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Surgery of Cerebrovascular Diseases. Subarachnoid Hemorrhages 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
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Subarachnoid HemorrhagesEtiologies: • 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 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
SAHRiscFactors: • Hypertension • Oral contraceptives • Cigarette smoking • Cocain • Alcohol? • Pregnancy
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 SAH
SAHDiagnosis • 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 SAH(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 SAH(Yaşargil) Grade 0: a, unruptured aneurysm b, unruptured aneurysm, neurological deficit (+) Grade 1: a, asymptomatic b, focal neurological deficit (+) Grade 2: a, headache, nuchal rigidity b, focal neurological deficit (+) Grade 3: a, lethargy, confusion, disorientation, agitation b, focal neurological deficit (+) Grade 4: semi coma Grade 5: deep coma
Grading 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)
SAHInitial 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 Admitting Order • Admit to ICU • Bed rest with head of bed at 30º • Low 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 anticonvulsants • Sedation, Analgesics, Dexamethasone • Antiemetics, H2 blockers, stool softener • Oxygenation • Cardiac rhythm monitor • Systolic blood pressure 120-150 mm Hg by cuff
SAH (Grade 1-2) • Cerebral angiography • If there is cerebral aneurysm, early surgery
SAH (Grade 3-4) • Arterial line • Central venous catheter • Urinary catheter • Nasogastric tube (if necessary) • External ventricular catheter (if necessary) • Endotracheal intubation(if necessary)
SAH • Rebleeding (70% mortality) • First 24 hours(4%) • 1.5% daily for 13 d. • 15-20% rebleed within 14 d • 50% will rebleed within 6 months • Thereafter the risk is 3%/yr • 50% of deaths occur in the 1st month • The rebleeding risk increases in patients with higher grades • Ventriculostomy and possibly lumbar spinal drainage increase the risk of rebleeding
CerebralVasospasm • 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
CerebralVasospasm • 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
VasospasmDiagnosis: • Delayed onset or persisting neuro deficit • Onset 4-20 days pos-SAH • Deficit appropriate to involved arteris • Rule-out other causes of deterioration • rebleeding • hydrocephalus • cerebral edema • seizure • metabolic disturbances (hyponatremia…) • hypoxia • sepsis • Ancillary tests • transcranial doppler • CBF studies • SPECT • cerebral angiography
Cerebral 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 AneurysmsAnterior Circulation (85-95%) • ICA • Oph A • P Com A (%25) • Ach A • ACoA (%30) • ACA • MCA (%20)
Cerebral AneurysmsPosterior Circulation (5-15%) • Vertebral Artery (%5) • PICA • VB Junction • Basilar Artery (%10) • Basilar trunk • AICA • SCA • Basilar Tip • PCA
Vascular Malformations • Arteriovenous malformations • Cavernous malformation • Venous angioma • Capillary telangiectasia
Arteriovenous Malformations • Dilated arteries and veins with dysplastic vessels,no capillary bed and no intervening neural parenchyma • Usually prents with hemorrhage, less often with seizures • Congenital lesions • Lifelong risk of bleeding of 2-4%/per year • Demonstrable on angiography, MRI, or CT • Prevalence 0.14%
Arteriovenous MalformationsPresentation • Hemorrhage (50%) (10% mortality, 30-50% morbidity). • Seizures • Mass effect • Ischemia • Headache • Bruit • Increased ICP
Arteriovenous Malformations Treatment • Microsurgery • Embolisation • Stereotactic Radiosurgery
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 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