Stroke management by skandhari06


									Acute Stroke Management

• Medical:


– Free radical scavengers and Antioxidants – Antithrombotic and Antiplatellet drugs – Thrombolysis

• Surgical
– Extracranial Carotid Recontruction
• Carotid endarterectomy

– Intracranial Procedures
• Extracranial Intracranial anastomoses • Embolectomy of intracranial vessels • Decompressive procedures

Free Radical Scavengers and Antioxidants
• Primary radical formation in most biological process is superoxide anion(O2) • Other sources are hydroxyl radical and iron oxygen complexes • Prostaglandins form important source for the free radicals ; prostaglandin inhibitors have antioxidant effect. • Scavenging the free radicals after formation : Vitamin E

Antithrombotics and Antiplatelet-aggregating Drugs
• Maintain or improve perfusion to the brain and to limit the area of ischemia by:
– preventing recurrent thromboembolism – halting propogation of thrombosis – helping with collateral flow

• Adjunct to carotid endarterectomy • Can prevent complications of ischemic stroke incuding DVT, pulmonary embolism and MI

• Bleeding : the most important complication involving bleeding are primary intracranial hemorrhage and symptomatic hemorrhagic transformation of an ischemic lesion. • Bleeding can occur at other sites also as GIT, urinary tract Retroperitoneum.

• Effects mediated through its action on antithrombin III. • aPTT value of 1.5 to 2 times of control is usually desirable. • Used for prophylaxis or acute treatment of DVT. Ischemic stroke predisposed to DVT and pulmonary embolism. • Complications - Bleeding, Heparin induced thrombocytopenia • C/I- CT evidence of ICH or large ischemic stroke.

LMW heparins and heparinoids
• Little interaction with endothelial cells or platelets ; lower risk of bleeding • Not bound to plasma proteins : have more bioavailability and longer half life.

Antiplatelet agents
• Aspirin: Most extensively tested and prescribed drug in the management of persons with ischemic vascular disease • Reduces the likelihood of major ischemic events by approx 22% in patients with TIA or ischemic stroke. • Ticlopidine and clopidogrel are marginally more effective than aspirin

• Brain damage after the onset of ischemia is gradual and early restoration of blood flow can interrupt the process. • Convert plasminogen to plasmin which lyses fibrin in the intravascular clots partial or complete dissolution of clot. • 30% increase in the number of patients who remained with minimal or no deficit after 3 months of stroke.

Limitations of thrombolytic agents
• Extent of damage prior to therapy
– Neuronal destruction : if neuronal destruction is inevitable or has already occurred , little use of thrombolysis. – Parenchymal destruction and hemorrhage: if vasculature is destroyed by the ischemic process - hemoorhage

• Pathogenesis of ischemia
– Arterial dissection – Age of clot – Atheromatous embolic material

Techniques of Delivery
• Intravenous
– Advantage :
• efficacious blood levels can be established rapidly.

– Disadvantage :
• Concentration of thrombolytic agent at the site of occlusion is similar to the concentration anywhere else in body; higher chances of hemorrhage • There may be a relatively static column of blood proximal to the site of occlusion ; can limit the rate at which thrombolytic agent can gain access to clot.

• Intra arterial:
– Advantage:
• imaging of vasculature can be done and clot site detected, effect of thrombolysis can be seen • delivery of drug directly into the clot- high local concentration of agent

– Disadvantage
• Time consuming

Agents and Doses
• Streptokinase, Urokinase ,Tissue Plaminogen Activator(tPA) • t-PA dose :
– ( within 3 hours) 0.9mg/kg , 10% given as initial bolus followed by infusion of remainder . A dose of 90mgm is not exceeded. – (Within 6 hours)- 1.1mgm/kg , maximim of 100mgm.

Clinical experience with thrombolysis
• Demonstration of efficacy:
– Lysis of clot - intraarterial - 90-100% success rate – Identify candidates for therapy:
• Patients who present within 3 hours of onset of stroke. • CT scans showing no evidence of hemorrhage and small area of involvement

• Problems of Recognizing infarction :
– Low density in NCCT : signifies established infarct. If large sized, withhold thrombolysis.

• Management of hypertension during thrombolysis : Thrombolysis withheld in patients with systolic BP > 185mm, diastolic Bp - >110mm

• Hemorrhage during and after thrombolysis:
– Most feared complication – Three patterns can be seen
• Hemorrhagic infarct • Hemorrhage into infarct • Primary hematoma

– Likelihood of hemorrhage into infarct seems greatest with increasing time of ischemia and increasing volume of ischemic tissue

Surgical therapeutic interventions
• Carotid endarterectomy: Not been consideration initially for reasons:
– noncarotid events as cause of the stroke – poor results

• Moderate successs with :
– Crescendo TIA in patients with severe stenosis – Stroke following angiography

• Indications:
– Documented carotid etiology for a progressive but non debilitating ischemic events – Evidence of acute thrombosis is present( loss of bruit, stroke following angiography – Ipsilaterral stenosis > 70%

• Complete carotid occlusion :To restore blood flow to the ipsilateral hemisphera and to prevent emboli originating from stump of occluded ICA from propogating distally • Duration of occlusion - around 100% success rate in reopening these arteries within 7 days • indications
– patients presenting with acute non debilitating deficit directly attributable to occlusion – Ischemic symptoms referable to embolization from an occluded stump

Timing of carotid surgery
• Neurologically stable- early • Unstable - 3-6 weeks after stroke

Intracranial Procedures
• EC- ICA anastomosis : results not favourable • Embolectomy of intracranial vessels : Restoration of flow seen in around 75% of cases • Decompressive craniotomy

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