Accidente Cerebro Vascular

Neurol Clin 26 (2008) 345–371

Management of Acute Ischemic Stroke
Anna Finley Caulfield, MD*, Christine A.C. Wijman, MD, PhD
Department of Neurology and Neurological Sciences, Neurocritical Care Program, Stanford Stroke Center, Stanford University School of Medicine, 701 Welch Road, B-325, Palo Alto, CA 94304, USA

Stroke is the third leading cause of death and the leading cause ofdisability in the United States and is associated with a tremendous cost burden to society [1]. Most strokes are ischemic, but about 15% of strokes are caused by intracerebral or subarachnoid hemorrhage. Currently, there is only one drug approved by the US Food and Drug Administration (FDA), intravenous tissue plasminogen activator (tPA), for the treatment of acute ischemic stroke within 3 hours ofsymptom onset [2]. Many stroke patients do not receive intravenous tPA, however, most commonly because they present beyond the 3-hour therapeutic window. More recently developed therapeutic strategies offer the hope of safe and effective treatment beyond the 3-hour time window in selected patients. This article is an update of a recent publication that reviewed established and novel treatments for acuteischemic stroke and the management issues that may arise in the first hours to days after symptom onset [3]. Blood pressure management, management of intracranial hypertension, and temperature management are discussed in greater detail elsewhere in this issue.

Initial management The initial management of acute ischemic stroke involves medical stabilization, including airway protection andventilatory and hemodynamic
Material for this article is reprinted in part from the American Academy of Neurology 2006 meeting syllabus titled ‘‘Critical Care for Cerebrovascular Patients: What General Neurologists Need to Know’’; with permission. This is an updated version of an article that originally appeared in Critical Care Clinics, volume 22, issue 4. * Corresponding author. E-mail address:afinley@stanford.edu (A. Finley Caulfield). 0733-8619/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved. doi:10.1016/j.ncl.2008.03.016 neurologic.theclinics.com

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support, followed by neurologic assessment, brain imaging, and evaluation of the appropriateness of thrombolytic therapy [4,5]. Airway and ventilatory support Patients with acute stroke areat risk for respiratory failure from aspiration and pneumonia [6,7] often in the setting of difficulty protecting the airway and clearing secretions because of facial or bulbar weakness or an altered level of consciousness [8]. Hypoxemia may worsen the injurious effects of cerebral ischemia, and patients must be monitored closely with a goal to keep oxygen saturation greater than 95% [4]. If apatient requires endotracheal intubation, short-acting sedatives should be used, and the hemodynamic changes associated with intubation should be minimized [5,9,10]. No prospective trials have been undertaken to establish the ideal mode of ventilation in intubated stroke patients. A commonly used mode for patients who are awake but in need of airway protection is pressure support ventilation, whereassynchronized intermittent mandatory ventilation or assist control ventilation is recommended for patients who have intracranial hypertension or are comatose [5]. Excessive positive end-expiratory pressures (ie, O10 cm H2O) may be deleterious in patients with elevated intracranial pressure (ICP) [11,12]. Mechanically ventilated patients frequently require sedation; however, sedatives may causehypotension and additional brain injury by lowering cerebral perfusion pressure [13–15]. Propofol, popular because of its short duration of action, has been associated with a ‘‘propofol infusion syndrome’’ when used at high doses for prolonged periods. This syndrome originally was described in pediatric patients, but it also can occur in adults. It presents with metabolic acidosis, rhabdomyolysis,...