Hypertensive emergencies: Malignant hypertension and hypertensive encephalopathy

DEFINITIONS

Hypertensive emergencies are acute, life-threatening, and usually associated with marked increases in blood pressure (BP), generally ≥180/120 mmHg (table 1) [1-3]. There are two major clinical syndromes induced by the severe hypertension:

• Malignant hypertension is marked hypertension with retinal hemorrhages, exudates, or papilledema. There may also be renal involvement, called malignant nephrosclerosis. Although papilledema had been thought to represent a more severe lesion, it does not appear to connote a worse prognosis than hemorrhages and exudates alone (so-called accelerated hypertension) [4]. Thus, treatment is the same whether or not papilledema is present.
• Hypertensive encephalopathy refers to the presence of signs of cerebral edema caused by breakthrough hyperperfusion from severe and sudden rises in blood pressure.

MECHANISMS OF VASCULAR INJURY

With mild to moderate elevations in blood pressure, the initial response is arterial and arteriolar vasoconstriction. This autoregulatory process both maintains tissue perfusion at a relatively constant level and prevents the increase in pressure from being transmitted to the smaller, more distal vessels [5].

With increasingly severe hypertension, however, autoregulation eventually fails (graph 1) [5]. The ensuing rise in pressure in the arterioles and capillaries leads to damage to the vascular wall. Disruption of the vascular endothelium then allows plasma constituents (including fibrinoid material) to enter the vascular wall, thereby narrowing or obliterating the vascular lumen. Within the brain, the breakthrough vasodilation from failure of autoregulation leads to the development of cerebral edema and the clinical picture of hypertensive encephalopathy [5].

The level at which fibrinoid necrosis occurs is dependent upon the baseline BP. Patients with chronic hypertension have arteriolar hypertrophy that minimizes the transmission of pressure to the capillary circulation. As a result, malignant hypertension is usually associated with a diastolic pressure above 120 mmHg. In comparison, hypertensive encephalopathy can be seen at diastolic pressures as low as 100 mmHg in previously normotensive patients with acute hypertension due to preeclampsia or acute glomerulonephritis; patients in whom autoregulation is impaired also may develop hypertensive injury at relatively mild degrees of hypertension [5].