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 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

SAH Risc Factors: Hypertension Oral contraceptives Cigarette smoking Cocain Alcohol? Pregnancy

SAH Symptoms Signs 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 Diagnosis 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 Grade 3: a, lethargy, confusion, disorientation, agitation 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)

SAH Initial 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

Cerebral 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

Cerebral Vasospasm 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

Vasospasm Diagnosis: 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: Unrupture aneurysm: 0.5-1% congenital predisposition (defect in the muscular layer) Atherosclerotic or hypertensive Unrupture aneurysm: 0.5-1% Risk of bleeding 1-2%/per year

Cerebral Aneurysms Anterior Circulation (85-95%) ICA Oph A P Com A (%25) Ach A ACoA (%30) ACA MCA (%20)

Cerebral Aneurysms Posterior 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 Malformations Presentation 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