Stroke

Introduction

Stroke involves abrupt onset of focal neurologic deficit that lasts at least 24 hours and is presumed to be of vascular origin. Stroke can be either ischemic or hemorrhagic. Transient ischemic attacks (TIAs) are focal ischemic neurologic deficits lasting less than 24 hours and usually less than 30 minutes.

CLINICAL PRESENTATION

Patients may be unable to provide a reliable history because of neurologic deficits. Family members or other witnesses may need to provide this information.

• Symptoms include unilateral weakness, inability to speak, loss of vision, vertigo, or falling. Ischemic stroke is not usually painful, but headache may occur in hemorrhagic stroke.
• Neurologic deficits on physical examination depend on the brain area involved. Hemi- or monoparesis and hemisensory deficits are common. Patients with posterior circulation involvement may have vertigo and diplopia. Anterior circulation strokes commonly result in aphasia. Patients may experience dysarthria, visual field defects, and altered levels of consciousness.

DIAGNOSIS

Laboratory tests for hypercoagulable states should be done only when the cause cannot be determined based on presence of risk factors. Protein C, protein S, and antithrombin III are best measured in steady state rather than in the acute stage. Antiphospholipid antibodies are of higher yield but should be reserved for patients younger than 50 years and those who have had multiple venous or arterial thrombotic events or livedo reticularis

• Computed tomography (CT) and magnetic resonance imaging (MRI) head scans can reveal areas of hemorrhage and infarction.
• Carotid Doppler (CD), electrocardiogram (ECG), transthoracic echocardiogram (TTE), and transcranial Doppler (TCD) studies can each provide valuable diagnostic information.

TREATMENT

• Goals of Treatment: The goals are to (1) reduce ongoing neurologic injury and decrease mortality and long-term disability, (2) prevent complications secondary to immobility and neurologic dysfunction, and (3) prevent stroke recurrence.

PHARMACOLOGIC THERAPY OF ISCHEMIC STROKE

• Alteplase (t-PA, tissue plasminogen activator) initiated within 4.5 hours of symptom onset reduces disability from ischemic stroke. Adherence to a strict protocol is essential to achieving positive outcomes: (1) activate the stroke team; (2) treat as early as possible within 4.5 hours of onset; (3) obtain CT scan to rule out hemorrhage; (4) meet all inclusion and no exclusion criteria (5) administer alteplase 0.9 mg/kg (maximum 90 mg) infused IV over 1 hour, with 10% given as initial bolus over 1 minute; (6) avoid anticoagulant and antiplatelet therapy for 24 hours; and (7) monitor the patient closely for elevated BP, response, and hemorrhage.
• Aspirin 160 to 325 mg/day started between 24 and 48 hours after completion of alteplase also reduces long-term death and disability.
• Secondary prevention of ischemic stroke.
• Statins reduce risk of stroke by approximately 30% in patients with coronary artery disease and elevated plasma lipids. Treat ischemic stroke patients, regardless of baseline cholesterol, with high-intensity statin therapy to achieve a reduction of at least 50% in LDL for secondary stroke prevention.
• Low-molecular-weight heparin or low-dose subcutaneous unfractionated heparin (5000 units three times daily) is recommended for prevention of deep vein thrombosis in hospitalized patients with decreased mobility due to stroke and should be used in all but the most minor strokes.

PHARMACOLOGIC THERAPY OF HEMORRHAGIC STROKE

• There are no standard pharmacologic strategies for treating intracerebral hemorrhage. Follow medical guidelines for managing BP, increased intracranial pressure, and other medical complications in acutely ill patients in neurointensive care units.
• SAH due to aneurysm rupture is often associated with delayed cerebral ischemia in the 2 weeks after the bleeding episode. Vasospasm of the cerebral vasculature is thought to be responsible for the delayed ischemia and occurs between 4 and 21 days after the bleed. The calcium channel blocker nimodipine 60 mg every 4 hours for 21 days, along with maintenance of intravascular volume with pressor therapy, is recommended to reduce the incidence and severity of neurologic deficits resulting from delayed ischemia.