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KEY POINTS

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  • Etiology

    • Cardioembolic and other nonarteriosclerotic causes of cerebral infarction occur more commonly in patients admitted to the ICU and should be carefully sought by appropriate diagnostic tests.

    • In hypertensive patients with hemispheric lobar hemorrhages and in patients without hypertension, causes for intracerebral hemorrhage such as coagulopathies, arteriovenous malformations, or saccular aneurysms should be sought.

    • Nontraumatic spontaneous subarachnoid hemorrhage is almost always due to a ruptured saccular aneurysm and should be evaluated by arteriography.

  • Clinical and Laboratory Diagnosis

    • X-ray computed tomography (CT) is the diagnostic neuroimaging test of choice for patients with acute stoke. It is rapid, can be performed easily on acutely ill patients and acute intracerebral or subarachnoid hemorrhage are easily identified.

    • Lumbar puncture is the most sensitive test for detection of SAH; it should be performed when there is a strong clinical suspicion and a negative CT scan, or when CT is not available or feasible.

    • In suspected ischemic stroke, diffusion-weighted MRI can be helpful for improving diagnostic certainty when there is no clear history of an abrupt onset or the localization of the neurological findings is confusing. MRI has not been shown to be of value in selecting patients for thrombolytic therapy.

    • Early electrocardiographic (ECG) monitoring detects previously unsuspected atrial fibrillation in 3% to 5% of patients with acute cerebral ischemia.

    • Patients with transient ischemic attacks (TIAs) or mild stroke who are good surgical candidates for carotid endarterectomy should be evaluated for symptomatic carotid stenosis immediately since the risk of stroke can be as high as 1 in 20 within the first 2 days.

  • Treatment of Cerebral Infarction

    The following statements can be made based on good clinical trial data.

    • Routine use of supplemental oxygen does not reduce mortality.

    • Early treatment of hyperglycemia to achieve levels <7 mmol/L does not improve outcome.

    • In patients with systolic blood pressures of 160 to 200 mm Hg, pharmacological reduction of systolic pressure by 20 to 25 mm Hg within the first 24 hours is safe, but does not improve outcome.

    • In hemiplegic patients, subcutaneous low-dose heparin or enoxaparin reduces deep venous thrombosis.

    • Intravenously administered t-PA improves outcome in carefully selected patients with acute ischemic stroke when instituted within 4.5 hours of onset.

    • The clinical value of any intra-arterial pharmacological or mechanical revascularization therapy for acute ischemic stroke has not been demonstrated.

    • Aspirin 160 or 300 mg/d of aspirin begun within 48 hours of the onset of ischemic stroke results in a net decrease in further stroke or death.

    • Full anticoagulation with heparin or similar drugs in patients with acute ischemic stroke provides no clinical benefit in general or in any subgroup, including those with atrial fibrillation or other cardioembolic sources.

    • Hemicraniectomy reduces mortality in patients with large hemispheric infarcts and depressed level of consciousness who are operated within 48 hours of stroke onset.

  • Treatment of Intracerebral Hemorrhage

    The following statements can be made based on good clinical trial data

    • Prophylaxis for deep venous thrombosis with low-dose subcutaneous heparin or heparinoids may be instituted safely on the second ...

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