22
3 Transient vertebral ndashbasilar ischemic attack
(1) Common symptoms
bull Vertigo nausea vomiting
(2) Characteristic symptoms
bull Drop attack
bull Transient global amnesia TGA
bull Cortical blindness
bull Crossed paralysis or sensory disturbance
Clinical feature
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
21032013
33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
21032013
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
23
(3) Symptoms may present
bull Dysphagia dysarthria
bull Ataxia
bull Disturbance of consciousness
bull diplopia
Clinical feature
21032013
24
Diagnosis
bull Clinical features
bull No signs between attack
21032013
25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
21032013
26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
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Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
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95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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Diagnosis
bull Clinical features
bull No signs between attack
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25
Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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26
Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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Differential diagnosis
bull Partial epilepsy
bull Meniere disease
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Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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Cerebral Thrombosis bull Infarction of an area of the brain secondary to
arterial occlusion by thrombosis of a major vessel with insufficient collateral circulation
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Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
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Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
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29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
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Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
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ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
27
Etiology
bull Atherosclerosis
bull Arteritis such as leptospirosis rheumatic fever
bull Rare cause
congenital vascular malformation polycythemia
blood hypercoagulability
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
28
Pathology
bull Vessel carotid gt middle gt posterior gt anterior gt vertebral-basilar
bull Super-early stage 1-6 hour
bull Necrosis rarr cyst
bull White infarct
bull Red infarct hemorrhagic infarct
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
21032013
33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
29
Pathophysiology
bull Neurons are sensitive to ischemia
bull Central necrosis
bull Ischemic penumbra
bull Super early stage lt 6 hours
21032013
30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
21032013
31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
21032013
32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
21032013
33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
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Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
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Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
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95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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30
Clinical feature
bull Onset is rapid
bull Usually occur in the rest and sleep
bull Premonitory symptoms such as weakness of a limb transient ischemic attack
bull The headache vomit and loss of consciousness may be absent or slight
bull Focal signs develop in several days
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31
Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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32
Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
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21032013
58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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Clinical type
bull Complete stroke
bull Progressive stroke
bull Reversible ischemic neurological deficit (RIND)
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Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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Clinical syndrome
1 Internal carotid artery
bull may have no signs (if the collateral supply from the other side is good )
bull amaurosis fugax uniocular blindness
bull Horners syndrome may present in the side of the occlusion
bull contralateral hemiplegia and hemianesthesia
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2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
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3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
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4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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Lacunar infarct
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Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
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103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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33
2 Middle cerebral artery
bull contralateral hemiplegia hemianesthesia hemianopia
bull aphasia (if the dominant hemisphere is affected)
bull disturbance of body image (non-dominant hemisphere)
Clinical syndrome
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
34
3 Anterior cerebral artery
bull contralateral hemiplegia the leg frequently being more affected than the arm
bull paracentral lobule regulation of sphincter function retention or incontinence
bull mental symptoms apathy euphoria
Clinical syndrome
21032013
