Hypertensive Encephalopathy

Although no specific blood pressure is pathognomic, the elevated pressure must exceed the limits of cerebral autoregulation of the small-resistance arteries, resulting in cerebral hyperperfusion with loss of integrity of the blood-brain barrier. In most cases, autoregulation usually cannot accommodate a constant cerebral blood flow above a MAP of 150 to 200 mmHg. Immediate reduction of blood pressure by 20 to 25 percent will help reverse the vasospasm that occurs at these pressures; however, excessive reduction in blood pressure must be avoided in order to prevent hypoperfusion and further cerebral ischemia. —I2

Hypertensive encephalopathy is usually acute in onset and reversible. It is characterized by severe headaches, nausea, and vomiting, and may also include altered mental status. Neurologic symptoms can range from confusion and drowsiness to seizures, decreased visual acuity, focal deficits, or even coma. Since the pathologic mechanisms are the same, accelerated hypertensive retinopathy is often seen. The differential diagnosis is wide and includes intracranial hemorrhage, stroke, meningoencephalitis, brain tumors, toxidromes, and metabolic coma. If hypertensive encephalopathy is suspected, antihypertensive therapy should be initiated while awaiting the results of certain key studies such as chemistry tests and CT scan.

Hypertensive encephalopathy is a true medical emergency and, if left untreated, can progress over hours and lead to coma and death. The treatment of choice is sodium nitroprusside infused at an initial dose of 0.5 (^g/kg)/min and titrated up to a maximum of 10 (^g/kg)/min. Intravenous nitroglycerin and labetalol have been successfully used, but they have not replaced nitroprusside as first-line therapy for hypertensive encephalopathy.

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