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  Time is brain. Time of symptom onset is key to acute stroke treatment.

  
  
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  Hypoglycemia and hypoxia can mimic stroke. Assess and treat these conditions early in the evaluation of patients with stroke-like symptoms.

  
  
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  Resist the urge to aggressively lower blood pressure. Hypertension is the body’s attempt to maintain perfusion to ischemic tissue. Hypotension can make things worse.

  
  
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  Transient ischemic attack (TIA) is a warning of a stroke to come (aborted stroke). Treat TIAs seriously and work up risk factors expediently.

Roughly 750,000 strokes occur annually in the United States, and this will increase as the population ages. Physical, emotional, and economic damages are multifactorial. The cost of initial care is only the beginning. Many stroke survivors are not only unable to return to work, they are unable to care for themselves, placing heavy demands on family and friends.

Stroke is defined as a neurologic deficit resulting from the interruption of blood supply to neuronal tissue. The brain is highly metabolically active, consuming roughly 25% of cardiac output, but has no mechanism for storing energy reserves. This makes it extremely sensitive to even transient interruption in its supply of oxygen and glucose. Vascular compromise may be caused by several different mechanisms, but the final common pathway is impaired neuronal perfusion and tissue starvation.

Strokes are often classified in 2 different ways: etiology and location. Etiologic causes can be classified as either hemorrhagic or ischemic. Hemorrhagic strokes account for 10–20% of all strokes. They sometimes result from the rupture of an aneurysm or arteriovenous malformation (AVM), usually causing bleeding on the surface of the brain. More commonly, the bleeding comes from disruption of an intracerebral arteriole, leading to bleeding inside the parenchyma of the brain. Uncontrolled hypertension is the most common precipitant of intracerebral bleeding, but other conditions such as amyloidosis and tumors can increase the chances of intracerebral bleeding. Vasospasm can occur from the irritant effects of blood on the surface of the brain, leading to an even greater decrease in blood flow.

Ischemic strokes are caused primarily by thrombosis of a blood vessel, very similar to mechanisms involved in myocardial infarction. Conditions such as atherosclerosis, hypercoagulable states, polycythemia, and vasculitis are common precipitants. About 20% of ischemic strokes result from embolic phenomenon. The carotid bifurcation is a common source of plaque embolism. Cardiac mural thrombus and valve disease are also likely sources of embolism.

Classification by location depends on the blood vessel or vascular distribution involved (Table 82-1). The blood supply to the brain comes from paired carotid and vertebral blood vessels. The carotid distribution (ie, anterior circulation) supplies primarily cerebral and cortical structures, whereas the vertebrobasilar vascular distribution (ie, posterior circulation) feeds the cerebellum and brainstem structures. The involved vessel can often be inferred from the clinical presentation. Carotid circulation strokes commonly present with motor and sensory deficits that are fairly obvious. Visual field defects, neglect, and language difficulties (eg, aphasia) are often apparent on exam. The internal carotid bifurcates into the anterior carotid artery (ACA), which feeds areas involved in control of the leg, and the middle carotid artery (MCA), which feeds areas more involved in control of the face and arm. Smaller branches penetrate deeper into areas such as the internal capsule. Strokes in these vessels can give pure sensory or motor deficits. Vertebrobasilar strokes cause ischemia in the brainstem or cerebellum. Large brainstem strokes are usually fatal. Smaller ones can lead to cranial nerve dysfunction and more subtle findings, such as vertigo. Cerebellar strokes can be much harder to recognize, emphasizing the importance of looking for ataxia, balance, and fine motor control on the neurologic exam. These signs are often not noticed by the patients themselves.

Until the mid 1990s, the treatment for acute ischemic stroke was almost entirely supportive care. In 1996, the Food and Drug Administration (FDA) approved the use of tissue plasminogen activator (TPA). Some facilities are employing intravascular catheter-guided clot lysis or evacuation. With the availability of these newer treatments, stroke patients now rank as true medical emergencies that warrant the focused resources of the emergency department (ED). With the time dependency of treatment options, much work has gone into increasing public awareness of stroke and enhancing prehospital recognition and transport. Many hospitals have developed dedicated stroke teams and stroke protocols to expedite care of acute stroke patients.

Transient ischemic attacks (TIAs) are defined as “a transient episode of neurologic dysfunction caused by focal brain, spinal cord or retinal ischemia, without acute infarction.” Symptoms typically last less than 1–2 hours. These patients should be assessed and treated as acute strokes, with the exception of fibrinolytic treatment. TIAs are the equivalent of unstable angina in coronary disease and should be treated as “warning signs of strokes to come.” Some studies estimate as many as 20% of TIA patients will suffer a stroke within 90 days, half of which may occur within 48 hours.

History

Reperfusion strategies are both time- and situation-dependant. Gathering accurate historical information as quickly as possible is a critical facet of treatment. Issues such as aphasia and cognitive dysfunction can make it very difficult to get information directly from the patient. Make efforts to contact others (family, nursing home staff) who can provide historical details. Hemineglect and gaze deviation may cause patients not to be aware of you. Be sure you are in the patient’s line of sight and touch them while you are talking to them.

One of the most important historical considerations is to determine when the symptoms began. If the patient had symptoms on awakening, or cannot clearly identify the time they started, the start time is considered the last time the patient was seen as normal. The “time last known well” is important to obtain early because it will determine whether fibrinolytics will be considered. The window to administer fibrinolytics intravenously (IV) is usually an onset of symptoms within the last 3 hours. If fibrinolytics are being considered, ask about contraindications to their administration. Is there a history of previous intracranial bleeding? Brain tumor? Head injury? Recent surgery? Is the patient on anticoagulants?

Ask the patient how he or she noticed the symptoms and what he or she was doing when it started. Is the patient dizzy, off balance, or falling? Is the patient having pain or weakness or both? Has the patient had these symptoms before? Extremity pain is an unusual feature of a stroke and suggests an alternate diagnosis. Onset of symptoms with severe headache, seizure, and syncope suggests a hemorrhage stroke. Neck pain or history of neck trauma or manipulation may indicate carotid or vertebral dissection.

When assessing the past medical history, determine whether a stroke mimic is possible. Diabetic patients may be presenting with hypoglycemia. Patients with a history of seizures may be postictal. Patients with a history of migraines may also present with stroke-like symptoms.

Lastly, elicit risk factors for stroke. Atrial fibrillation and valvular disease are common risk factors for emboli. Diabetes and hypertension are risk factors for thrombotic strokes.