35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
21032013
36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
21032013
37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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35
4 Posterior cerebral artery
bull contralateral hemianopia or quadrantanopia
bull thalamic syndrome contralateral hemianesthesia thalamic pain ataxia tremor athetosis
Clinical syndrome
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36
5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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5 Vertebro-basilar artery
(1) Main trunk
bull nausea vomiting tetraplegia coma death
(2) Weber syndrome
bull Unilateral lesion of midbrain
bull Ipsilateral oculomotor nerve paralysis contra lateral hemiplegia
Clinical syndrome
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bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
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Investigation 1 CT
Low density focus after 24-48 hours
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bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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44
Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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63
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64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
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68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
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70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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37
bull (3) locked-in syndrome
bull Bilateral infarction in the basis pontis
bull Tetraplegia can not speak can not swallow
bull Conscious
bull Can only respond by vertical gaze and blinking
Clinical syndrome
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38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
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82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
38
6 posterior inferior cerebellar artery
Wallenbergs syndrome Lateral medullary syndrome
bull Vertigo vomiting nystagmus
bull Crossed sensory disturbance
bull Ipsilateral Horner sign
bull Dysphagia dysarthria
bull Ipsilateral ataxia
Clinical syndrome
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
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81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
39
Investigation 1 CT
Low density focus after 24-48 hours
21032013
40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
21032013
41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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40
bull 2 MRI
Investigation
A right carotid artery occlusion low signal of T1 and high signal of T2 weighted image
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41
3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
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44
Lacunar infarct
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45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
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59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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3 Lumbar puncture
bull Normal
bull Large infarct pressure uarr
bull Hemorrhagic infarction RBC
4 DSA
5 TCD
Investigation
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Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
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43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
42
Diagnosis
bull after middle or old age
bull rapid onset focal cerebral symptoms
bull premonitory symptoms
bull occurs in rest or sleep
bull CTMRI find cerebral infarction focus
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
43
Differential diagnosis
bull Cerebral hemorrhage
bull Cerebral embolism
bull Intracranial tumor
21032013
44
Lacunar infarct
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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44
Lacunar infarct
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Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
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Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
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Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
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53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
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Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
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Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
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56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
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74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
45
Pathology
bull 3-4mm lt15-20mm
bull Small liquid cavity
bull Basal ganglia thalamus brain stem
bull Small artery 100-200μm
bull Atherosclerosis
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
46
Clinical feature
bull 40-60 years of age
bull Always combined with hypertension
Lacunar syndrome
bull 1 Pure motor hemiparesis
bull 2 Pure sensory stroke
bull 3 Ataxic-hemiparesis
bull 4 Dysarthric-clumsy hand syndrome
bull 5 Sensorimotor stroke
bull 6 Lacunar state
21032013
47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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47
Cerebral embolism
Occlusion of a major cerebral artery by an embolus with resultant infarction of part of the brain
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48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
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49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
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50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
