bimbingan ukmppd (ukdi) - anestesi-bedah
TRANSCRIPT
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BIMBEL UKDI MANTAPdr. Andreas W Wicaksono
dr. Anindya K Zahradr. Arius Suwondo
dr. M. Dzulfikar Lingga Q M
dr. Marika Suwondo
Anesthesiology
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Algorhythm
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Patient Assesment
• Level of consciousness
• Spontaneous effort vs apneu
• Airway and cervical spine injury
• Chest expansion
• Sign of airway obstruction
• Signs of respiratorry distress
• Protective airway reflexes
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Airway and C – Spine control
Problem Airway
Trauma Maksilofasial
Trauma Leher
Trauma Laryngeal
Pasien Berbicara Lancar ‐>
airway baik
Look : Agitasi, penkes,
retraksi, otot bantu nafas
Listen : suara nafas abnormal
Feel : lokasi trakea
Adakah patensi jalan
nafas ?
•liquid or semisolid foreign material in the main airway ‐> SuctioningGurgling
•pharyng is partially occluded by soft palate or epiglottis.
Snoring•sound of laryngeal spasm.Crowing
•obsruction at laryngeal level or above.Inspiratory stridor
•obstruction of the lower airway.Expiratory wheeze
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Pengelolaan Jalan Nafas
Oksigenasi dan pasang pulse oxymetri
Chin– lift manuver atau jaw – trust manuver (pada
curiga C‐spine terganggu ‐> dipertahankan dengan
nasofaringeal airway atau orofaringeal airway
Bersihkan jalan nafas dari corpal, suctioning
Dapat teroksigenasi Definitif airway
surgicalNO
Assess airway anatomy ‐>
LEMON Difficult
Call assistance
or Awake
intubationIntubation – drug – assistanceCricoid pressure
unsuccesfull
Consider adjunct ‐> GEB/LMA/LTA
Definitif arway
surgical
NPA
OPA
Intubation
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Opening the Airway – Triple AirwayManeuver
• Slightly extend neck
(when cervival spine
injury not suspected)• Elevated mandible
• Open mouth
Head Position
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Oropharingeal Airway
• Digunakan untuk ventilasi sementara pada pasien yang tidaksadar sementara intubasi pasien sedang disiapkan
• Tidak boleh digunakan pada pasien yang sadar karena dapatmenyebabkan sumbatan, muntah dan aspirasi.
Nasopharingeal Airway
• Prosedur ini digunakan apabila pasien terangsang untukmuntah pada penggunaan OPA
Laryngeal Mask Airway
• Digunakan untuk pertolongan dengan airway yang sulit untukintubasi endotracheal atau bag mask gagal. Ingat LMA bukandefinitif
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Laryngeal Tube Airway
• Suatu alat airway diluar glotis untuk memberi ventilasi pasiendengan baik.
Gum Elatic Bougie
• Diikenal dengan nama Eschmann tracheal tube introducer(ETTI)
Multilumen Esophageal Airway
• Dapat dihunakan apabila airway definit belum dapatdilakukan.
• Alat ini memiliki lubang udara yang mengarah ke salurannafas . Sedangkan lubang lain mengarah ke esofagus.
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Airway definitif
Kebutuhan Untuk PERLINDUNGANAIRWAY
Kebutuhan Untuk VENTILASI
Penurunan Kesadaran (GCS < 9) Apneu :
‐Paralisis neuromuscular
‐Tidak sadar
Fraktur Maxilofacial berat Usaha Nafas tidak adekuat
‐Takipneu
‐Hipoksia
‐Hiperkarbia
‐Sianosis
Resiko Aspirasi : Perdarahan, muntah
muntah
Cedera kpala tertutup berat yang
membutuhkan hiperventilasi
Resiko Sumbatan : Hematoma leher,
cedera laring, trachea, stridor
Kehilangan darah yang masif dan
memerlukan resusitasi volume
Orotracheal Tube
Nasotracheal Tube
Airway surgical :
Krikotiroidotomi
Trakheostomi
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Nasotracheal intubation
Cricothyroidotomy Tracheostomy
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Bronchus Primarius
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• Apply face mask – Oro/naso‐pharyngeal
airway adjuncts
– Mouth opening – Hand positioning
• Elevate mandible and chin
• Resuscitation bagcompression – volume andfrequency
• Apply face mask – Oro/naso‐pharyngeal
airway adjuncts
– Mouth opening – Hand positioning
• Elevate mandible and chin
• Resuscitation bagcompression – volume andfrequency
Manual Assisted Ventilation
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Single‐Hand Method of FacemaskApplication
• Base of mask placedover chin and mouthopened
• Apex of mask overnose
• Mandible elevated,
neck hyperextend (nocervical injury), anddownward pressure bymask hand
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Two‐Hand Method of FacemaskApplication
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Inadequate Mask‐to‐Face SealInadequate Mask‐to‐Face Seal
• Identify leak• Reposition face mask
• Improve seal along
cheeks• Slightly increase
downward pressure over
face or neck extension ifno cervical injury
• Use two hand technique
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TemporoMandibular Joint Dislocation
(Locked Jaw)
Type :
• Anterior• Posterior
• Superior
Unilateral /
Bilateral
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The patient is unable to close the mouth and may have garbled speech,
drooling and in pain .
