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Life-threatening neurologic illness may be caused by a primary disorder affecting any region of the neuraxis or may occur as a consequence of a systemic disorder such as hepatic failure, multisystem organ failure, or cardiac arrest (Table 275-1). Neurologic critical care focuses on preservation of neurologic tissue and prevention of secondary brain injury caused by ischemia, edema, and elevated intracranial pressure (ICP). Management of other organ systems proceeds concurrently and may need to be modified in order to maintain the overall focus on neurologic issues.

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Table 275-1 Neurologic Disorders in Critical Illness 
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Pathophsiology

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Brain Edema

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Swelling, or edema, of brain tissue occurs with many types of brain injury. The two principal types of edema are vasogenic and cytotoxic. Vasogenic edema refers to the influx of fluid and solutes into the brain through an incompetent blood-brain barrier (BBB). In the normal cerebral vasculature, endothelial tight junctions associated with astrocytes create an impermeable barrier (the BBB), through which access into the brain interstitium is dependent upon specific transport mechanisms. The BBB may be compromised in ischemia, trauma, infection, and metabolic derangements. Typically, vasogenic edema develops rapidly following injury. Cytotoxic edema refers to cellular swelling and occurs in a variety of settings, including brain ischemia and trauma. Early astrocytic swelling is a hallmark of ischemia. Brain edema that is clinically significant usually represents a combination of vasogenic and cellular components. Edema can lead to increased ICP as well as tissue shifts and brain displacement from focal processes (Chap. 274). These tissue shifts can cause injury by mechanical distention and compression in addition to the ischemia of impaired perfusion consequent to the elevated ICP.

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Ischemic Cascade and Cellular Injury

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When delivery of substrates, principally oxygen and glucose, is inadequate to sustain cellular function, a series of interrelated biochemical reactions known as the ischemic cascade is initiated (see Fig. 370-2). The release of excitatory amino ...

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