Malignant hypertension and hypertensive encephalopathy are two acute, life-threatening clinical syndromes usually associated with marked

increases in blood pressure (BP), generally 180/120 mmHg. Malignant hypertension refers to marked hypertension with retinal hemorrhages, exudates, or papilledema. There may also be renal involvement, called malignant nephrosclerosis. Hypertensive encephalopathy refers to the presence of signs of cerebral edema caused by breakthrough hyperperfusion from severe and sudden rises in blood pressure. With increasingly severe hypertension, autoregulation fails (figure 1), and the ensuing rise in pressure in arterioles and capillaries leads to disruption of the vascular endothelium. Plasma constituents (including fibrinoid material) enter the vascular wall, 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. (See 'Mechanisms of vascular injury' above.) Malignant hypertension most often occurs in patients with long-standing uncontrolled hypertension, many of whom have discontinued antihypertensive therapy. (See'Clinical manifestations' above.) In addition to marked elevation in BP, the major clinical manifestations of malignant hypertension include: (See 'Clinical manifestations' above.) Retinal hemorrhages and exudates Malignant nephrosclerosis, with acute kidney injury, hematuria, and proteinuria Neurologic symptoms due to intracerebral or subarachnoid bleeding and lacunar infarcts Hypertensive encephalopathy is characterized by the insidious onset of headache, nausea, and vomiting, followed by nonlocalizing neurologic symptoms such as restlessness, confusion, and, if the hypertension is not treated, seizures and coma. (See 'Clinical manifestations' above.) In the presence of neurologic symptoms, a magnetic resonance imaging (MRI) study should be obtained to exclude a stroke, which is not usually treated with aggressive BP reduction. With hypertensive encephalopathy, MRI may reveal edema of the white matter of the parieto-occipital regions, a finding termed reversible posterior leukoencephalopathy syndrome. (See 'Clinical manifestations' above.) Malignant hypertension and hypertensive encephalopathy should be initially treated with parenteral antihypertensive medications. Commonly used agents includeNitroprusside, Nicardipine, Labetalol, Clevidipine, and Fenoldopam. (See 'Antihypertensive drugs' above.) The initial aim of treatment in malignant hypertension and hypertensive encephalopathy is to lower the diastolic pressure to about 100 to 105 mmHg within two to six hours, with the maximum fall in BP over this period of time not exceeding 25 percent of the original value. More aggressive antihypertensive therapy is both unnecessary and may reduce the BP below the autoregulatory range, possibly leading to ischemic events (such as stroke or coronary disease). (See 'Goal of therapy'above.) Once the BP is controlled, the patient should be switched to oral therapy, with the diastolic pressure being gradually reduced to 85 to 90 mmHg over two to three months. (See 'Goal of therapy' above.) Even with effective antihypertensive therapy, most patients who have had malignant hypertension still have moderate to severe chronic and acute vascular damage and are at continued risk for coronary, cerebrovascular, and renal disease. (See 'Prognosis' above.)

Hypertensive emergencies require rapid lowering of the blood pressure (BP). (See 'Introduction' above.) A variety of antihypertensive drugs can be used to treat hypertensive emergencies; an overview of the mechanism of action, doses, and routes of administration of these agents is provided in the following table (table 1). (See 'Antihypertensive drugs' above.) Malignant hypertension and hypertensive encephalopathy can be managed with various parenteral antihypertensive medications, most commonly nitroprusside,nicardipine, labetalol, or fenoldopam. The blood pressure should not be lowered by more than 25 percent of the original value. (See 'Malignant hypertension and hypertensive encephalopathy' above and "Malignant hypertension and hypertensive encephalopathy in adults".) The optimal antihypertensive regimen, rapidity of blood pressure lowering, and blood pressure goal varies in patients with severe hypertension who have an ischemic stroke or subarachnoid or intracerebral hemorrhage. (See 'Ischemic stroke or subarachnoid or intracerebral hemorrhage' above and "Antihypertensive therapy to prevent recurrent stroke or transient ischemic attack" and "Spontaneous intracerebral hemorrhage: Treatment and prognosis", section on 'Blood pressure' and"Treatment of aneurysmal subarachnoid hemorrhage", section on 'Intracranial pressure'.) Severe hypertension in patients with acute left ventricular failure due to systolic dysfunction should be principally treated with vasodilators (eg, nitroprusside or nitroglycerine). Drugs that increase cardiac work (hydralazine) or decrease cardiac contractility (labetalol or other beta blocker) should be avoided. (See 'Acute pulmonary edema' above and "Treatment of acute decompensated heart failure: General considerations".) Acute coronary insufficiency frequently increases the systemic blood pressure. Beta adrenergic blockers should be administered to all patients without contraindications who experience a myocardial infarction. Intravenous parenteral vasodilators, principally nitroglycerin, effectively lower blood pressure and reduce symptoms in patients with acute myocardial infarction. Drugs that increase cardiac work (hydralazine) are contraindicated. (See 'Angina pectoris or acute myocardial infarction' above and "Overview of the acute management of ST elevation myocardial infarction" and "Overview of the acute management of unstable angina and non-ST elevation myocardial infarction".) In patients with aortic dissection, an intravenous beta adrenergic blocker should be given to reduce the heart rate below 60 beats/min and maintain the systolic blood pressure between 100 to 120 mmHg or the lowest level that is tolerated. Nitroprusside can be added to further control blood pressure but should not be given without first controlling the heart rate with beta blockade. (See 'Aortic dissection' above and "Management of aortic dissection", section on 'Acute management'.)