A depression may be noted in the preauricular area. Palpation of the TMJ
reveals one or both of the condyles trapped in front of the articular eminence
and spasm of the muscles of mastication.
In addition, the coronoid process of the mandible becomes prominent and
palpable just below the maxilla
Treatment depends on
patient status and varies
from simple reduction to
surgical intervention.
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Manual closed Reduction (Classic)
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Barton bandage
• Application of a Barton bandage
after reduction.
• Apply warm compresses to the TMJ
area for 24 hours• Avoid extreme opening of the jaw
for three weeks. In some patients,
placement of a padded rigid cervical
collar.
• Support the lower jaw when
yawning.
• Maintain a soft diet for one week.
• Take nonsteroidal anti‐inflammatory
agents (eg ibuprofen 10 mg/kg orally
every six hours as needed, maximum
single dose : 800 mg) as needed for
pain and swelling.
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Brain Death
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Shock – DefinitionA physiological state characterized by a
significant, systemic reduction in tissueperfusion, resulting in decreased tissue oxygen
delivery and insufficient removal of cellular
metabolic products, resulting in tissue injury.
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Classification of Shock
HypovolemicHypovolemic CardiogenicCardiogenic
ObstructiveObstructive DistributiveDistributive
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Pathophysiology• BP = CO x R
• CO = SV x HR
• SV components = Preload, Afterload,
Contractility
• DO2 = CO x CaO2
• CaO2= (Hb x sat x 1.34) + (PaO2 x 0.003)
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Pathophysiology
Shock CO SVR
Hipovolemik
(termasuk perdarahan)
(preload dan
afterload)
sebagai
kompensasi
Kardiogenik (kontraktilitas) sebagai
kompensasi
Distributif
(termasuk anafilaktik,
septik, neurogenik/
spinal)
sebagai
kompensasi
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Characteristics of Shock
End organdysfunction:
reduced urine
output
altered mentalstatus
poor peripheralperfusion
Metabolicdysfunction:
acidosis
altered metabolicdemands
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HYPOVOLEMIC SHOCK
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Perkiraan Kehilangan DarahKelas I Kelas II Kelas III Kelas IV
Kehilangan darah
(mL)*
2000
Kehilangan darah
(% volume darah)
40%
Nadi 100 >120 >140
Tekanan darah Normal Normal Menurun Menurun
Tekanan nadi Normal atau naik Menurun Menurun Menurun
Frekuensi nafas 14‐20 20‐30 30‐40 >35
Produksi urin
(ml/jam)
>30 20‐30 5‐15 Tidak berarti
Status mental Sedikit cemas Agak cemas Cemas, bingung Bingung, letargis
Penggantian
cairan
Kristaloid Kristaloid Kristaloid dan
darah
Kristaloid dan
darah
*) untuk laki‐laki dengan berat badan 70kg
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Estimated Blood Volume (EBV)• Laki –laki = 75 cc/kgBB (70‐75 cc/KgBB)
• Perempuan = 65 cc/kgBB
• Infant = 80 cc/kgBB
• Neonatus = 85 cc/kgBB• Premature neonatus = 96 cc/kgBB
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Therapy ‐ HypovolemicPRINSIP TERAPI : CAIRAN
TUJUAN• VOL. INTRAVASKULER TERCUKUPI
• KOREKSI ASIDOSIS METABOLIK
• OBATI PENYEBAB
REASSES PERFUSI, UO, TANDA VITAL
PILIHAN :
• KRISTALOID ISOTONIK : 20 CC/KG SCR CEPAT BILA FUNGSIJANTUNG NORMAL
• NS DAPAT MENYEBABKAN ASIDOSIS HIPERCHLOREMIK
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IV fluidsCrystalloid solutions (isotonic)
• Both 0.9% saline and RL are equally effective
• RL may be preferred in hemorrhagic shock because itsomewhat minimizes acidosis and will not causehyperchloremia.
• For patients with acute brain injury, 0.9% saline is preferred.
Colloid solutions (eg, HES, albumin, dextrans)
• also effective for volume replacement during major
hemorrhage.• offer NO major advantage over crystalloid solutions, and
albumin has been associated with poorer outcomes in patientswith traumatic brain injury.
Sumber: Merck Manuals
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IV Fluids Composition
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n point n onitoring
M
The actual end point of fluid therapy in shock is normalization
of DO2
Adequate end‐organ perfusion is best indicated by urineoutput of > 0.5 to 1 mL/kg/h
Central Venous Pressure
• is the pressure in the superior vena cava, reflecting right ventricular end‐
diastolic pressure or preload.
