the skull the brain’s protector made of 8 irregularly fused bones smooth on the outside, folds and...

The Skull The brains protector

Made of 8 irregularly fused bones Smooth on the outside, folds and ridges on the inner surface THE SKULL

The Cranial Vault

Foramen magnum

The Brain (80%)

Increased Brain Volume Mass Cerebral Swelling

Blood (10%) Normally about 750cc of circulating volume 20% of the Cardiac Output

Increased Blood Volume Hemorrhage Vasodilatation

Cerebrospinal Fluid (10%)

Hydrocephalus Increased CSF Volume

Intracranial Pressure (ICP) The pressure exerted by the brain tissue, intracranial blood, & CSF

Tough Mother

Dura Mater Double layered Inelastic, fibrous membrane Holds the brain in place

Epidural Space Space that is directly above the Dura Middle Meningeal Artery is present here

Cerebral lobes

MovementImpulses Frontal lobe

Spoken Language Personality Frontal lobe

Sight UnderstandingTouch Understanding Parietal lobe

Distance and Position to Objects Parietal lobe

Temporal lobe Memory Hearing Written Words

Damage Causes Ipsilateral Movement

Pons Mid Brain Medulla Oblongata

ABCs First Quick History LOC Vital Signs Pupils Early or Late? Early: restlessness, disorientation, lethargy Late: Increase BP, pupillary changes, seizures Down and Dirty

Assessment GLASGOW COMA SCALE Best Eye Opening Best Verbal Response Best Motor Response

Best Eye Opening Spontaneously-4 To Verbal Command-3 To Pain-2 No Response-1

Best Verbal Response Oriented, Converses-5 Disoriented, Converses-4 Inappropriate words-3 Incomprehensible sounds-2 No Response-1

Best Motor Response Obeys Commands-6 To Pain Localizes Pain-5 Flexion Withdrawal-4 Abnormal Flexion-3 Abnormal Extension-2 No Response-1

Glasgow Coma Scale Pediatrics Verbal (2 to 5 years) Appropriate words or -5 Inappropriate words-4 Persistent cries and/or screams-3

Glasgow Coma Scale Pediatrics Verbal (0 to 23 months) Smiles or coos appropriately-5 Cries and consolable-4 Persistent inappropriate crying and / or screaming-3

Mild GCS Score 14-15 Moderate GSC Score 9-13 Severe GCS Score 3-8 Severity of Injury

A desk scores a 3

Loss of Consciousness A,E,I,O,U TIPS A Alcohol E Epilepsy I Insulin (too much, too little) O Oxygen (too much, too little) U Uremia or other metabolic issues T Trauma, toxicity, tumors, thermoregulation I Infections, ischemia P Psychiatric, poisonings S Stroke, syncope or other neurologic / cardiovascular causes

Babinskis Reflex Present when stroking of Planter surface of foot causes Flexing of great toe Fanning of other toes Normally present in children 2yo indicates problem in corticospinal tract (nerve path spine to brain)

Abnormal posturing is a late sign of increasing ICP Decorticate Abnormal flexion Decerebrate Abnormal extension

Meningeal Signs Nuchal rigidity Stiff neck, pain on flexion Photophobia Positive Brudzinskis Involuntary flexion of knees/hips when neck flexed Positive Kernigs Unable to straighten leg when hip fully flexed in supine patient

Increased Intracranial Pressure

Intracranial Pressure Intracranial pressure reflects Brain Cerebrospinal fluid Blood As intracranial pressure increases, cerebral perfusion pressure decreases Leads to cerebral ischemia and hypoxia In a hypotensive patient, even a marginally elevated ICP can be harmful Adequacy of cerebral perfusion pressure is most important

Increased Intracranial Pressure Initially -intracranial volume increases- ICP remains stable. System becomes less compliant, or less able to tolerate increases in volume Later, intracranial volume conts to increase, less compliance will be unable to buffer the increases and ICP will rise

Increased Intracranial Pressure Assessment Early picture of increased intracranial pressure (IICP) LOC Loss of insight Loss of recent memory Restless, irritable, uncooperative behavior Requires more stimulation to get same response Speech less distinct Sudden quietness in a very restless patient

