Ramani Balu and Scott E. Kasner

Definitions and Classification of Strokes

Stroke is broadly defined as the abrupt onset of persistent neurologic symptoms caused by inadequate blood flow to a particular area of the brain or by hemorrhage into the brain, which compresses brain tissue and secondarily compromises perfusion. Ischemic strokes—which are caused by inadequate blood flow to the brain—constitute ∼80% of all strokes and can be caused by a variety of mechanisms, including large artery atherothromboembolic disease, small artery disease, cardioembolism, or less common causes including hypercoagulable states, cocaine abuse, arterial dissection, and hypoperfusion. A transient ischemic attack (TIA) is a temporary focal neurologic deficit caused by an abrupt decrease in cerebral blood flow that does not cause permanent infarction. TIA and ischemic stroke represent two points along a continuum of acute ischemic cerebrovascular disease (analogous to unstable angina and myocardial infarction in coronary artery disease) and are therefore managed similarly in the acute setting. Patients with a single TIA, however, are unlikely to be admitted to an ICU.

Hemorrhagic strokes—which are caused by abrupt bleeding into the brain—make up the remaining 20% of strokes and can be further divided into primary intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH). ICH most commonly results from hypertension (which usually results in deep subcortical, brain stem, and cerebellar hemorrhage), cerebral amyloid angiopathy (CAA, which results in predominantly superficial and lobar hemorrhage), rupture of an arteriovenous malformations (AVM), or as a complication of systemic anticoagulation (for example, supratherapeutic dosing of warfarin). In contrast, SAH is generally caused by a ruptured aneurysm. Ischemic strokes can often have hemorrhagic transformation, because infarcted tissue is friable and susceptible to bleeding; however, hemorrhagic transformation is more appropriately thought of as a potential complication of ischemic stroke, rather than a subtype of hemorrhagic stroke.

Initial Diagnosis and Management

The initial diagnosis and management of stroke patients typically occur in the emergency department. Because different stroke types have markedly divergent management strategies and potential acute treatments (such as thrombolysis using intravenous [IV] tissue plasminogen activator, described later) that can only be given within a short time window, a directed approach is required when evaluating patients who present with acute neurologic deficits (Figures 71.1 to 71.3). A clear history of the time of symptom onset is needed to determine whether the patient may be eligible for thrombolysis. If the patient or family members cannot provide an exact time when symptoms occurred, the time when the patient was last seen normal is assumed to be the time of symptom onset. Certain historical features may help distinguish stroke subtypes. For example, sudden-onset “thunderclap” headache, neck stiffness, and nausea that coincide with neurologic symptom onset strongly suggest SAH (although headache is often nonspecific and does not reliably distinguish ischemic from hemorrhagic stroke). In contrast, symptoms that develop over minutes are more likely to be associated with ICH.

A brief, directed neurologic examination helps to localize the lesion and quantify the extent of neurologic impairment. Aphasia, neglect, and forced gaze deviation away from the hemiparetic side suggest cortical involvement. Pure motor hemiparesis or hemisensory loss affecting the face, arm, and leg equally occur with subcortical injury. Finally, “crossed signs” (such as ipsilateral facial weakness and contralateral arm and leg weakness), cranial nerve abnormalities, and ataxia localize to the posterior fossa (brain stem and cerebellum). The NIH Stroke Scale (NIHSS) (see stroke.nih.gov/documents/NIH_Stroke_Scale.pdf for description) provides a quick, reliable metric to measure of extent and severity of neurologic injury and can be used to track clinical changes over time.

Laboratory blood work, including electrolytes, renal function panel, complete blood count, coagulation panel, and troponin, should be obtained on presentation to help identify (1) metabolic stressors that may mimic stroke, (2) coagulopathies that may contribute to intracerebral hemorrhage, and (3) acute cardiac ischemia that can lead to cardioembolism. An electrocardiogram (ECG) is indicated to identify cardiac ischemia and rhythm disturbances (such as atrial fibrillation), both of which can cause cardioembolic strokes.

After a clinical diagnosis of acute stroke has been made, it is imperative to distinguish hemorrhagic from ischemic stroke as rapidly as possible and initiate appropriate therapy. A computed tomographic (CT) scan is usually the first neuroimaging study to be performed because it is readily available and highly sensitive for acute bleeds (see Figures 71.1 to 71.3 and Figure 71.E1) . Intraparenchymal or intraventricular hyperdense lesions suggest ICH, whereas hyperdensities within the sulci and basal cisterns imply SAH. In the absence of evidence for hemorrhage, an ischemic infarct is presumed because radiologic signs of cerebral ischemia may be subtle or undetectable within the first 12 hours. It is important to realize, however, that CT can miss a small proportion of SAH (< 5%). Thus, if clinical suspicion for SAH is high, a negative CT should prompt further testing with lumbar puncture to look for red blood cells or xanthochromia (yellowish discoloration of CSF) or with a magnetic resonance imaging (MRI) scan.

Management of Ischemic Stroke

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