• Normal CVP: 2 to 7 mm Hg (3 to 9 cm H2O)
• CVP > 12 to 15 mm Hg : fluid administration risks fluid overload
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CARDIOGENIC SHOCK
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Therapy ‐ Cardiogenic
• Terapi Inisial Dg. Pemberian Cairan
• Bila Tak Ada Perbaikan→ memburuk → susp.
Syok Kardiogenik Inotropik
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zdvnk
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DISTRIBUTIVE SHOCK
Anaphylactic – Septic – Neurogenic
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Distributive Shock• Inflammatory mediators disruption of cellular
metabolism peripheral vasodilationdecreased PVR
• Etiology
– Anaphylaxis
– Septic
– Neurogenic
• Sign & symptoms
– Febrile, tachycardia, clear lungs, warm extremities,flat neck veins, oliguria
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Anaphylactic ShockAnaphylactic shock
• a type of distributive shock, which involves the immune system(Hurst, 2008)
Type 1 hypersensitivity
• antigen binds to IgE antibodies on mast cells, which leads todegranulation of the mast cells
Sign & symptoms
• itching, hives, and swelling
• circulatory collapse (vasodilatation)
• suffocation (bronchial and tracheal swelling)
Hipersensitivity reactions
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Figure 12‐2
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Neurogenic Shock
Neurogenic shock is the rarest form of shock.
It is caused bytrauma to the spinal cord
sudden lossof autonomic and motor reflexes below the injury level
Stimulation by sympathetic nervous system (‐) the vesselwalls relax uncontrollably sudden decrease in peripheralvascular resistance vasodilation and hypotension
Gambar 4. Patofisiologi spinal shock
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Septic Shock Tx• O2
• Antibiotics• Fluids
• Vasopressor
– Indication: persistent hypotension* once
adequate intravascular volume expansion has
been achieved
– DOC: NOREPINEPHRINE
*systolic blood pressure
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OBSTRUCTIVE SHOCK
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Obstructive ShockCO↓akibat OBSTRUKSI FISIK terhadap ALIRAN DARAH
KOMPENSASI →SVR ↑
PENYEBAB :
• TAMPONADE PERIKARD• TENSION PNEUMOTHORAX
• CRITICAL COARCTASIO AORTA
• STENOSIS AORTA
TERAPI
• CAIRAN
• ATASI PENYEBAB
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START
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STARTSimple Triage and Rapid Treatment
• TRIASE
– proses pemilihan pasien berdasarkan beratnya kondisi
pasien
• Terdiri dari 4 prioritas penanganan:
– Merah immediate care/life‐threatening
– Kuning urgent care/can delay up to 1 hour
– Hijau delayed care/can delay up to 3 hours
– Hitam dead/no care required
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RPMrespirasi, perfusi, mental
‐ Semua proses evaluasi
dalam START harus
dilakukan dalam waktu
kurang dari 60 detik.
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Keterangan: angka normal analisis gas darah (arteri): pH: 7,35-7,45 ; PCO2: 35-45 mmHg ; HCO3: 22-26 mmol/L.
Gangguan Asam Basa
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Gangguan asam
basa
pH PCO2 HCO3 Penyebab umum
Asidosis respiratorik jikaterkompensasi
PPOK, asma, ARDS
Alkalosis respiratorik jika
terkompensasi
Hiperventilasi,
sepsis
Asidosis metabolik
jikaterkompensasi
Dehidrasi berat,
DM, gagal ginjal,
starving, Diare
Alkalosis metabolik jika
terkompensasi
Muntah
Gangguan Asam Basa
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Tanda
Terkompensasi(sebagian/sepe
nuhnya)
ditandai dgn
ARAH panah
yang SAMAAntara PaCO2
dengan HCO3
CO Poisoning
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Cyanide Poisoning
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y g
• Naturally in foods (some fruits, lima beans, SINGKONG)
• Cyanide salts used in industry• Produced in smoke of burning plastics/synthetics, electroplating,
metal polishing
Sources
• Inhibits cellular respiration
• Tissue cannot utilize O2
• “Arterialization” of venous blood
Mechanism
• Smells like “almonds”
Characteristics
Cyanide inhibit cellular respiration
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Clinical Effects of Cyanide• Headache • Hypertension,
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• Dizziness
• Seizures
• Coma
CNS
yp ,
bradycardia
• Hypotension, later incourse
• Cardiovascularcollapse
Cardiovascular
• Dyspnea
• Tachypnea
• Pulmonary edema
• Apnea
Pulmonary
• Nausea, vomiting
• Caustic effects
Gastrointestinal
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Cyanide Diagnosis
• Clinical picture : sweet almond breath• Lactic acidosis
• ABG:
– metabolic acidosis
ABG sample
Treatment
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• Remove from source
• Oxygen• Cyanide antidote kit:
– Amyl nitrite perle until IV established
– Sodium Nitrite (300mg IV)
• Peds: 0.33 ml/kg of 10% solution)
– Sodium Thiosulfate (12.5gm IV)
• Peds: 1.65 ml/kg of 25% solution
Djengkolic Acid Poisoning
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• JENGKOL bean
Sources
• poor solubility under acidic conditions
• the amino acid precipitates into crystals• mechanical irritation of the renal tubules and urinary tract
Mechanism
• abdominal discomfort, loin pains, severe colic, nausea,vomiting, dysuria, gross hematuria, and oliguria, occurring 2 to6 hours after the beans were ingested.