Increased Intracranial Pressure Early Increasing ICP Motor function Usually contralateral to lesion Pronator drift Loss of one or more grades on the strength scale Increased tone

Increased Intracranial Pressure Early Increasing ICP Pupils Sluggish to light response Usually unilateral Ipsilateral to lesion Papilledema or bulging of optic discs Blurred vision

Increased Intracranial Pressure Early Increasing ICP Vital signs Occasionally tachycardic Occasional hypertensive swings

Increased Intracranial Pressure Late Increasing ICP LOC Arousable only with deep pain Unarousable Motor function Dense hemiparesis Abnormal flexion Abnormal extension No response (flaccidity preliminary to death)

Abnormal posturing is a late sign of increasing ICP Decorticate Abnormal flexion Decerebrate Abnormal extension

Increased Intracranial Pressure Decreased LOC Motor Dysfunctions Pupillary abnormalities Impaired Reflexes Changes in Vital Signs Irregular respirations Sign & Symptoms- Impending Herniation

Increased Intracranial Pressure Late Signs Increasing ICP Vital signs Cushings triad Very late sign of increasing ICP, last ditch effort to perfuse brain Elevated SBP Bradycardia Widening pulse pressure

Increased Intracranial Pressure Interventions ABCs Mechanically decrease ICP Oxygenate Osmotic Agents

Increased Intracranial Pressure Osmotic Agents Mannitol: reduces ICP within 15 minutes with continued effectiveness for 2-3 hours Monitor serum osmolarity

Increased Intracranial Pressure Treatment of ICP Easiest to manipulate is BP and CSF proper head alignment sedation Surgery

Goal Keep SBP>90

Traumatic Brain Injury Injury to skull, brain, or both that is of enough magnitude to interfere with normal neurological function

Nearly 2 million people sustain head injuries each year

70,000 die prior to hospitalization

TBI Another 25,000 die following hospitalization

90,000 people will have significant permanent neurological disabilities for the rest of their lives

Traumatic Brain Injury The peak age for neurotrama is 15 to 30 years of age

Causes of TBI

Concussion Transient impairment of neurological function caused by a mechanical force Rapid acceleration-deceleration if repeated can produce a permanent deterioration in intellect recent studies suggest long term impairment even with moderateconcussion moderate if loss of consciousness

Concussion Diagnosis CT scan Rule out other injury Clinical picture History of injury

Concussion Interventions Assess neuro status Patient/Family education return to facility Change in LOC Change in pupils Projectile vomiting Seizure Inability to arouse

Interventions Educate patient/family Post concussion syndrome H/A Dizziness (positional) Tinnitus Inability to concentrate Personality change Memory disturbances

Interventions Educate patient/family Post concussion syndrome Duration Days to years Social/occupational Difficulty school/work

Diastatic Skull Fractures Fracture along suture line Often seen in children

Depressed Skull Fracture A break in a cranial bone (or "crushed" portion of skull) with depression of the bone in toward the brain May require surgical elevation

Compound Skull Fracture A break in or loss of skin and splintering of the bone.

Basilar Skull Fracture A Fracture that occurs somewhere in the Cranial Vault

Basal Skull Fractures Periorbital ecchymosis (Raccoon sign) Anterior fracture

Basal Skull fracture Retroauricular ecchymosis (Battles sign) --Posterior fracture Blood behind tympanic membrane --Middle Fracture

Basilar Fractures contd If Basilar skull fracture suspected NO nasal intubation NO nasal gastric tubes

Basal Skull Fractures CSF leaks -rhinorrhea (nose) -otorrhea (ear) Tests for CSF: Positve glucose Positive Halo

Basal Skull Fracture VIIth (Facial) Nerve Palsy Occur immediately Occur a few days after initial injury

Cerebral Contusion Cerebral contusions fairly common Mostly occur in frontal and temporal lobes Bruising of the brain tissue without puncture of pia Petechial hemorrhages Extravasation of fluid from vessels

Cerebral Contusion Distinction between contusion and traumatic intracerebral hematoma ill defined. Contusions, can evolve into an intracerebral hematoma

