Hypertensive Encephalopathy Management

A hypertensive emergency is severe hypertension with signs of damage to target organs (primarily the brain, cardiovascular system, and kidneys). Diagnosis is by BP measurement, ECG, urinalysis, and serum BUN and creatinine measurements.

Treatment is immediate BP reduction with IV drugs (eg, clevidipine, fenoldopam, nitroglycerin, nitroprusside, nicardipine, labetalol, esmolol, hydralazine).

Target-organ damage includes hypertensive encephalopathy, preeclampsia and eclampsia, acute left ventricular failure with pulmonary edema, myocardial ischemia, acute aortic dissection, and renal failure.

Damage is rapidly progressive and often fatal.

Hypertensive encephalopathy may involve a failure of cerebral autoregulation of blood flow. Normally, as BP increases, cerebral vessels constrict to maintain constant cerebral perfusion.

Above a mean arterial pressure (MAP) of about 160 mm Hg (lower for normotensive people whose BP suddenly increases), the cerebral vessels begin to dilate rather than remain constricted.

As a result, the very high BP is transmitted directly to the capillary bed with transudation and exudation of plasma into the brain, causing cerebral edema, including papilledema. Pathophysiology of other target-organ manifestations is discussed elsewhere in The Manual.

Although many patients with stroke and intracranial hemorrhage present with elevated BP, elevated BP is often a consequence rather than a cause of the condition. Whether rapidly lowering BP is beneficial in these conditions is unclear; it may even be harmful.

Hypertensive urgencies: Very high blood pressure (eg, diastolic pressure > 120 to 130 mm Hg) without target-organ damage (except perhaps grades 1 to 3 retinopathy—see Diagnosis) may be considered a hypertensive urgency. BP at these levels often worries the physician; however, acute complications are unlikely, so immediate BP reduction is not required.

However, patients should be started on a 2-drug oral combination (see Drugs), and close evaluation (with evaluation of treatment efficacy) should be continued on an outpatient basis.

Symptoms and Signs

BP is elevated, often markedly (diastolic pressure > 120 mm Hg). CNS symptoms include rapidly changing neurologic abnormalities (eg, confusion, transient cortical blindness, hemiparesis, hemisensory defects, seizures).

Cardiovascular symptoms include chest pain and dyspnea. Renal involvement may be asymptomatic, although severe azotemia due to advanced renal failure may cause lethargy or nausea.

Physical examination focuses on target organs, with neurologic examination, funduscopy, and cardiovascular examination.

Global cerebral deficits (eg, confusion, obtundation, coma), with or without focal deficits, suggest encephalopathy; normal mental status with focal deficits suggests stroke. Severe retinopathy (sclerosis, cotton-wool spots, arteriolar narrowing, hemorrhage, papilledema) is usually present with hypertensive encephalopathy, and some degree of retinopathy is present in many other hypertensive emergencies.

Jugular venous distention, basilar lung crackles, and a 3rd heart sound suggest pulmonary edema. Asymmetry of pulses between arms suggests aortic dissection.


Complications of hypertensive encephalopathy result in neurologic deficits from hemorrhage and strokes, which can progress to death. Complications of hypertension include the following:

  • Coma
  • Death
  • Stroke
  • Nephropathy
  • Myocardial ischemia or infarction
  • Nephropathy
  • Retinopathy
  • Peripheral vascular disease


Very high BP

Identify target-organ involvement: ECG, urinalysis, BUN, creatinine; if neurologic findings, head CT
Testing typically includes ECG, urinalysis, and serum BUN and creatinine.

Patients with neurologic findings require head CT to diagnose intracranial bleeding, edema, or infarction. Patients with chest pain or dyspnea require chest x-ray.

ECG abnormalities suggesting target-organ damage include signs of left ventricular hypertrophy or acute ischemia. Urinalysis abnormalities typical of renal involvement include RBCs, RBC casts, and proteinuria.

Diagnosis is based on the presence of a very high BP and findings of target-organ involvement.

Laboratory Studies

Hypertensive encephalopathy is a diagnosis of exclusion; other potential causes of the symptoms must be evaluated in the workup as indicated by the clinical findings.

Evaluation includes determining the extent of hypertensive damage and excluding intracranial processes. Laboratory and radiologic studies do not take the place of a careful history and physical examination (see Presentation).

Obtain a complete blood count (CBC) to determine whether microangiopathic hemolytic anemia is present. Perform a urinalysis, and measure blood urea nitrogen (BUN) and creatinine levels; with hypertensive nephropathy, an elevated creatinine with hematuria and casts may be present.

Order cardiac enzyme studies to exclude myocardial ischemia. Perform a urine toxicology screen to help exclude drug-induced hypertensive encephalopathy.


  • Admit to ICU
  • Short-acting IV drug: nitrates, fenoldopam, nicardipine or labetalol
  • Goal: 20 to 25% reduction MAP in 1 to 2 h
  • Hypertensive emergencies are treated in an ICU; BP is progressively (although not abruptly) reduced using a short-acting, titratable IV drug. Choice of drug and speed and degree of reduction vary somewhat with the target organ involved, but generally a 20 to 25% reduction in MAP over an hour or so is appropriate, with further titration based on symptoms. Achieving “normal” BP urgently is not necessary.

Source & More Info: E Medicine and Merck Manuals



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