Characteristics
Djengkolic Acid Poisoning
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• Urine analysis erythrocytes, epithelialcells, protein, and the needle‐like crystals ofdjenkolic acid.
Supporting examination
• Hydration to increase urine flow• Alkalinization of urine by sodium
bicarbonate.
Treatment
Organophosphate Poisoning
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• Insecticides, herbicides
Sources
• Inhibit acethylcholinesterase• ACh accumulates throughout the nervous system
• Overstimulation of muscarinic and nicotinic receptors
Mechanism
• SLUD + GEM
Characteristics
Organophosphate Poisoning
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Atropine
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Competitive inhibitor at autonomic postganglionic cholinergic receptors (GI &pulmonary smooth muscle, exocrine glands, heart, and eye)
Dosis awal dewasa: 2 mg IM. Dosis dapat digandakan setiap 10 menitsampai teratropinisasi.
“The main concern with OP toxicity is respiratory failure fromexcessive airway secretions. The endpoint for atropinization
is dried pulmonary secretions and adequate oxygenation.
Tachycardia and mydriasis must not be used to limit or to stopsubsequent doses of atropine.”
Opiates Intoxication
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• Antidote for Opiate Intoxication:
NALOXONE
Dosage
Adult: As hydrochloride: 0.4‐2 mg repeated if necessary at 2‐3 min intervals. If there is noresponse after a total of 10 mg has been given, consider the possibility of overdosage with
other drugs. Reduce dose for opioid‐dependent patients: 0.1‐0.2 mg. IM/SC routes may be
used (at IV doses) if IV admin is not feasible.
Child: As hydrochloride: Initially 10 mcg/kg IV followed by 100 mcg/kg IV if necessary.
Alternatively, 0.4‐0.8 mg IM or SC, repeated as necessary, if IV admin is not feasible.
Parenteral
Amphetamine Intoxication
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Management
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• Airway Management
• Gastrointestinal decontamination : activatedcharcoal and gastric lavage
• Psychomotor agitation : lorazepam 2 mg IV or
Diazepam 2 mg IV• Hyperthermia : ice packs and evaporative cooling
• Hypertension : Anti HT such as nitroprusside
• Seizure : diazepam IV
Arsenic Toxicity
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Management
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• Decontamination
– Skin Decontamination
– Gastrointestinal decontamination : nasogastricsuction, and administer activated charcoal
• Fluids – Administer intravenous fluids to maintain
adequate urine flow.• Monitoring – Patients should have continuous
cardiac monitoring. Additionally, fluid and
electrolyte balance should be monitored.• Chelation – Dimercaprol and DMSA
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Therapy
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Therapy
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• Hemodialysis can easily remove methanol and
formic acid.
Mercury Poisoning
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• Sensory disturbance – peripheral neuropathy paresthesia, itching,
burning
• Visual field constriction• Ataxia
• Cognitive decline
• Bizarre behavior
– excessive shyness or aggression• Tremor
• Gingivitis
• Acrodynia
• Neuropsychiatric – emotional lability or subtle performance
decline
• Death
Mercury Poisoning
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Congenital Minamata Disease:
CP, MR, seizure
Management
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• Chelating agent – Penicillamine is given at doses of 500 mg PO every six
hours for five days, often in combination withpyridoxine (vitamin B6) in doses of 10 to 25 mg/day.
– DMPS is administered according to the followingregimen: 250 mg intramuscular (IM) or intravenous
(IV) every four hours on day 1, 250 mg IM or IV everysix hours on day 2, and 250 mg IM or IV every six toeight hours for days 3 to 5. DMPS is not approved foruse in the United States.
– DMSA is given at a dose of 10 mg/kg PO every eighthours for five days.
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Botulinum Toxin
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Alcohol Withdrawal Syndrome
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Management
Benzodiazepines IV are used to control psychomotor agitation, seizure , DT and
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prevent progression to more severe withdrawal.
(DOC : Diazepam, lorazepam, or chlordiazepoxide)
Volume deficits replacement, isotonic intravenous fluid can be infused rapidly untilpatients are clinically euvolemic
Deficiencies of glucose, potassium, magnesium, and phosphate should becorrected as needed.
Patients being treated for moderate or severe alcohol withdrawal must be closelymonitored (vital signs, pulse oximetry, fluid status, and neurological function) andmay require admission to an intensive care unit (ICU).
