Ischemic Stroke

Ischemic Stroke


Mohamed Teleb and Paul Singh


BACKGROUND


Stroke is the fourth leading cause of mortality in the United States and incurs an estimated cost of 38.6 billion dollars anually.1 Although the overall mortality from this disease has declined over the last decade, 50% of individuals who suffer a stroke at an age of >65 will die within 5 years.1 Traditionally a clinical diagnosis, evaluation of stroke is now highly reliant on imaging. While new multimodality radiologic technologies are being developed to determine brain ischemia and penumbral tissue, the most important imaging for acute care remains the noncontrast computed tomography (CT) of the head. With this in mind, this chapter reviews both the pathogenesis and clinical manifestation of stroke as well as a basic approach to its image interpretation in the acute setting.


HISTORY AND PHYSICAL EXAM


Patient History


Obtaining a quick and accurate history in patients with stroke facilitates optimal clinical care. It is essential to determine the exact time at which brain ischemia started. Because this can be a difficult task unless bystanders are present at the onset of symptoms, the practitioner should rely on the time of “last seen normal,” as opposed to when the patient was first witnessed having symptoms. For example, if a patient were to wake up with symptoms of a stroke, his or her time last seen normal would be the night before when he went to sleep. This information is required to determine a patient’s eligibility to receive specific interventions, including intravenous tissue plasminogen activator (IV tPA) or endovascular intra-arterial (IA) thrombolysis/thrombectomy. In addition to the time of onset and duration of symptoms, delineating the progression of neurologic findings is also important. Most vascular events result in immediate deficits; exceptions to this include stuttering transient ischemic attacks and flow related symptoms caused by an intracranial or extracranial stenosis.


The emergency provider should also attempt to identify nonstroke conditions, referred to as “stroke mimics” that can produce focal neurologic deficits (Table 20.1).



TABLE 20.1 Stroke Mimics and Their Features


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BPPV, benign paroxysmal positional vertigo; PNC, peripheral nerve compression; CN, cranial nerves ; HSV, herpes simplex virus; ICP, intracranial pressure; CPP, cerebral perfusion pressure.


A thorough history and exam can help distinguish brain infarction from stroke mimics, and, in the event of a true central ischemic process, help pinpoint the specific etiology of the neurologic insult. Stroke symptoms accompanied by severe chest pain radiating to neck are suggestive of a myocardial infarction with associated cardiac emboli. Stroke symptoms accompanied by severe chest and back pain can suggest an aortic dissection with extension into the carotid or the vertebral arteries. Such combinations of findings not only help identify a specific pathologic process but also may dramatically alter patient management by avoiding hemorrhagic complications of thrombolytic therapy in patients with specific contraindications, for example, an intracerebral tumor.


The diagnosis of stroke mimics can often be difficult during the acute phase. Studies show anywhere between 3% and 16% of patients treated with tPA are stroke mimics.2,3 Fortunately, multiple studies have reported stroke mimics treated with tPA to have no increased rate of symptomatic intracranial bleeds.3 The pathogenesis of intracranial hemorrhage after tPA is secondary to reperfusion hemorrhage into a region of infarcted brain tissue. Because stroke mimics do not have actual brain ischemia, they are less likely to have hemorrhage after tPA. The exception to this is patients with intracranial tumors, but these are typically visualized on a CT scan prior to IV tPA administration.


In addition to accompanying symptoms, the patient’s past medical and surgical history needs to be quickly established, focusing on exclusion and inclusion criteria for administration of IV tPA. IV tPA is the current standard of care for patients who present within 3 hours of symptoms and is recommended in patients up to 4.5 hours if they meet the criteria (Table 20.2).4



TABLE 20.2 Pertinent History in Stroke Patients


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HPI, history of present illness; PMH, past medical history; PSH, past surgical history.