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51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
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52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
48
Etiology
bull Cardiac cause
Atrial fibrillation rheumatic valve disease endocarditis atrial myxoma myocardial infarction
bull Non-cardiac
Atherosclerosis plaque pus embolus fat embolus tumor embolus
bull Embolus of unknown origin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
49
Clinical feature
bull Left middle cerebral artery
bull abrupt onset maximum disability occurring at once
bull In some cases there is rapid improvement
bull The primary disease such as rheumatic heart disease
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
50
Vertebrobasilar Ischemia
Symptoms Commonly manifested as vertigo visual disturbances progressive neuro deficit
Mechanisms Microembolization from heart or more proximal arteries Less
common bull innominate prox subclavian and vertebrals
ndash Low-flow lack appropriate inflow from the vertebral artery and have inadequate compensation from the carotid bull More frequent
bull Stenosisocclusion of vert also extrinsic compression
bull Orthostatic hypotension antihypertensive meds arrythmias CHF pacemaker malfunction anemia
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
51
Evaluation of Patients
bull Dizziness vertebral artery stenosis are common complaintsfindings
bull Imaging brain to ro tumor investigate for infarctions
bull Check bilateral arm BPrsquos to ro subclavian steal syndrome ndash Document reversal of flow by duplex
bull Extrinsic compression by osteophytes ndash Turning head side to side slowly then briskly to differentiate from BPV
ndash Confirm with angiogram
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
52
Global ischemia
bull ldquoDrop attacksrdquo comprise roughly 30 of presentations
bull One or both internal carotid arteries occluded or with severe siphon stenosis
bull Vertebral arteries important pathways for cerebral revascularization when they are critically stenosed or occluded ndash Minimal anatomic req to justify vert reconstruction is
gt60 stenosis in dominant if contra is hypoplastic or gt60 in both
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
53
Head Injury
bull 15 million Non-fatal TBIrsquos
bull 370000 Hospitalizations
bull 80000 cases of neurological sequela
bull 52000 Die from TBIrsquos
bull 4 billion annually for cost of treatment
bull Peak incidence ndash Males age 15-24 years
bull Causes of TBI ndash Young GSW
ndash Old Falls
Epidemiology
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
54
Head Injury-Anatomy
bull Scalp
bull Blood supply
bull Calvaria
bull Brain
ndash Occupies 80 of calvarium
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
55
Head Injury-Pathophysiology
bull Primary injury
ndash Irreversible cellular injury as a direct result of the injury
ndash Prevent the event
bull Secondary injury
ndash Damage to cells that are not initially injured
ndash Occurs hours to weeks after injury
ndash Prevent hypoxia and ischemia
21032013
56
Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
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103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
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107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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Head Injury-Normal Physiology
bull Brain consumes 20 of total O2
bull Receives 15 of Cardiac Output
bull Brain tissue perfusion
bull CPP versus CBF ndash CPP=MAP-ICP
bull MAP=(SBP-DBP3) + DBP ndash ICP=IVM
bull Autoregulation ndash 50-150 mm Hg
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ICP
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Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
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Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
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Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
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Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
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Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
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Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
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Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
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Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
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Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
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Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
57
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
58
ICP
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
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98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
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99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
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100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
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101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
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102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
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104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
59
Spectrum of Traumatic Brain Injury
bull Mild TBI
ndash GCS 14-15
ndash 80 of all TBI
ndash Low Risk
bull GCS 15 and no LOC amnesia vomiting or diffuse HA
bull Less than 01 risk of hematoma requiring evacuation
ndash Medium Risk
bull GCS 15 and LOC amnesia vomiting or Diffuse HA
bull 1-3 risk of hematoma requiring evacuation
bull CT should be done in medium risk mild TBI
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