Cerebral Contusion Blunt force High velocity Low velocity

Cerebral Contusion Intervention Decrease ICP Mannitol to decrease water content in brain Increase venous outflow Discuss with family/patient evolution of contusion and need for monitoring Discuss bizarre behavior- frontal lobe Assist family in understanding a contusion to brain stem has injured awake center in brain

Epidural Hematoma Located outside the dura, within the skull Biconvex or lenticular in shape Mostly located in temporal or temporoparietal region

Epidural Hematoma Result from tearing of middle meningeal artery D/T fracture Bleeds arterial in origin Does not tamponade 50% mortality

Epidural Hematoma Brief loss of consciousness followed by lucid interval then rapidly progressive deterioration Talk and die

Epidural Hematoma Bleeding can rapidly become mass lesion Cause IICP Brain shift Uncal herniation

Subdural Hematoma More common than epidural hematomas 30% of severe head injuries Tearing of bridging vein between cerebral cortex and a draining venous sinus

Subdural Hematoma Cover entire surface of hemisphere

Subdural Hematoma Presentation can be Acute < 48 hours Subacute 2 days to 3 weeks More frequent in elderly Chronic > 3 weeks

Subdural Hematoma Clinical findings range from headache with nausea to comatose and flaccid

Subdural Hematoma Non-contrast CT scan Crescent shaped mass Ancillary tests CBC Chemistry Coag studies T&C

Subdural Hematoma Interventions Acute Decrease ICP Nonacute Burr holes

Subarachnoid Hemorrhage/Aneurysm rupture worst h/a of my life Aneurysms result from thinning vascular wall Precipitated by hypertensive event Straining Sex Heavy lifting

Subarachnoid Hemorrhage/Aneurysm rupture After rupture vessel clamps down to prevent further bleeding Result in Ischemia/infarction Blood in subarachnoid space is irritant Meningeal signs

Subarachnoid Hemorrhage/Aneurysm rupture Complications Increased ICP Vasospasm Rebleeding Ischemia Infarction Hydrocephalus

Subarachnoid Hemorrhage/Aneurysm rupture Interventions ABCs Monitor neuro status Fluids within normal range avoid dehydration increases hemoconcentration, increases vasospasm Monitor sodium usually falls Normotensive BP until clipped then can be elevated

Penetrating/ Perforating Injuries A foreign object penetrates into the skull and brain

Perforating & Penetrating Trauma PerforatingPenetrating

Causes of Secondary Injury Hypoxia

Causes of Secondary Injury Hypotension

Causes of Secondary Injury Cerebral edema 1.Cerebrum 2. Skull 3. Cerebellum 4. Herniation of Brain Into Spinal Column

Causes of Secondary Injury Sustained hypertension

Causes of Secondary Injury Hypercapnia

Causes of Secondary Injury Seizures

Causes of Secondary Injury Vasospasm

Causes of Secondary Injury Metabolic abnormalities (hypoglycemia)

Causes of Secondary Injury Ischemia (#1 cause) Normal Ischemic

MAP & ICP GO HAND IN HAND MAP= Diastolic x2 Plus Systolic Divide that by 3 ICP= The Brain The CSF The Blood

Cerebral Perfusion Pressure (CPP) Pressure required to maintain adequate perfusion to cerebral tissues MAP ICP = CPP Normal: 70-100 mmHg

CPP < 50 mmHg Results in Ischemia

Spinal Cord Injuries Involve bruising or tearing of spinal cord substance from penetrating trauma or a fracture/dislocation of spinal column 15-35 year olds Usually due to trauma

Spinal Cord Injuries Mechanism of Injury Axial loading Hyperflexion Hyperextension Injury may involve only Spinal cord Vertebral body Both

Spinal Cord Injuries Damage to cord From extrinsic(bony and soft tissue injury) From intrinsic (hemorrhage, edema, hypoxia, biochemical changes

Spinal Cord Injuries Classification Complete Transection of the cord, no preservation of motor or sensory function Incomplete Some cord sparing