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SurgeryBEDAH
BIMBEL UKDI MANTAP
NEURO SURGERY
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NEURO SURGERY
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Epidural Hemorrhage
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>>a. meningea media, temporo parietal,
biconvex/lenticular, lucid interval
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Epidural Hemorrhage
Signs and Symptoms :
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g y p
• Most patients are unconscious
when first seen. A “lucidinterval” of several minutes to
hours before coma supervenes
is most characteristic of
epidural hemorrhage• Deterioration of consciousness
• Unilateral dilated pupil on side
of injury
• Hemiparesis or hemiplegia onside of body opposite injury
Biconvex / lenticular
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Subarachnoid hemorrhage
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Aneurisma, AVM
Thunderclap headache, Muntah, stiff neck, meningeal
irritation, confusion / penkes
Intracerebral hemorrhage
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Parenkim otak
Brain trauma atau spontan pada hemorrhagic stroke.
CT‐Scan
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MRI
Specific for
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Soft Tissue
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Brain Herniation
Supratentorial herniation
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Supratentorial herniation• Subfalcine (Cingulate) herniation
• Central herniation
• Transtentorial lateral (Uncal) herniation
• Transcalvarial herniation
Infratentorial herniation
• Upward cerebellar herniation
• Downward cerebellar (Tonsillar) herniation
Uncal herniation
• Herniation of the medial temporal lobe inferiorly throughthe tentorial notch
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Clinical triad associated with uncal herniation : – Dilated pupil ipsilateral
– Hemiplegia contralateral
– Coma
• compressed ipsilateral to herniation: hemiplegia will be onthe contralateral side of the body (axons decussate atpyramidal decussation)compressed contralateral to herniation: If the herniation is
very severe, the contralateral cerebral peduncle may becompressed by the opposite side of the tentorial notchleading to an ipsilateral (to the herniation) hemiplegia(Kernohan's phenomenon).
Glasgow Comma Score
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• Motor response 2
• Motor response 3
CEDERA KEPALA
ATLS
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Klasifikasi klinis cedera kepala
berdasarkan GCS :
• Cedera Kepala Ringan (CKR)
GCS 13-15
• Cedera Kepala Sedang (CKS)GCS 9-12
• Cedera Kepala Berat (CKB)
GCS 3-8
Basis Cranii
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CLASSIFICATION
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• Posterior frontal sinus, roof of ethmoid,cribriform, and orbital roof, sphenoidbone
• Posterior frontal sinus, roof of ethmoid,cribriform, and orbital roof, sphenoidbone
Anterior Skull
Base Fracture
• Temporal bone• Temporal boneMiddle Skull
Base Fracture
• Clivus occipital, condylar occipital• Clivus occipital, condylar occipitalPosterior Skull
Base Fracture
Clinical sign :
• Presentation with anterior cranial fossa fractures is with CSF rhinorrhea
and bruising around the eyes "raccoon eyes."
f f l b h
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• Patients with fractures of the petrous temporal bone present with CSF
otorrhea and bruising over the mastoids “Battle sign. “
• Longitudinal temporal bone fractures result in ossicular chain disruption
and conductive deafness of greater than 30 dB that lasts longer than 6‐7
weeks.
• Transverse temporal bone fractures involve the VIII cranial nerve and thelabyrinth, resulting in nystagmus, ataxia, and permanent neural hearing
loss.
• Occipital condylar fracture is a very rare and serious injury. Most of thepatients are in a coma and have other associated cervical spinal injuries.
These patients may also present with other lower cranial nerve injuries
and quadriplegia.
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Halo Sign
(Ring sign/Target sign)
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• Tanda CSF leak:
– Glucose (+)
– Halo sign (+) – Beta‐2‐transferrin (+) highly specific to CSF, not present
in plasma, nasal secretion, tear, saliva, or other fluid.
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THORAX AND CARDIOVASCULAR SURGERY
Trauma Algorythm
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Trauma Thorax“PRIMARY SURVEY” – Mengancam Jiwa
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• Gangguan jalan nafasAirway
• Pneumotoraks terbuka
• Pneumotoraks tension• “Flail Chest”Breathing
• Hematoraks masif • Tamponade kordis
Circulation
Hematothorax
Definition :
accumulation of blood
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accumulation of blood
in pleural cavity• Simple
• Massive :
> 1.5litres blood on
chest drainage or >
200cc blood/ hour on
drainage
Etiology
• Trauma : ruptur arteri di dinding thorax
ataupun internal organ di thorax
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ataupun internal organ di thorax
– A. thoracica interna and it’s branches – A. intercostalis
– A. bronchialis
Physical Exam
• Sign : dyspneu
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• I : Jejas (+), ketingalan gerak (+)
• P : Fremitus taktil menurun
• P : Redup (+)
• A : Vesikuler turun, normal heart sound
Tube Thoracostomy / Chest Tube
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Water Sealed Drainage
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Cardiac Tamponade
• Etiology : blunt orpenetrating trauma
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penetrating trauma
in mid‐chest• Nomal breath sound
• Sign Trias Beck
1. Increase JVP2. Hypotension
3. Muffled Heartsound
• Tx :pericardiocentesis
Pericardiocentesis
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Pneumothorax
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Definition :
accumulation of air
or gas in pleuralcavity
Classification
• Spontan (primer dan sekunder) and Trauma
O d Cl d
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• Open and Closed
• Simple and Tension
Physical Exam
• Sign : Dyspneu, subcutis emfisem
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• I : Jejas (+), ketingalan gerak (+)
• P : Fremitus taktil menurun
• P : Hipersonor
• A : Vesikuler turun/hilang, normal heart sound
Open Pneumothorax
Etiology : Penetrating Trauma lubang dindingdada (ukuran mendekati diameter trakea)
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( )
“Mediastinal Flutter“ “Sucking Chest Wound“
TreatmentOcclusive dressing tape in 3
sides.
