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The three broad categories of stroke are hemorrhagic, thrombotic, and embolic (i.e., artery to artery and chamber to artery).
Carotid plaque, unlike coronary lesions, most often causes symptoms due to atheroembolization rather than thrombotic occlusion.
The size of a brain infarction is determined by the time it takes for reperfusion to occur, the patency of the circle of Willis as a collateral source, and the viability of the surrounding penumbra of ischemic tissue.
The only approved treatment for acute ischemic stroke is intravenous thrombolysis within 3 to 4.5 hours of onset and without contraindications.
The risk of intracranial hemorrhage complicating intravenous thrombolytic therapy for stroke is increased in direct relation to the size of the stroke, time to treatment (>3 hours), patient age (>85 years), and uncontrolled hypertension.
Recently completed randomized controlled trials involving ischemic stroke have established that mechanical thrombectomy in patients with large-vessel occlusions with or without intravenous tissue-type plasminogen activator (IV tPA) is preferred over IV tPA alone, yielding higher recanalization rates, higher rates of favorable clinical outcomes, and similar complication rates.
Outcomes of endovascular stroke therapy given by interventional cardiologists on a stroke team are not inferior to the outcomes of therapy given by neurovascular specialists.
Stroke affects approximately 70,000 Americans each year, resulting in almost 150,000 deaths. Stroke is the third leading cause of death in the United States, after heart disease and cancer. It is the number one cause of disability and the number one reason for rehabilitation. There are more than 3 million stroke survivors in the United States, and one-third of them are young adults with long-term disabilities.
The causes of stroke include hemorrhage, thrombus, and embolus. Embolic strokes may extend artery to artery or from a heart chamber (left atrium or ventricle) to an artery, particularly in patients with atrial fibrillation. A major tenet of the treatment of ischemic stroke is that time is brain .
The extent of ischemic brain injury is determined by the time from the onset of symptoms to reperfusion; the collateral circulation, including an intact circle of Willis; and the penumbra of viability surrounding the infarcted brain tissue. The penumbra is the region of brain surrounding the infarct area where the blood supply is significantly reduced but energy metabolism is maintained due to collateral flow. The viability of this area depends on the severity and duration of ischemia. If blood flow is rapidly restored, some ischemic brain tissue can be saved. For ischemic and hemorrhagic strokes, there are opportunities to minimize injury early after the onset of the stroke. This puts a premium on the rapid assessment of patients with stroke ( Table 47.1 ).
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The goals of treatment include preventing or limiting the mortality and morbidity of the acute event and preventing recurrent events. More than 80% of strokes are ischemic. Ischemic stroke therapy, designed to achieve reperfusion as quickly as possible and to minimize further damage, consists of intravenous thrombolysis with or without catheter-based reperfusion therapy, which can include intra arterial thrombolysis, mechanical thrombectomy, or balloon angioplasty with or without stent placement.
Rapid initiation of intravenous tissue-type plasminogen activator (IV tPA) with a door-to-needle time of less than 60 minutes is important for a good outcome. However, the American Heart Association’s Get With the Guidelines–Stroke national registry has reported that fewer than one in three stroke patients are treated within less than 60 minutes of arrival at the hospital. Although a national heart attack quality initiative has enabled interventional cardiologists to achieve dramatic reductions in door-to-balloon times, acute stroke therapy languishes without a mandate to provide early reperfusion. Currently there is no goal for time to reperfusion or door-to-treatment time in the United States, and it is not the standard of care for stroke therapy as it is for heart attacks. Unfortunately, owing to a variety of issues—including time to presentation, availability of stroke programs, and a lack of national focus on time to treatment—the majority of patients with ischemic stroke in the United States do not receive reperfusion therapy.
The American Heart Association/American Stroke Association (AHA/ASA) has a class I recommendation to perform noncontrast computed tomography (CT) or magnetic resonance imaging (MRI) for patients who are evaluated within 3 hours of stroke symptom onset so as to exclude intracranial bleeding. Imaging is the cornerstone for triaging candidates for stroke therapy. The purpose of the baseline CT is to detect conditions that make the patient ineligible for thrombolysis, such as subdural, subarachnoid, or parenchymal intracranial hemorrhage (ICH). CT may also detect mass lesions or hemorrhagic infarctions.
Brain imaging in the setting of an acute stroke has four major goals. First, ICH must be excluded. The patient with ICH has a neurosurgical emergency, and the neurosurgeon must be involved immediately. Second, CT and MRI can be used to identify intravascular thrombus noninvasively. Data regarding the geographic distribution and size of the thrombus burden can assist in deciding between IV tPA and endovascular mechanical thrombectomy. Third, the ratio of the volume of viable to nonviable brain (penumbra) predicts the patient’s potential for recovery.
Multimodal CT includes unenhanced CT, CT angiography (CTA), and CT perfusion. Noncontrast CT can identify ICH and detect early signs of acute ischemic stroke. CTA can identify the occlusion site, detect arterial dissection, and grade collateral blood flow, whereas CT perfusion can differentiate between tissue at risk (the so-called penumbra) and irreversibly damaged brain tissue.
A cornerstone of managing acute stroke is reducing the risk of recurrent events and minimizing the disability due to the established stroke. Acute therapy involves the management of physiologic variables, reperfusion of ischemic tissue, and reduction of the risk of ICH. The patient’s level of consciousness, airway status, and oxygenation must be determined immediately. An electrocardiogram is needed to rule out a concomitant myocardial infarction.
Most patients with stroke have arterial hypertension, which is associated with a poorer outcome, but lower blood pressure may decrease perfusion to the ischemic penumbra, extending the size of the infarction. Hypertensive patients who are eligible for treatment with IV tPA should have their blood pressure carefully lowered so that their systolic blood pressure is <185 mm Hg and their diastolic blood pressure is <110 mm Hg before fibrinolytic therapy is initiated. If medications are given to lower blood pressure, the clinician should be sure that the blood pressure is stabilized at the lower level before beginning treatment with IV tPA and that it is maintained below 180/105 mm Hg for at least the first 24 hours after intravenous IV tPA treatment.
In patients with markedly elevated blood pressure who do not receive fibrinolysis, a reasonable goal is to lower blood pressure by 15% during the first 24 hours after the onset of stroke. The level of blood pressure that would mandate such treatment is not known, but consensus exists that medications should be withheld unless the systolic blood pressure is >220 mm Hg or the diastolic blood pressure is >120 mm Hg. Restarting antihypertensive medications is reasonable after the first 24 hours for patients who have preexisting hypertension and are neurologically stable unless a specific contraindication to restarting treatment is known. Patients who have malignant hypertension or other medical indications for the aggressive treatment of blood pressure should be treated accordingly.
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