Subarachnoid HemorrhagesSubarachnoid HemorrhagesEtiologies:Etiologies:

intracranial aneurysms (%75-80) cerebral AVMs (%4-5) vasculopathy tumors cerebral artery dissections coagulation disorders dural sinus thrombosis spinal AVM pretruncal nonaneurysmal SAH pituitary apoplexy no cause can be determined (%14-22)

Subarachnoid HemorrhageSubarachnoid Hemorrhage

Incidence: 6-8/100 000 10-15% of patients die before reaching medical care Overall mortality is 45% peak age for aneurysmal SAH is 55-60 years. 20% of cases occur

between ages 15-45 yrs 30% of aneurysmal SAHs occurs during sleep SAH is complicated by intracerebral hemorrhage in 20-40%, by

intraventricular hemorrhage 13-28%, and by subdural blood in 2-5% rupture incidence is higher in spring and autumn

SAHSAHRiscRisc Factors:Factors:

Hypertension Oral contraceptives Cigarette smoking Cocain Alcohol? Pregnancy

SAH SAH

Symptoms Sudden unset of severe headache Usually with vomiting, syncope, neck

pain, and photophobia Loss of consciousness Focal cranial nerve deficits

Signs meningismus hypertension focal neurological deficits ocular hemorrhage coma

SAHSAHDiagnosisDiagnosis

Non-contrast high resolution CT will detect SAH in 95% of cases if scanned within 48 hours of SAH

If CT is negative: Lumbar punction in questionable cases CT angiography MR angiography Cerebral angiography

Grading SAHGrading SAH(Hunt and Hess) (Hunt and Hess)

Grade 1: asymptomatic, or mild headache and slight nuchal rigiditity

Grade 2: moderate to severe headache, nuchal regidity, cranial nerve palsy

Grade 3: mild focal deficit, lethargy, or confusion

Grade 4: stupor, moderate to severe hemiparesis, early decerebrate rigidity

Grade 5: deep coma, decerebrate rigidity, moribound appearance

*add one grade for serious systemic disease or severe vasospasm on angiography

Grading SAHGrading SAH(Yaşargil)(Yaşargil)

Grade 0: a, unruptured aneurysmb, unruptured aneurysm, neurological deficit (+)

Grade 1: a, asymptomaticb, focal neurological deficit (+)

Grade 2: a, headache, nuchal rigidityb, focal neurological deficit (+)

Grade 3: a, lethargy, confusion, disorientation, agitationb, focal neurological deficit (+)

Grade 4: semi comaGrade 5: deep coma

Grading system of FisherGrading system of Fisher

Grade 1: no subarachnoid blood detected (5.8% mortality)

Grade 2: diffuse or <1 mm blood (10.3% mortality)

Grade 3: localized clot and/or >1 mm blood (32.8% mortality)

Grade 4: intracerebral or intraventricular clot (45% mortality)

SAHSAH Initial Management ConcernsInitial Management Concerns

rebleeding hydrocephalus

acute (obstructive) hydrocephalus (20-27%) chronic (communicating) hydrocephalus (14-23%)

delayed ischemic neurological deficit (DIND) attributed to vasospasm

Hyponatremia with hypovolemia (10-34%) DVT and pulmonary embolism seizures (10.5%)

SAH SAH Admitting OrderAdmitting Order

Admit to ICUBed rest with head of bed at 30ºLow level of external stimulation, restricted visitation, no loud noises IV fluids: 2ml/kg/h or 150ml/h (normal saline + 20 mEq KCl/L)Medications

Prophylactic anticonvulsantsSedation, Analgesics, DexamethasoneAntiemetics, H2 blockers, stool softener

OxygenationCardiac rhythm monitorSystolic blood pressure 120-150 mm Hg by cuff

SAH (Grade 1-2)SAH (Grade 1-2)

Cerebral angiography If there is cerebral aneurysm, early surgery

SAH (Grade 3-4)SAH (Grade 3-4)

Arterial line Central venous catheter Urinary catheter Nasogastric tube (if necessary) External ventricular catheter (if necessary) Endotracheal intubation (if necessary)

SASAHH

Rebleeding (70% mortality)

First 24 hours (4%) 1.5% daily for 13 d.15-20% rebleed within 14 d50% will rebleed within 6 monthsThereafter the risk is 3%/yr50% of deaths occur in the 1st month The rebleeding risk increases in patients with higher gradesVentriculostomy and possibly lumbar spinal drainage increase the risk of rebleeding

CerebralCerebral Vasospasm Vasospasm

A delayed focal ischemic neurologic deficit following SAH. Clinically characterized by confusion or decreased level of consciousness with focal neurological deficit

Findings usually develop gradually, and my progress or fluctuate

Radiographic cerebral vasospasm is identified in 30-70% of arteriograms

Symptomatic cerebral vasospasm occurs in only 20-30% of patients

Pathogenesis of cerebral vasospasm is poorly understood

CerebralCerebral VasospasmVasospasm

Almost never before day 3 post-SAH Maximal frequency of onset during days 6-8 post SAH Rarely can occur as late as day 17 Usually resolves in 2-4 weeks

VasospaVasospassmmDiagnosis:Diagnosis:

Delayed onset or persisting neuro deficitOnset 4-20 days pos-SAHDeficit appropriate to involved arterisRule-out other causes of deterioration

rebleedinghydrocephaluscerebral edemaseizuremetabolic disturbances (hyponatremia…)hypoxiasepsis

Ancillary teststranscranial dopplerCBF studiesSPECTcerebral angiography

Cerebral AneurysmsCerebral Aneurysms

Etiology: congenital predisposition (defect in the muscular layer) Atherosclerotic or hypertensive

Unrupture aneurysm: 0.5-1% Risk of bleeding 1-2%/per year

Cerebral AneurysmsCerebral AneurysmsAnterior Circulation (85-95%)Anterior Circulation (85-95%)

ICA Oph A P Com A (%25) Ach A

ACoA (%30) ACA MCA (%20)

Cerebral AneurysmsCerebral AneurysmsPosterior Circulation (5-15%)Posterior Circulation (5-15%)

Vertebral Artery (%5) PICA VB Junction

Basilar Artery (%10) Basilar trunk AICA SCA Basilar Tip PCA

Vascular MalformationsVascular Malformations

Arteriovenous malformationsCavernous malformationVenous angiomaCapillary telangiectasia

Arteriovenous MalformationsArteriovenous Malformations

Dilated arteries and veins with dysplastic vessels,no capillary bed and no intervening neural parenchymaUsually prents with hemorrhage, less often with seizuresCongenital lesions Lifelong risk of bleeding of 2-4%/per yearDemonstrable on angiography, MRI, or CTPrevalence 0.14%

Arteriovenous MalformationsArteriovenous MalformationsPresentationPresentation

1. Hemorrhage (50%) (10% mortality, 30-50% morbidity).2. Seizures3. Mass effect4. Ischemia5. Headache6. Bruit7. Increased ICP

Arteriovenous Malformations Arteriovenous Malformations TreatmentTreatment

1. Microsurgery2. Embolisation3. Stereotactic Radiosurgery

Cavernous Malformations (Cavernomas)Cavernous Malformations (Cavernomas)

Usually not demonstrable on angiography Usually present with seizures, rarely with hemorrhage No intervening neural parenchyma, no arteries Low-flow Surgery best for symptomatic accessible lesions

Venous AngiomasVenous Angiomas

Abnormally medullary vein Usually demonstrable on angiography as a starburst pattern Represents the venous drainage of the area, and intervening

brain is present Seizures rare, hemorrhage even more rare Low flow, low pressure Should not be treated