Subarachnoid Hemorrhage

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SUBARACHNOID HEMORRHAGE DIAH MUSTIKA HW SpS,KIC INTENSIVE CARE UNIT of NAVAL HOSPITAL dr RAMELAN SURABAYA

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Transcript of Subarachnoid Hemorrhage

  • SUBARACHNOID HEMORRHAGE

    DIAH MUSTIKA HW SpS,KIC

    INTENSIVE CARE UNIT of NAVAL HOSPITAL dr RAMELAN SURABAYA

  • EPIDEMIOLOGY

    Subarachnoid hemorrhage include the subset of intracranial hemorrhage

    Traumatic SAH : traumatic brain injury

    Spontaneous SAH :

    - Ruptured intracranial aneurysm (75-80%)

    - Cerebral arteriovenous malformation (AVMs; 4-5%)

    - Carotid or cerebral dissection

    - Coccaine use

    - Sickle cell disease

    - Pituitary apoplexy

  • Risk Factor of aneurysmal SAH

    Increasing age

    Smoking: Relative risk is 3.0 for men, 4.7 for women

    African American

    Moderate to excessive alcohol intake

    Hypertension

    Cocaine use

    Autosomal dominant polycystic kidney disease (ADPKD)

    Fibromuscular dysplasia (FMD)

    Arteriovenous malformation

    Moyamoya disease

    Connective tissue disease: Ehlers-Danlos type IV, Marfans syndrome, pseudoxanthoma elasticum

    Multiple family members with intracranial aneurysms

    Coarctation of the aorta

    Osler-Weber-Rendu syndrome

    Atherosclerosis

    Bacterial endocarditis

  • CLINICAL PRESENTATION

    Headache : sudden, severe, unremitting headache accompany with nausea and vomiting

    Warning headache or sentinel leak

    Photophobia

    Neck stiffness

    Meningismus

    Impairment of consciousness

    Cranial neuropathies

    Seizure

  • DIAGNOSIS

    Simple nonenhanced brain CT scan

    Lumbar puncture if negative head CT scan but the presentation is typical RBC> 100000 cells/mm3 in 3rd tube and xanthochromia

    CT Angiography (CTA)

    Magnetic Resonance angiography (MRA)

    Conventional Cerebral angiography gold standard

    CA is negative in 10-15% in aSAH

  • PROGNOSTIC INDICATORS

    Hunt and Hess Classification Scale

    Grade Neurologic Status %risk of death I Asymptomic; or minimal headache and slight nuchal

    rigidity 11

    II Moderate to severe headache; nuchal rigidity; no

    neurologic deficit except cranical nerve palsy 26

    III Drowsy; minimal neurologic deficit 37

    IV Stuporous; moderate-to-severe hemiparesis; possibly

    early decerebrate rigidity and vegetative distirbance 71

    V Deep coma; decerebrate rigidity; moribund

    appearance 100

  • CRITICAL CARE MANAGEMENT

    GCS 8 or unable to protect the airway should be intubated

    Anticonvulsant prophylaxis

    Blood pressure should be controlled aggressively. Hypotension

    or hypertension should be avoided

    Coagulation parameters should be examined and corrected

    promptly

    Give the stool softener

    Pain management should be optimized

    ICU

  • Complication and its therapy

    Rebleeding

    Broderick et al , 22% aSAH mortalities as a result of rebleeding

    First 24 hours the risk is 4% and 1.5% per day for the following 13 days

    The first 14 days the total risk of rebleeding is 15-20% and at 6 months is 50%

    In the longterm, rebleeding at 3% per year and mortality is 2% per year

    Treatment for prevention rebleeding is aneurysm obliteration (open aneurysm clipping or endovascular coil embolization procedures)

  • Hydrocephalus

    communicating

    obstructive

    Treatment : External Ventricular Drainage (EVD)

    50% improve spontaneously

  • Vasospasm :

    o inflammatory reaction in blood vessel bathed in subarachnoid

    blood, resulting in luminal narrowing

    o 60- 70% after SAH, maximal severity in 2nd weeks after SAH

    and typically resolves spontaneously in 3rd or 4th weeks

    o Vasospasm cause death or serious disability Delayed Ischemic Neurological Deficit (DIND)

    o Demonstrated radiographycally by transcranial Doppler (TCD),

    cerebral angiography or CT angiography

    o Treatment : hyperdynamic therapy or triple H therapy

    (hypertension, hypervolemia and hemodilutions)

  • o Administration 23,4% saline improve CBF, CPP and decrease ICP significiantly at 90 and 180 minute after administration. Limited by hiperchloremia, hypernatremia and hyperosmolality

    o Selective Calsium Channel Blocker (nimodipin) improve outcome by measure Glasgow Outcome Scale (GOS)

    o Endovascular and surgical treatment if hyperdynamic and pharmacologic fail to reserve neurologic defisit

  • OUTCOME

    Fairly poor as a whole

    Overall mortality of aSAH is 45-50%

    The most common predictor of death is the clinical

    conditions at presentation, age, medical morbidities,

    severity of hemorrhage on CT and aneurysm type

  • THANK YOU