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75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
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77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
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Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
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80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
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83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
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84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
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85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
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86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
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87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
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88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
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89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
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90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
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91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
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92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
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93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
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94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
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95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
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96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
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105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
60
Spectrum of Traumatic Brain Injury
bull Mild TBI ndash High Risk
bull GCS 14-15
bull Neurologic deficits
bull Up to 10 risk of hematoma requiring evacuation
bull Anyone with coagulopathy drugalcohol consumption epilepsy age gt60 and previous neurosurgery
ndash Disposition bull No CT indicated or negative CT with GCS 15-Home
bull GCS 14 and negative CT-Observation admit
21032013
61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
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76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
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79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
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81
BRAIN TUMOR
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82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
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106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
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61
Spectrum of Traumatic Brain Injury
bull Moderate TBI
ndash GCS 9-13
ndash 10 of all TBI
ndash lt20 mortality
bull Severe TBI
ndash GCS lt9
ndash 10 of all TBI
ndash 40 mortality
ndash 50 morbidity
ndash 40 positive CT
ndash 8 NS intervention
ndash lt10 make moderate recovery
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
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66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
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72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
62
Intracerebral Pressure
bull Normal lt15 mm Hg
bull ICP gt20-25 mm Hg
ndash Increases morbidity and mortality
bull ICP monitoring rarely available in the ED
bull Must use physical findings
ndash Neurologic deterioration
ndash Unilaterally dilated pupil
ndash Hemiparesis
ndash Posturing
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
63
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
64
Specific Head Injuries
bull Scalp Lacerations
ndash May lead to massive blood loss
ndash Small galeal lacerations may be left alone
bull Skull Fracture
ndash Linear and simple comminuted skull fractures
bull Exploration of wound
bull Prophylactic antibiotics are controversial
bull Occipital fractures have a high incidence of other injury
bull If depressed beyond outer table-requires NS repair
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
65
Specific Head Injuries
bull Skull Fractures
ndash Basilar Fracture
bull Most common-petrous portion of temporal bone the EAC and TM
bull Dural tear ndash CSF otorrhea
ndash CSF rhinorrhea
ndash Battle Sign
ndash Raccoon Sign
bull CSF testing ndash Ring sign glucose or CSF transferrin
bull Should be started on prophylactic antibiotics ndash Ceftriaxone 1-2 gm
ndash Hemotympanum
ndash Vertigo
ndash Hearing loss
ndash Seventh nerve palsy
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
66
The Ring Sign bull Ann Emerg Med 1993 Apr22(4)718-20 bull
The ring sign is it a reliable indicator for cerebral spinal fluid Dula DJ Fales W Department of Emergency Medicine Geisinger Medical Center Danville Pennsylvania STUDY OBJECTIVE To study the development of a ring sign when blood is mixed with various fluids METHODS One drop of blood and one drop of either spinal fluid saline tap water or rhinorrhea fluid were placed simultaneously on filter paper and the specimens were examined after ten minutes for the development of a ring A variety of filter paper agents were used including standard laboratory filter paper paper towels coffee filters and bed linens RESULTS All fluids when mixed with blood gave rise to a ring sign blood alone did not The type of filter paper did not affect the development of a ring CONCLUSION In this experimental setting the ring or halo sign is reliable for detecting cerebrospinal fluids but is not exclusive for cerebrospinal fluid
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
67
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