• the dressing prevents atmosphericair from entering the chest wall
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gduring inspiration but allows any
intrapleural air out duringexpiration
Closed Pneumothorax
• Etiology : blunt trauma,
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gy ,
spontaneous rupture ofpleurae air leakage to
pleural cavity
• Can developed intoTension Pneumothorax
• Tx : Chest Tube
Tension Pneumothorax
• Clinical sign :• Himpitan vena cava
• Shock
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• Shock
• JVP ↑• Himpitan paru
kontra lateral• distress nafas
• deviasi trakhea
• Tx :
– Neddle
thoracostomy(decompression)
– Chest tube
Tension Pneumothorax
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• Fraktur costae segmental, multipel,berurutan
Flail Chest
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• Severe respiratory distress• Paradoxal movement
• Asymmetrical and uncoordinated chest wall
movement
• Crepitation on palpation
• Pain>>>>
Flail Chest
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• ABCDE
• Adequate ventilation, oxygenation,
Management
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analgesia
Chest X‐Ray
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Penyakit Oklusi Arteri Perifer
• Nama lain : Peripheral ArteryOcclusive Disease (PAOD),Peripheral Artery Disease
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p y
(PAD), Peripheral VascularDisease (PVD)
• Definisi : gangguan alirandarah akibat penyempitanatau kerusakan pembuluhdarah perifer (selainpembuluh darah koroner dan
pembuluh darah otak)• Etiologi : aterosklerosis (>>>),
non‐aterosklerosis
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Penyakit Oklusi Arteri Perifer
• Penyebab Non‐aterosklerosis
– Raynaud’s syndrome
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– Buerger’s disease (Thromboangiitis Obliterans)
– Vasculitis
• Large‐vessel vasculitis = Giant Cell Arteritis (Temporal
Arteritis), Takayasu’s Disease
• Medium‐vessel vasculitis = Polyarteritis Nodosa,
Kawasaki’s Disease, Behcet’s Disease, Cogan’s Syndrome,
• Small‐vessel vasculitis = Antineutrophil CytoplasmicAntibody‐associated Vasculitidies, Vasculitis Associated
with Connective Tissue Diseases
Penyakit Oklusi Arteri Perifer
• Penyebab Non‐aterosklerosis (con’t)
– Heritable arteriopathies
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• Cystic Medial Necrosis• Pseudoxanthoma Elasticum
• Arteria Magna Syndrome
– Congenital Conditions Affecting the Arteries• Persistent Sciatic Artery
• Popliteal Entrapment Syndromes
• Adventitial Cystic Disease
– Peripheral Artery Aneurysms• Femoral Artery Aneurysms
• Popliteal Artery Aneursyms
Claudicatio Intermitten
• Definition : pain incalf region during
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exercise (walking)cause narrowing ofvessel due toatheroscleroticplaque (e.c PeripheralArtery Disease)
Penyakit Oklusi Arteri Perifer
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Critical Limb Ischemia
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Tatalaksana PAD ‐ Revaskularisasi
• Prosedur endovaskular (angioplasti, stenting),
• Pembedahan (bypass, profundoplasty),
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simpatektomi
Acute Limb Ischemia
• 5 P Pain, Pallor, Pulseless,Paresthesia, Paralysis
• Chronic Limb ischemia adakolateralisasi, Acute Limb
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ischemia tidak ada / sedikitkolateralisasi, kurang bisamenolerir iskemia
• Etiologi tromboembolism
(atrial fibrilasi, valvularleaflets, riwayat bypass ataustent placement)
Acute Limb Ischemia
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Acute Limb Ischemia
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I, IIA revaskularisasi dengan trombolitik
IIB revaskularisasi dengan intervensi operatif
Thromboangitis Obliterans
• Also called as “Buerger Disease”
• Male, 20‐40 y.o
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• An acute inflammation and trombosis of
vessel on peripeheral region (foot and hand)
that associate with smoking.• Symptom : claudicatio intermitten
Raynaud Phenomenon
• May appear as a component of otherconditions.
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• Causes: – connective tissue diseases (scleroderma & SLE)
– arterial occlusive disorders.
