Introduction to cerebrovascular diseases

Introduction to cerebrovascular diseases - Introduction to...

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Unformatted text preview: Introduction to cerebrovascular Introduction to cerebrovascular diseases SAH SAH Subarachnoid haemorrhage Subarachnoid haemorrhage Blood within the CSF Trauma: most common. Spontaneous Causes: Ruptured berry aneurysms;75­80% AVM;4­5% Vasculitis, tumours, carotid dissection ,HTN, 3­5% Unknown; 10­15% Annual rate:10­28/100,000 10­15% die before reaching the hospital Some facts Some facts Among survival rebleeding is the major cause of M&M risk is at 38% 8% die from progressive deterioration from the initial bleed 7% die from vasospasm Anther 7% will have severe deficit Overall one third will have good results 85­95% of aneurysms occur in ICA 5­15% in posterior circulation 20­30% of aneurysm patients have multiple aneurysms Berry aneurysms Berry aneurysms Incidence of aneurysms are 5% of population Aneurysm rupture 6­12/ 100 000/ y Ruptured to unruptured ratio 5:3 Peak age is 55­65 Peak age is 55­65 females more than males 3:2 females more than males 3:2 of aneurysmal SAH occurs during sleep 30% of aneurysmal SAH occurs during sleep 50%of patients have warning symptoms 1­3 weeks before SAH SAH complicated with ICH 20­40%,IVH in 15-35% The 30 day Mortality rate is 50­60% Those who survive initial bleed 6 month mortality rate is Those who survive initial bleed 6 month mortality rate is 60% Aetiology Aetiology Congenital predisposition due to defect in the arterial wall Atherosclerosis HTN presumed to be the most implicated factor for initiation, growth and subsequent rupture due to variable hemodynamic changes Infectious or mycotic aneurysm Traumatic as in dissecting aneurysms Genetics as seen in familial aneurysms is well established such as in PCK. Marfam’s, EDS. Risk factors Risk factors HTN Diurnal variation in blood pressure Smoking Alcohol consumption Coffee consumption Oral contraceptives Drug abuse Clinical features Clinical features 1­rupture 95­97% Sudden onset of severe headache Associated with vomiting and kneeling LOC Focal cranial nerve deficits Back pain Nuchal rigidity, Kernig's, Brudzinski's sign Sentinel haemorrhage causes warning headache Continued Continued 2­ mass effect 2­ 3% Giant aneurysm as any mass lesion Compression of neural structure 3ed CN as in P­com CONTINUED CONTINUED 3­ Incidental finding Natural history of ruptured aneurysm Natural history of ruptured aneurysm if treated conservatively studies in 60’s Of 100 patients 15% die before reaching hospital 15% die in first 24 h in hospital 15% die between 1­14 days 15% die between 2­8 weeks 15% die between 2­24 months 25% may survive > 2 years Evaluation Evaluation Non contrast high resolution CT scan is positive in 95­98% Ct can also assess the following Hydrocephalus which occurs in 21% ICH Infarction Amount of blood in cisterns which is a prognosticator in vasospasm Ct may predict the aneurysm location continued continued CSF in questionable cases Pressure is elevated 3 tube test Xanthochromia after 6 hours MRI is not sensitive acutely May be helpful after 4­10 days Angiogram DSA Angiogram DSA Demonstrate the cause of the SAH usually aneurysm in 85­95% Study the 4 vessels to rule out additional aneurysms and collateral circulation 3 views for each vessel Obtain 3­D views for Grading SAH Grading SAH Hunt & Hess 0: unruptured 1: asymptomatic, mild headache, slight nuchal rigidity 2: Cr N palsy, severe headache & nuchal rigidity 3: focal deficit, lethargy or confusion 4:stuper, hemiparesis, decerebrate 5:deep coma moribund appearance WFNS GRADING WFNS GRADING WFNS grade WFNS grade GCS Score Major deficit 0 - - 1 15 absent 2 13-14 absent 3 13-14 present 4 7-12 Present or absent 5 3-6 Present or absent Fisher grading system Fisher grading system correlates between blood on CT and the risk of vasospasm 1 No blood detected 2 Diffuse < 1 mm thick 3 Localized clot or and > 1mm 4 ICH, IVH Initial management Initial management Once SAH is documented admit to ICU Arterial &Venous catheters, bloods Intubation if necessary EVD ? VS with crani checks q 1 hr BR, Head up 30,foley I’S & O’s 100­125 cc/h N/S vs. D/W+ 20 meq kcl continued continued Medications Codeine phosphate 30­60 mg q3h Stool softeners, H2 blockers Ca channel blockers Nimodipine 60mg q 4h PO OR 0.2 mg/kg/h IV Dexamethasone may help with headache and neck pain Prophylactic anticonvulsant usually phenytoin is controversial Blood pressure volume management Blood pressure volume management Unsecured aneurysm: gentle volume expansion& hemodilution may help prevent vasospasm HTN must be avoided keep at 120­150 Clipped aneurysm Aggressive 3 H treatment is recommended Keep SBP at 140­160 may be as high as 180 Hyponatremia is common Over hydration or SIADH vs CSWS REBLEEDING REBLEEDING 1st day 4%, then 1.5 % /d Mortality rate is 70% 15­20% within 2 w 50% will bleed within 6 m 3% will bleed annually with 2% mortality 50% of deaths occur in the 1st m Early surgery prevents rebleeding Vasospasm Vasospasm It is also called cerebral angiopathy or DIND. First Introduced in1951 by Ecker Commonly seen after aneurysmal SAH but may occur with trauma Never before day 3 post SAH peak day 5­7 The most significant cause of M &M in patient surviving SAH long enough to reach medical care Mortality rate is 7%, severe morbidity 7% Blood clot is spasmogenic