68
Specific Head Injuries
bull Brain Herniation
ndash Four Types
bull Uncal Transtentorial
bull Central Transtentorial
bull Cerebellotonsillar
bull Upward Posterior Fossa
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
69
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
70
Specific Head Injuries
bull Traumatic Subarachnoid Hemorrhage ndash Most common CT finding in moderate to severe
TBI
ndash If isolated head injury may present with headache photophobia and meningismus
ndash Early tSAH development triples mortality
ndash Size of bleed and outcome
ndash Timing of CT
ndash Nimodipine reduces death and disability by 55
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
71
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
72
Specific Head Injuries
bull Epidural Hematoma
ndash Occurs in 05 of all head injuries
ndash Blunt trauma to temporoparietal region
ndash Eighty percent with associated skull fracture
ndash May occur with venous sinus tears
ndash Classic presentation only 30 of the time
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
73
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
74
Specific Head Injuries
bull Subdural Hematoma
ndash Sudden acceleration-deceleration injury with tearing of bridging veins
ndash Common in elderly and alcoholics
ndash Classified as acute subacute or chronic
bull Acute lt2 weeks
bull Chronic gt2 weeks
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
75
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
76
Specific Head Injuries
bull Diffuse Axonal Injury
ndash Disruption of axons in white matter and brainstem
ndash Injury occurs immediately and is irreversible
ndash Seen after MVC or shaken baby syndrome
ndash Usually have persistent vegetative state
ndash CT usually normal
ndash MRI with multiple diffuse abnormalities
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
77
Specific Head Injuries
bull Penetrating Injury
ndash Gunshot Wounds
bull Injury due to direct brain injury and cavitary effects
bull GCS predicts prognosis ndash GCS gt8 and reactive pupils = 25 mortality
ndash GCS lt5 = nears 100 mortality
ndash Stab wounds
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
78
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
79
Complications-Long Term Sequela
bull Seizure Disorder
ndash 2 Early post-traumatic incidence
ndash Increased to 30 in children alcoholics and with intracranial hematoma
bull Prophylactic antiepileptics reduce early occurrence
bull Use not supported by the literature
bull Concussion
- Brief LOC - Vertigo - Nausea
- Dizziness - Headache - Vomiting
- Photophobia - CognitiveMemory dysfunction
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
80
Complications-Long Term Sequela
bull Concussion
ndash Up to 80 may have symptoms at 3 months
ndash 15 may have symptoms at 1 year
ndash Persistence of these symptoms is termed Postconcussive Syndrome
ndash 85-90 recover after 1 year
ndash Risk factors
- Female - Litigation - Low socioeconomic status
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
81
81
BRAIN TUMOR
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
82
82
INSIDEN 1 Tumor otak memp 2 puncak pertama usia anak-anak
3-12 tahun puncak kedua 50-70 tahun 2 Dua pertiga terjadi pd anak-anak terletak infra
tentorial berasal dari serebellum batang otak dan mesensefalon
3 Pada orang dewasa terletak supra tentorial dan berasal dari korteks dan hemisfer otak
4 Insiden pd pria hampir sama dg wanita astrositoma gt pd pria sedang meningioma gt pd wanita
5 Di USA 1998 tumor otak primer 34000 170000 tumor otak metastasis Tahun 2003 18300 kasus baru dg kematian 13100 orang
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
83
83
DEFINISI
Tumor otak adalah pertumbuhan jinak atau ganas dari jaringan otak selaputnya yang menyebabkan proses desak ruang dan menyebabkan perubahan patologis Tumor primer (50) dari seluruh tumor otak td glioma 50 meningioma (20) adenoma (15) neurinoma (7) Tumor sekunder (50 ) td tumor metastasis Letak tumor pada dewasa (60) supratentorial pada anak (70) infratentorial
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
84
84
ETIOLOGI TUMOR OTAK (1) Penyebab pasti belum diketahui
1 Bawaan Dijumpai pada anggota keluarga mis meningioma astrositoma neurofibroma
2 Sisa jaringan embrional mengalami degenerasi perubahan neuroplastik mis kraniofaringioma teratoma intra kranium kordoma (berasal dari kantung rathke mesenkim-ektoderma embrional korda dorsalis)
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
85
85
ETIOLOGI TUMOR OTAK (2)
3 Radiasi Dosis subterapi dapat merang sang pertumb sel mesenkim mjd tumor
4 Virus Telah terbukti oleh Burkitt bahwa limfoma pd penduduk Afrika disebabkan oleh infeksi virus
5 Zat karsinogenik Methylcholantrone nitrose- ethyl-urea dpt menyebabkan tumor otak pada percobaan binatang
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
86
86
ISI KRANIUM (1)
1 Isi kranium selalu konstan yaitu otak cairan serebrospinal pembuluh darah dg isinya
2 Otak mikroskopis td NEURON NEUROGLIA (Astrosit fibosa amp protoplasmatis mikroglia oligodendroglia dan sel ependim) MENING PEMBULUH DARAH
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
87
87
ISI KRANIUM (2)
Volume otak 1400 ml cairan LCS 150 ml darah 150 ml
Hukum Monro Kellie total volume dr ketiga komponen selalu konstan
Bila ada kenaikan volume salah satu komponen akan terjadi kompresi komponen lainnya
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
88
88
NEOPLASMA OTAK
NEOPLASMA INTRA - AKSIAL GLIAL GLIOM
ndash Asal parenkim otak neuron neuroglia
ndash Sifat infiltratif
ndash Contoh Astrositoma Ependimoma Meduloblastoma Oligodendroglioma
NEOPLASMA EKSTRA - AKSIAL NON GLIAL
ndash Asal luar otak meningen Hipofisis embrional metas
ndash Sifat ekspansif
ndash Contoh Meningioma neurinoma akus tikus adenoma hipofise kranio paringioma tumor epider moid
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
89
89
I SIGN AND SYMPTOMS OF INCREASED INTRACRANIAL PRESSURE
THREE MAJOR SIGNS
bull HEADACHE