– carpal tunnel syndrome, – thermal or vibration injury.
• Pale > Cyanosis > Redness
• Aggrevated with cold
Raynaud’s
Phenomenon vs
Syndrome• Vasospastic disorder causing
discoloration of the fingers, toes,
d ll h
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and occasionally other areas.
– Raynaud's disease ("Primary
Raynaud's phenomenon") →
idiopathic
– Raynaud's syndrome
(secondary Raynaud's), →
commonly connective tissue
disorders such as Systemiclupus erythematosus
Takayashu
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Deep Vein Thrombosis
(Trias Virchow)
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Deep Vein Thrombosis
Sign and Symptoms :
• Leg swelling
P i f th ff t d l
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• Pain of the affected leg
• Erythema or discolored skin ofthe affected leg
• Warmth of the affected leg skin
• Leg fatigue
Commonly affects leg veins –popliteal, femoral, pelvic
(Half of all DVT cases cause no symptoms)
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PLASTIC SURGERY
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Burn Injury
Etiology The Depth of
skin burn
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Size and extent of
the burn wound
Burn Injury
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prick test (+)
Superficial PartialThickness Burn (IIa)
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Deep Partial
Thickness Burn (IIb)
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Full Thickness Burn
(III)
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Total Body
Surface Area
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To estimate scattered burns: patient's
palm surface = 1% total body surface
areaParkland formula = baxter formula
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Labio‐Gnato‐Palato Schisis
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The Neonatal Period
• Surgical Repair
– Cleft Lip
• In US ‐ “the rule of tens” ‐ 10 wks, 10 lbs, Hgb 10
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• Lip adhesion vs baby plates
– Cleft Palate
• Varies from 6‐18 months ‐ most around 10 mo• Early repair may lead to midface retrusion
• Early repair improves speech
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PEDIATRIC SURGERY
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Urachal anomaliesare due to failure of complete obliteration of the lumen during gestation.
Presenting symptoms :
Umbilical drainage or a mass and/or pain due to infection. The umbilicaldrainage may be clear, serous, purulent, or bloody.
Urachal abnormalities are a frequent concern in newborns with umbilicaldrainage that persists beyond a few weeks.
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drainage that persists beyond a few weeks.
A patent urachus or urachal sinus can appear as a dimple or indentation in
the base of the umbilicus.
In general, symptomatic urachal remnants should be treated with surgicalexcision. This should include complete excision of the urachus from theumbilicus to the dome of the bladder.
If the urachal disorder presents with an infection, the infection is treatedfirst. This requires antibiotics, possible admission for intravenous antibiotics,and occasional surgical drainage of any infected cyst or poorly draining cavity.
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Sign and Symptoms
• Symptoms may recur after previouslyresolving with laxatives, or feeding
changes.
• Digital Rectal examination maydemonstrate a tight anal sphincter
d l i di h f t l d
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and explosive discharge of stool and
gas.‐ Frog‐like abdomen
‐ Darm contour
‐ Darm steifung‐ Metallic sound
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Atresia Esophageal
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• The first sign of esophageal atresia in the fetus may be polyhydramnios in
the mother.
• Prematurity has also been associated with esophageal atresia.
• Classically, presents with copious, fine, white, frothy bubbles of mucus inthe mouth and, sometimes, the nose.
• The infant may have rattling respirations and episodes of coughing, choking
and cyanosis, may be exaggerated during feeding.
Diagnosis
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• (A) Diagnosis of esophageal atresia is confirmed when a 10‐gauge(French) catheter cannot be passed beyond 10 cm from the gums.
• (B) A smaller‐caliber tube is not used because it may curl up in the upper
esophageal segment, giving a false impression of esophageal continuity.
• The normal distance to an infant's gastric cardia is approximately 17 cm
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Hypertrophy Pyloric Stenosis
• Hipertrofi m.sphincter pylorus
• Stenosis > canalis pyloricus
• Klinis :
– Muntah proyektil, bile free,bolus+gastric juice
B b l k h
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– Baby looks hungry
– Palpable mass (olive)
• Dx : – Plain photo (Single bubble sign) – Barium meal / OMD (Umbrella sign)
• Komplikasi : dehidrasi & aspirasi
• Tx : – Non surgery : resusitasi cairan
– Surgery : pyloromyotomy
HPS
• Typical presentation is onset of non‐bilious vomiting at 1‐12 weeks of age
(3‐4 weeks), becomes more predictable, occurring at nearly every feeding.
• Vomiting intensity also increases until pathognomonic projectile vomiting
ensues
• Slight hematemesis of either bright‐red flecks or a coffee‐ground
appearance is sometimes observed.
• Persistent hunger, weight loss, dehydration, lethargy, and infrequent or
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g , g , y , gy, q
absent bowel movements may be seen. Stomach wall peristalsis may be
visible.