when indirect contact with the proximal 9 cm of ACA, MCA The high grade the high risk The more blood on CT scan the more risk continued continued Clinical vasospasm 20­30% of patient symptoms usually develop gradually Criteria: increased symptoms headache and lethargy, new focal deficits, or hyponatremia ACA> MCA Radiological vasospasm 30­70%. Arterial narrowing demonstrated on angiogram with slowing of contrast filling Pathogenesis Pathogenesis Poorly understood Proposed mechanisms Contraction of the smooth muscle as a result of the vasoconstrictors or vasoactive substances released into the CSF Neuronal mechanism via nervi vasorum as a result of sympathetic hyperactivity Impairment of endothelial derived relaxant facto Mechanical phenomenon Components implicated :oxyhemoglobin, iron, noradrenalin, thromboxane­A2 and free radicals Management for vasospasm Management for vasospasm Non contrast CT scan to rule out hydrocephalus, oedema, infarction or rebleed Electrolytes and ABGs Angiogram?, TCD? Numerous treatment have been proposed medical and invasive Calcium channel blockers Nimodipine vs Nicardpine for 21 days May improve the outcome, more beneficial in neuroprotection than in preventing vasospasm 3 H Protocol Dexamethasone Balloon angioplasty Intra­arterial papaverine ICP monitor Treatment options Treatment options Best treatment depends the patient’s condition, anatomy of the aneurysm, ability of the surgeon Clipping of the aneurysm at the neck to exclude it from the circulation is considered the optimal treatment Goal of surgery to prevent rupture or further enlargement while preserving all normal vessels and minimizing injury to brain :Alternatives Alternatives Wrapping Trapping Hunterian ligation Endovascular techniques GDC Intra­aneurysmal placement of detachable balloon Coiling Coiling coiling coiling Decision regarding the management by Decision regarding the management by GDC vs surgical repair Unruptured aneurysm are not to be coiled as the long term efficacy has yet to be established Ruptured aneurysm Following aneurysms are considered for GDC Posterior circulation (except PICA and BASA pointing up), A com. If the N:F ratio <2:1 or neck is >4mm those are not for GDC Multiple aneurysms which can be dealt with same approach Timing of surgery Timing of surgery Controversy exists between what so called Early surgery within first 3 days and late surgery after 10 days. early is advocated for following reasons Reduce the risk of rebleeing Facilitate treatment of vasospasm May remove potentially vasospasomgenic agents Factors favoring early Good medical and neurologic condition Associated ICH Rebleeding or imminent rebleeding CONTINUED CONTINUED Against early brain is red and swollen, may increase vasospasm, high incidence of rebleeding Factors favoring late Poor condition Difficult aneurysm because of site and size FOLLOW UP FOLLOW UP Patients should be followed up on regular basis as follows 3,6,12,24,36 months Investigation of asymptomatic first degree siblings is recommended Genetic screen is under evaluation Giant aneurysms Giant aneurysms Less than 1 cm is small 1­2.5 large More than 2.5 is giant Saccular and fusiform 3­5% of all aneurysms Peak 30­60 F: M 3:1 35% present with bleeding The rest present with TIAs or seizures or mass effect Angiogram often underestimates the actual size because of the thrombus CT,MRI with and without contrast are more informative Treatment options are variable: direct clipping is the ideal if applicable, clipping with EC­IC ICA bypass, trapping, ligation GIA GIA Vascular malformation Vascular malformation 4 types described by McCormick Arterio­venous malformation Cavernous angioma Venous angioma Capillary telangiectasia AVM AVM AVM AVM Definition: A collection of blood vessels wherein arterial blood flows directly into draining veins without normal interposed capillary beds Appears as a tangle of vessels A congenital lesion progresses from low flow at birth to high flow in adult hood Presentation Bleeding 50%, mainly from small lesions peak age 15­20 y, mortality is 10% from each bleeding, morbidity is 30­50%, risk of bleeding is 4% per year Seizures more frequent with large AVM Mass effect Headache, bruits, heart failure, hydrocephalus as seen in vein of Galen aneurysm 7% of AVM patients have aneurysms AVM AVM Evaluation Evaluation CT flickers of calcifications MRI flow void on TI,T2,feeding arteries, and draining veins, ischemic changes, size and site, better for cavernous angiomas Angiogram reveals tangle of vessels (nidus), feeders and draining veins Can not show up cavernous angiomas Spetzler and Martin grading system Spetzler and Martin grading system GRADED FEATURE Size Small<3cm Small<3cm Medium3­6cm large >6 POINTS 1 2 3 Eloquence of adjacent brain Non eloquent Non eloquent eloquent 0 1 Pattern of venous drainage Superficial deep deep 0 1 Treatment Treatment Excision is the treatment of choice Adjunctive treatment may help includes conventional radiotherapy, radiosurgery and embolization Pre op consider B­ blockers dexamethasone, and phenytoin Cavernous angiomas Cavernous angiomas Sinusoidal vascular channels located within the brain but lacking intervening neural parenchyma, feeders and draining veins usually present with seizures, bleeding, mass effect or incidental CT, MRI show the lesion Symptomatic lesion showed be excised ...
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