bull VOMITING
bull CHOKED DISK
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
90
90
1HEADACHE
1 A QUARTER OF PATIENTS WITH INCREASED ICP 2 NOT SO SEVERE GENERALLY OCCURS IN THE MORNING EARLY
MORNING HEDACHE 3 MAY BE PULSATILE N BECOME WORSE WITH VOLUNTARY STRAINING 4 MAINLY GENERATED BY THE EXTENSION AND DISPLACEMENT OF OF
SUCH PAIN ndashSENSITIVE TISSUES AS DURAMATER N CEREBRAL VESSELS (TRACTION HEADACHE)
5 GENERALLY THERE IS NO CORRELATION BETWEEN THE SIDE OF HEADACHE N THE LOCATION OF THE TUMOR
6 SUPRATENTORIAL TUMOR FOREHEAD PARASELLAR TUMOR PAIN SPREDING OVER AN ORBIT POSTERIOR FOSSA TUMOR PAIN SPREADING OVER NUCHAL AREA
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
91
91
2VOMITING
1 OCCURS AT THE END OF INTRACRAN HYPERTENSION
2 NOT RELATED TO INGESTION PROJECTILE TYPE
3 AN EARLY N SOLE SYMPTOM IN CASE OF CHILDREN
4 PROBABLY CAUSED BY DIRECT STIMULATION OF THE VAGUS NERVE
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
92
92
3CHOKED DISC (CD) N VISUAL DITURBANCE
1 NOT ALL BT CAUSE CD 2 IF CD IS PRESENT IT IS USUALLY DUE TO A (S O L) SUCH AS
BT 3 CD IS SELDOM SEEN IN INFANTS 4 WHEN ICP INCREASE GRADUALLY THE EDEMA OF THE DISC
MAY NOT BE OBSERVED AND IT WILL BE CONVERTED INTO ATROPHIC STAGE
5 BESIDES DOUBLE VISION MAY OCCUR DUE TO PRESSURE ON THE ABDUCENS NERVE AND THE SIDE OF LESION( FALSE LOCALIZING SIGN)
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
93
93
4ENLARGEMENT OF THE HEAD
WHEN ICP INCREASES THE HEAD USUALLY ENLARGES IN A CHILD LESS THAN 2 YEARS OF AGE WHERE SKULL SUTURES HAVE NOT BEEN CLOSED YET
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
94
94
5NUCHAL RIGIDITY
bull WHEN THE CEREBELLAR TONSIL HERNIATES RIGIDITY WILL BE OBSERVED N THEREFORE IS A DANGEROUS SIGN IN PATIENT WITH INCREASED ICP
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
95
95
6INTELLECTUAL DETERIORATION( ID)
1 ID MAY BE PRESENT WITH INTRACRAN HYPERTENSION
2 INDIFFERENCE N APATHY ARE OBSERVED
3 NEXT MENTAL N PHYSICAL FATIQUE
4 FOLLOWED BY MEMORY DISTURBANCE
5 FINALLY AROUSAL DIORDER RESULTING IN GENERALIZED CONSCIOUSNESS DISTURBANCE
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
96
96
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
97
97
7SIGN N SYMPTOMS OF TRANSTENTORIAL HERNIATION (TTH)
1 FOUND IN BT GENERALLY PRESENT DISTANT SYNDROME ( PLUM amp POSNERrsquoS CENTRAL SYNDROME)
2 COURSE 0F WORSENING FROM ROSTRAL TO CAUDAL DIRECTIO BY TTH( DISTANT SYNDROME)
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
98
98
MANIFESTASI KLINIK TUMOR OTAK (1)
1 Tanda amp gejala lokalisatorik yg benar Dasar Bagian otak ttt punya fungsi ttt Bila ada ggnndashfs ttt pasti ada ggn organik pd otak ttt Tanda-gejala ini sering luput pengamatan luput dihargai setelah ada proses desak ruang baru disadari
2 Gejala ini timbul sebelum ada manifestasi TIK meninggi mis monoparesishemiparesis hemianopsia anosmia
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
99
99
MANIFESTASI KLINIK TUMOR OTAK (2)
3 Gejala dan tanda lokalisatorik yang menyesatkan Tak sesuai dengan ggnndashfs bagian otak di mana tumor berada Misal - kelumpuhan N III IV VI
- refleks pathologis ke-2 sisi
- gangguan mental
- gangguan endokrin
- encephalomalasia
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
100
100
MANIFESTASI KLINIK TUMOR OTAK (3)
4 Tanda dan gejala akibat TIK meninggi Misal gangguan kesadaran sefalgia muntah kejang gangguan mental rasa abnormal papiledema pembesaran kepala anak bradikardi-tensi meninggi gangguan irama napas dll
Gejala umum ini terjadi akibat langsung dari masa tumor edema otak atau obstruksi LCS
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
101
101
MANIFESTASI KLINIK TUMOR OTAK (4)
Tanda ndashtanda fisik diagnostik
bull Papil edema
bull Pembesaran kepala anak dgn pelebaran sutura
bull Hipertensi yang progresif sbg mekanisme kompensasi bradikardi
bull Irama amp frekuensi pernapasan yg berubah
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
102
102
MANIFESTASI KLINIK TUMOR OTAK (5)
GANGGUAN KESADARAN Akibat tekanan intrakranial meninggi timbul ancaman herniasi otak dgn akibat penurunan kesadaran Misalnya Sindroma unkus atau kompresi diensephalon ke lateral sindroma kompresi sentro rostrokaodal thd BO herniasi otak kecil ke foramen magnum Keadaan ini menyebabkan kegawatdaruratan medik
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
103
103
DIAGNOSIS TUMOR OTAK (1)
ANAMNESIS
bull Keluhan yang sifatnya kronis-progresif
bull Misalnya Nyeri kepala mlm hebat dlm bbrp minggu bulan
bull Atau nyeri kepala kemudian diikuti defisit neurologik yang lain Misal gangguan motorik sensorik sensibel
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
104
104
DIAGNOSIS TUMOR OTAK (2)
INGAT GEJALA UMUM
1 Sefalgiaberdenyut terasa pagi hari meningkat bila mengejan batuk atau angkat berat
2 Muntah pagi hari tak bhb dg makanan sifatnya proyektil
3 Kejang fokal umum tumor dekat girus pre sentralis
4 Perubahan mental demensia apatis gangg berpikir dan daya ingat
5 Papiledema dgn pem funduskopi
6 Pembesaran kepala anak
7 Bradikardi dan hipertensi
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
105
105
DIAGNOSIS TUMOR OTAK (3)
INGAT SINDROM FOKAL LOKALISATORIK
bull Lobus Frontalis sefalgia amp gangguan mental bull Lobus Temporalis tinitus halusinasi auditorikafasi
sensorik bull Daerah Pre Sentralis kejang dan hemiparesis kontralateral bull Lobus Parietalis gangg sensibilitas
asteriognosia (tak mampu mengenal barang yang dipegang)
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
106
106
DIAGNOSIS TUMOR OTAK (4)
INGAT SINDROM FOKAL
bull Lobus Oksipitalis sefalgia gangguan medan penglihatan agnosia visual
bull Serebelum ataksia disdiadokokinesis dismetri rebound phenomen disartri
bull Batang Otak gangguan kesadaran amp gangguan saraf spinal
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin
21032013
107
107
DIAGNOSIS TUMOR OTAK (5)
INGAT TANDA2 LOKALISATORIK YG MENYESATKAN
bull Kelumpuhan N III IV VI
bull Refleks patologis positif
bull Gangguan mental lt demensia dll
bull Gangguan endokrin