• An enlarged pylorus, classically described as an "olive," can be palpated in
the right upper quadrant or epigastrium of the abdomen in 60‐80% of
infants
• Pre‐operative management is directed at correcting the fluid deficiencyand electrolyte imbalance.
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Atresia / Stenosis Duodeni
• Atresia: completeobstruction; stenosis:partial obstruction
• Lokasi tersering diduodenum pars
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horizontal
• Symptom: regurgitasi &vomit (bilous vomit)
• Dx : (double bubble)
– Plain photo – Barium meal / OMD
In approximately 80% of affectedneonates, the site of duodenal atresia is
postampullary, so that the patient may
present with bilious vomiting.
Double bubble Sign
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• Plain film radiograph
“Double bubble” Sign
(gas‐filled stomach and duodenum
dilatation with no distal gas)
• Without abdominal distension
Barium meal / OMD
Intestinal Obstruction(jejunoileal obstruction)
Classic signs of patients with jejunoileal atresia :
• Bilious vomit
• Abdominal distention (in distal atresia)
• Jaundice (32%) which is characteristically due to indirect
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Jaundice (32%) which is characteristically due to indirect
hyperbilirubinemia
• Failure to pass meconium in the first 24 hours (rule out Hirschsprung
disease; passage of meconium does not rule out intestinal atresia)
• Abdominal distention is most evident in cases of ileal atresias, in which it
is diffuse, as opposed to proximal jejunal atresias, in which the upper
abdomen is distended and the lower abdomen is scaphoid.
• Intestinal loops and their peristalsis may be seen through the thinabdominal wall of newborns.
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Anorectal
Malformations
• The resulting malformations range from
isolated imperforate anus to persistent cloaca.
• Atresia ani (imperforate anus) is a congenital abnormality characterized by
persistence of the anal membrane resulting in a thin membrane covering
the normal anal canal or is the failure of the anal membrane to break
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down (Noden and Lahunta 1985)
• If, after 24 hours, there is no meconium on the perineum, we recommendperforming a cross‐table lateral x‐ray with the baby in knee chest (prone)
position.
useful in determining the
level of atresia
Klasifikasi
• Menurut Berdon, membagi atresia ani berdasarkan tinggi rendahnya
kelainan, yakni :~ Atresia ani letak tinggi : bagian distal rectum berakhir di atas muskulus
levator ani (jarak > 1,5 cm dengan kulit luar)
~ Atresia ani letak rendah : bagian distal rectum melewati musculus
levator ani (jarak < 1,5cm dari kulit luar)
• Menurut Stephen, membagi atresia ani
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Menurut Stephen, membagi atresia ani
berdasarkan pada garis pubococcygeal :
~ Atresia ani letak tinggi : bagian distal rectumterletak di atas garis pubococcygeal.
~ Atresia ani letak rendah: bagian distal rectum
terletak di bawah garis pubococcygeal.
“high” supralevator lesions are typically associated
with fistulas
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Intussusception(Invagination)
• Invagination of a proximal portion of intestine (intussusceptum) into a
more distal portion (intussuscipiens), is one of the most common causesof bowel obstruction in infants and toddlers.
• > 80% involves the ileocecal region.
• Occur in children less than one year of age, with a peak incidenceof between 6‐10 months. (>> 9 months)
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TRIAS :
• Colicky & Cramping abdominal pain
• Bilious vomiting
• Mucous‐red “currant jelly stools”
Physical Exam :
• Palpable abdominal mass
(Sausage Appearance)
• Dance ‘s sign
Radiographic Features Intussusception
USG :• Target or doughnut sign (Transverse cross section)
• Sandwich sign, pseudokidney sign (Longitudinal
section)
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Pseudokidney sign
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Barium Enema : Cupping sign(as a diagnostic) or therapeutic (non‐operative reduction)
Volvulus
• Volvulus of the intestine, the twisting of a segment of intestine on its
mesentery, can be a primary pathology or secondary to malrotation of theintestine. Clinical presentations vary from acute abdominal emergency
requiring immediate surgical intervention to insidious history of colicky
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abdominal pain.
• Volvulus of the small intestine is commonly associated with abnormality
of intestinal rotation and fixation. This is due to failure of fixation and
narrow mesenteric base which allow volvulus to occur. Midgut volvulus
can lead to irreversible intestinal necrosis, which is potentially fatal.
• Large bowel volvulus on the other hand is rare in children; it usually
occurs as a result of redundant sigmoid colon and affects mainly adults.
• Up to 80% of patients present in the first month of life (20% of patients
present after the first year of life) and in this age group the cardinal
symptom is bile (green) vomiting due to duodenal obstruction through
midgut volvulus.
• Pain, irritability, and other non‐specific symptoms (anorexia or nausea was
noted) are more common in toddlers and older children.
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• The coffee‐bean sign (also known as bent inner tube sign) is a sign on anabdominal plain film.
• This thick 'inner wall' represents the double wall thickness of opposed
loops of bowel, with thinner outer walls due single thickness.
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TERIMA KASIH