Spinal Cord Injuries Respiratory Complications Phrenic nerve innervates diaphragm, exits cervical cord at C-3, C-4, C-5 if involved diaphragm involved Compromises ability to breath Intercostal muscles (T-1 to T-12) involved becomes difficult to deep breath, cough

Neurogenic Shock Eliminates the fight or flight protective response and permits the parasympathetic system to function unopposed Results in vasodilation below level of the injury, pooling of blood, decreased venous return to the heart, and decreased cardiac output

Neurogenic Shock Loss of ability to sweat Below level of injury D/T lack of innervation of sweat glands Temperature lower than normal D/T break in connection between hypothalamus and sympathetic nervous system Loss of body heat by passively dilated vascular bed of skin

Neurogenic Shock Blood pressure may not be restored by fluids alone In trying to normalize BP may cause fluid overload, pulmonary edema BP best restored by judicious use of vasopressors May perfuse adequately without normal BP

Intravenous Fluids Quadriplegic patients-may fail to become tachycardic or may even become bradycardic in the presence of shock- due to loss of cardiac sympathetic tone.

Intravenous Fluids Hypovolemic Shock Patient usually presents with tachycardia Neurogenic Shock Patient usually presents with bradycardia Overzealous fluids may cause PULMONARY EDEMA in Spinal Cord Injury Patients If blood pressure does not improve after fluid challenge, judicious use of vasopressors, may be indicated

Neurogenic Shock Orthostatic Hypotension Rapid drop in BP when vertical position assumed. Blood supply to brain inadequate, syncope results. (brain damage and death can result) D/T loss of arteriole vasomotor tone below level of lesion so there is pooling of blood in abdomen and LEs when upright. Seen in patients with lesions above T-7

Spinal Cord Injuries Interventions ABCs Cervical Spine Immobilization O2 Monitor VS, CO2 Mechanical ventilation if needed Monitor LOC, UOP Enhance venous return to the heart Interventions Support BP if needed Atropine if needed Methylprednisolone NG tube Foley Attempt to have someone with patient most of the time

Autonomic Hyperreflexia Noxious stimuli produces sympathetic discharge that causes reflex vasoconstriction of blood vessels in skin and visceral bed below level of the injury Vasoconstriction of visceral bed distends baroreceptors in the carotid sinus and aortic arch, body attempts to lower hypertension by superficial dilation of vessels above level of injury

Autonomic Hyperreflexia As spinal shock reverses, potential for dysreflexia should be considered in patients with injuries T-6 or above Nursing intervention prevent conditions that are know to trigger autonomic hyperreflexia Causative noxious stimulus most common Distended bladder d/t kinked drainage tube

Autonomic Hyperreflexia Clinically Sudden hypertension 240/120 Pounding headache Anxious Flushed face, neck, upper chest moistened with perspiration Blurred vision Nasal congestion Nausea Lower extremities goose flesh, cold

Autonomic Hyperreflexia Interventions Elevate HOB Relieve trigger mechanism Treat hypertension as needed Resources for family/patient for self care

Headaches Occur when there is traction, pressure, displacement, inflammation or dilation of pain receptors in brain or surrounding tissues Two types: Primary No organic cause consistently identified (migraines, cluster, tension) Secondary Organic etiology (tumor, aneurysm, meningitis, temporal arteritis)

Headaches Affects up to 75% population per year 5% will seek treatment 50 % of people with headache suffer migraine Mechanism unknown Blood vessels that supply brain and surrounding tissue narrow, reduced blood flow, followed by reflex vasodilatation, swelling, and inflammation of cerebral blood vessels

Headaches Assessment Hx of present illness Time frame onset (migraines early morning) Occurrence (in groups, then period of remission) Aura (migraines with/without aura) Duration (tension 7 days, migraine 4-72 hours)

Headaches Pain Character and quality Intensity Therapeutic measures implemented Success of therapeutic measures Location Unilateral (migraine), bilateral (tension), hatband

Headache Symptoms with migraines Aura possible without aura most common Nausea/vomiting Photophobia Difficulty concentrating Visual changes May see neurodeficits in complicated migraine

Headache Cluster Headaches Burning, sharp, severe unilateral orbital or temporal pain Photophobia Tearing, nasal congestion on affected side May have lid edema, red eye on affected side. Usually lasts < 1 hour, but may have multiple per day