Physical Exam


Assessment of the ABCs (airway, breathing, circulation) and vital signs may also provide clues as to the nature and cause of the stroke (whether hemorrhagic or ischemic). Tachycardia with an irregular heartbeat may support a cardioembolic ischemic stroke. Elevated blood pressure in the setting of headache, nausea/vomiting, and obtundation is more likely to be indicative of a hemorrhagic stroke, although posterior circulation strokes (e.g., a basilar artery occlusion) can present similarly. Once the ABCs are stabilized, a rapid neurologic examination using the National Institutes of Health Stroke Scale (NIHSS) should be obtained (Table 20.3).5,6



TABLE 20.3 NIHSS (National Institutes of Health Stroke Scale)


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Available at www.ninds.nih.gov/doctors/NIH_Stroke_Scale.pdf


The NIHSS is easy to perform, helps predict short-term and long-term outcomes, and can help identify large-vessel occlusion (LVO) strokes.7,8 The scale has been demonstrated to be reliable and reproducible, but proper use requires training and certification, which can be obtained through the American Stroke Association’s Web site (www.strokeassociation.org).9,10


Common clinical syndromes ascribed to specific subtypes of stroke are listed in Table 20.4.1113 While not an exhaustive list, familiarity with these signs and symptoms can help providers localize the region of ischemia. Stroke patients often present with dramatic findings, such as hemiparesis; in isolation, however, weakness can be representative of both large- and small-territory strokes. The presence of cortical signs, such as aphasia, visual field deficits, or a gradient in weakness (face and arm greater than leg involvement), suggests a LVO that may eventually require endovascular therapy. The presence of cranial nerve deficits or cerebellar findings, such as ataxia or dysmetria, may help localize a stroke to the brainstem or posterior fossa.14



TABLE 20.4 Common Signs and Symptoms by Type of Stroke


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MCA, middle cerebral artery; ACA, anterior cerebral artery; PCA, posterior cerebral artery; SCA, superior cerebellar artery; AICA, anterior inferior cerebellar artery; PICA, posterior inferior cerebellar artery.


From Levine J, Johnston K. Diagnosis of stroke and stroke mimics in the emergency setting. Continuum Lifelong Learning Neurol. 2008; Jones HR, Srinivasan J, Allam GJ, et al. Netter’s Neurology. W. B. Saunders Co; 2011; Uchino K, Pary J, Grotta J. Acute Stroke Care. 2011.


PATHOGENESIS


Ischemic stroke is commonly classified according to the following subtypes: small-vessel atherosclerosis, large-artery atherosclerosis, cardioembolic, cryptogenic, or other.15 Other known causes include arterial dissections, infections, trauma, sickle cell disease, and hypercoagulable states. A patient’s particular diagnostic course will depend in part on his or her history of illness and clinical presentation. For example, a patient who presents with heart palpitations followed by stroke symptoms will require a cardiac evaluation for arrhythmias; whereas a patient with stroke symptoms who has sustained neck trauma would need vascular imaging of the chest, neck, and head to identify potential arterial dissections.


DIAGNOSTIC EVALUATION


The initial ED diagnostic workup should consist of a focused history, exam, labs, and imaging. Per the American Heart Association/American Stroke Association (AHA/ASA) guidelines, only a noncontrast CT of the head is required, even though advanced imaging, if available, may help delineate the stroke.4 The rationale for this recommendation is that a noncontrast head CT is sufficient to determine a patient’s eligibility for IV tPA, provided that clinical criteria are already met. Although other imaging such as CT angiogram or MRI may ultimately be required, the decision to give tPA should be made immediately following noncontrast CT so as to avoid delays that can lessen benefit from IV tPA (Table 20.5).



TABLE 20.5 Diagnostic Approach by Time Line


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aThis is a relative time scale and defines the maximum allotted time to complete each step.


bImaging will differ depending on the institution. Only CT of the head is required.