Headaches Tension Dull, nonpulsating pain No photophobia, aura Usually starts at occiput and moves around bilaterally to frontal area (band like)

Headaches Precipitating event Emotional (stress/depression) Metabolic (fever/menses) Flickering lights/television Alcohol abuse/withdrawal Food Fatigue or altered sleep wake cycle

Headaches Physical Exam Neuro exam Edema over the sinuses Distended, twitching scalp vessels Flushed, pale, or shiny skin

Headaches Diagnostic procedures (organic) Skull x-rays CT scan

Headaches Interventions/Planning Physical measures Heat (muscular) or cold (vascular) Darkened room Massage Psychological measures Stress mgt Relaxation techniques Behavior modification

Headaches Interventions Pharmacological measures Preventive drugs Vasoconstrictor agents Beta blockers Anticonvulsants Analgesics Oxygen

What Is Stroke ? A stroke occurs when blood flow to the brain is interrupted by a blocked or burst blood vessel.

What Is the Impact of Stroke? Stroke is the third leading cause of death in the United States On average, someone suffers a stroke every 53 seconds About 600,000 Americans suffer strokes each year Every 3.3 minutes, someone dies of a stroke Stroke is the third leading cause of death in the United States On average, someone suffers a stroke every 53 seconds About 600,000 Americans suffer strokes each year Every 3.3 minutes, someone dies of a stroke

What Is the Impact of Stroke? n Stroke is a leading cause of serious, long-term disability n About 4 million Americans are stroke survivors n Stroke costs the U.S. $30 to $40 billion a year n Stroke is a leading cause of serious, long-term disability n About 4 million Americans are stroke survivors n Stroke costs the U.S. $30 to $40 billion a year

Stroke Clinical syndrome consisting of a neurological deficit resulting from an interuption of blood flow to an area of the brain, rapid or gradual in onset, which persists for more than 24 hours. Two types Ischemic: Thrombotic or embolic occlusion of a cerebral artery resulting in infarction Hemorrhagic: Spontaneous rupture of a vessel resulting in intracerebral or subarachnoid hemorrhage

Stroke Assessment Hx present illness (time pattern) Classifications of stroke: TIA brief, lasting seconds to hours; < 24 hrs RIND lasting 48 hours or less, complete resolution of deficit, reversible ischemic neuro deficit Stroke in evolution/progressive Symptoms last >24 hrs with progressive neurologic deterioration. Completed stroke permanent neurologic damage

Stroke Medical History Diabetes Rheumatic heart disease Recent MI CHF Migraines Hypertension A-Fib

Stroke Physical Exam Anterior Circulation Alteration in LOC Motor deficit Contralateral hemiparesis, hemiplegia Sensory deficit Contralateral

Stroke Physical Exam Anterior Circulation Speech deficit Dysphasia Expressive or receptive Dominant hemisphere Visual deficit Loss of vision in half of the visual field on same side

Stroke Physical Exam Posterior Circulation (vertebral basilar) Alteration in LOC Motor deficit more than one limb

Stroke Physical Exam Cranial nerve deficit Dysphonia difficulty producing voice sounds Dysarthria difficulty in articulation Dysphagia difficulty in swallowing

Stroke Physical Exam Posterior Circulation (vertebral basilar) Visual deficits field defects, cortical blindness diplopia Loss of coordination Ataxia

Stroke Ischemic Sudden, rapid onset Occurs at sleep, rest Hemorrhagic Severe headache More gradual onset Symptoms of increasing ICP Occurs during activity

Stroke Interventions Maintain airway, breathing, circulation Monitor neuro status for change Maintain venous outflow (head neutral position) Frequently monitor Cerebral function LOC Blood pressure

Stroke Interventions Supplemental oxygen, pulse oximetry RSI: sedation, neuromuscular blockers, analgesics Initiate measures to normalize blood pressure Keep SBP < 180, DBP

the skull the brain’s protector made of 8 irregularly fused bones smooth on the outside, folds and...

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parietal lobe slide

tough mother slide

ipsilateral movement

cranial vault slide