Recommended initial orders and labs include (per AHA/ASA guidelines)



  • Vital Signs
  • ECG and cardiac enzymes
  • INR, PT, PTT, BMP, CBC, troponin, urinalysis, and toxicology (urine studies help in identification of stroke mimics such as hypo/hyperglycemia, DKA, infection, metabolic encephalopathy)
  • Noncontrast CT of the head

The noncontrast CT allows a radiologist to distinguish hemorrhagic from ischemic stroke; the relative acuity of an ischemic stroke; the presence of mass effect or imminent midline shift that would necessitate more aggressive treatment; and the degree of brain parenchyma that is unsalvageable. In patients with stroke onset >3 hours, a hypodensity of greater than or equal to one-third of middle cerebral artery (MCA) territory excludes use of tPA. For ischemic stroke, the emergency physician should be aware of the following radiographic findings indicative of a stroke (Fig. 20.1); these findings may sway the decision to administer IV tPA based on the presumed degree of infarcted brain tissue:



  • A hyperdense MCA
  • Blurring of the insular ribbon
  • Sulcal effacement
  • Blurring of the gray–white junction, especially of the deep structures of the caudate, internal capsule, and putamen


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FIGURE 20.1 A: A hyperdense left MCA with blurring of the insular ribbon and sulcal effacement of the left temporal lobe. B: Blurring of the gray–white junction involving the right caudate, internal capsule, and putamen. C: Sulcal effacement and blurring of the gray–white junction over the entire left MCA territory.


In addition to the subtle findings above, one should evaluate for midline shift, masses/mass effect, blood (in the brain or at the base of the skull), cerebral edema, or herniation. A frequently used tool for the evaluation of ischemic stroke on a head CT is the Alberta Stroke Program Early CT Score (ASPECTS).16 The ASPECTS tool evaluates 10 commonly viewed areas of the MCA territory. Every area of hypodensity is subtracted from 10; a lower composite score indicates more areas of infarcted brain. This tool can be used to evaluate functional outcome (a score of 7 or less associated with poor functional outcome) as well as to estimate the size of any MCA stroke (Fig. 20.2).



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FIGURE 20.2 ASPECTS stroke regions (10 regions assessed). (A) Lower cross-sectional region of interest with deep structures. (B) Higher cross-sectional region of interest for cortex evaluation. C, caudate; L, lentiform nucleus; IC, internal capsule; I, insula; M1–6, corresponding regions of the MCA territory.


MANAGEMENT GUIDELINES


The treatment of acute ischemic stroke centers on urgent revascularization of occluded vessels or augmentation of collateral cerebral blood flow in order to minimize brain infarct size and salvage penumbra. Equally important is the provision of supportive care to minimize stroke complications, including intracerebral hemorrhage, increasing stroke size, and brain herniation, as well as identification of concomitant disease processes such as myocardial infarction, aortic dissection, aspiration pneumonia, or drug intoxication. Management aims to provide appropriate treatment, and to proceed as rapidly as possible to improve neurologic outcome with an acceptably low risk of complications. A decision tree for the management of ischemic stroke is provided in Figure 20.3. Guidelines for standard medical management are detailed in Table 20.6. Potential complications of stroke therapy and their management are reviewed in Table 20.7. Additional standard ischemic stroke protocols, criteria, and order sets are provided in Table 20.8.4,1719 Indications and contraindications to IV tPA are listed in Table 20.9.



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FIGURE 20.3 Acute-Stroke Flow Chart. ^Meta-analysis of stroke mimics treated with IV tPA revealed no adverse events (involve stroke team in decision). From Chang J, Teleb M, Yang JP, et al. A model to prevent fibrinolysis in patients with stroke mimics. J Stroke Cerebrovasc Dis. 2011;21(8):839843. doi:10.1016/j.jstrokecerebrovasdis.2011.04.018; Tsivgoulis G, Alexandrov AV, Chang J, et al. Safety and outcomes of intravenous thrombolysis in stroke mimics: a 6-year, single-care center study and a pooled analysis of reported series. Stroke. 2011;42(6):17711774. doi:10.1161/STROKEAHA.110.609339

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Dec 22, 2016 | Posted by in CRITICAL CARE | Comments Off on Ischemic Stroke
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