Hypertensive Encephalopathy: Definition, Causes, Symptoms, Treatment and Laboratory Studies

High blood pressure in the brain.

Hypertensive encephalopathy is a syndrome that consists of a sudden rise in blood pressure usually preceded by severe headache and followed by seizures, coma, or a variety of transient brain phenomena.

The syndrome can complicate acute glomerulonephritis, toxemia of pregnancy, and essential or malignant hypertension. Two syndromes of true hypertensive encephalopathy should be differentiated:

  1. Critical anxiety state with labile hypertension
  2. Acute pulmonary edema due to hypertensive heart disease.

At least in patients with acute anxiety states, the use of antihypertensive drugs is generally not indicated.

Since encephalopathy is always accompanied by increased vascular resistance and clinical experience has shown the cessation of seizures and release of vasoconstriction after reducing blood pressure, the main objective of therapy should be a prompt reduction of blood pressure. The two agents of choice are diazoxide and sodium nitroprusside.


The clinical manifestations of hypertensive encephalopathy are due to increased cerebral perfusion of the loss of integrity of the blood-brain barrier, which results in fluid exudation in the brain.

In normotensive individuals, an increase in systemic blood pressure in a particular range (i.e., 60-125 mm Hg) induces cerebral arteriolar vasoconstriction, thus preserving a constant cerebral blood flow (CBF) and an intact blood-brain barrier.


In chronic hypertensive people, the brain range gradually shifts to higher pressures as an adaptation to the chronic elevation of systemic blood pressure; this adaptive response since it is overwhelmed during a hypertensive emergency in which the acute increase in systemic blood pressure exceeds the individual’s brain range, resulting in hydrostatic loss through capillaries within the central nervous system (CNS).

Brain scans have shown a pattern typically in the posterior brain (frontal superior occipital) edema that is reversible.

This is usually called reversible posterior leukoencephalopathy or reversible posterior encephalopathy syndrome (PRSS).

With the persistent elevation of systemic blood pressure, necrosis, and arteriolar damage, the progression of vascular pathology leads to generalized vasodilation, cerebral edema, and papilledema, which manifest clinically as neurological deficits and alter the sensorium in hypertensive encephalopathy.

The most common cause of hypertensive encephalopathy is the sudden rise in blood pressure in a chronic hypertensive patient. Other conditions that may predispose a patient with high blood pressure and cause the same clinical situation include the following:

  • Chronic renal parenchymal disease
  • Acute glomerulonephritis
  • Renewcular hypertension
  • Withdrawal of hypertensive agents (e.g., clonidine)
  • Encephalitis, meningitis
  • Pheochromocytoma, tumors that secrete renin
  • Sympathomimetic agents (e.g., cocaine, amphetamines, phencyclidine [PCP], and lysergic acid diethylamide [LSD])
  • Eclampsia y preeclampsia
  • Cranial trauma, cerebral infarction
  • Collagen vascular disease
  • Autonomic hyperactivity
  • Vasculitis
  • Ingestion of antidepressants, foods, or tricyclic antidepressants containing tyramine in combination with monoamine oxidase inhibitors (MAOIs)

Symptoms of Hypertensive Encephalopathy

The majority of patients with hypertensive encephalopathy have a history of hypertension. In patients who do not have a history of hypertension, emphasis should be placed on the medical history of the past, the list of medications and compliance with the medication, actively seeking causes of drug-induced, for example, sympathomimetic agents and illicit drugs such as cocaine.

Patients usually present with vague neurological symptoms and may show signs of headache, confusion, visual disturbances, seizures, nausea, and vomiting.

Symptoms usually occur for 24-48 hours, with neurological progression for 24-48 hours.

Patients can also present symptoms that result in damage to other organs; some examples that illustrate these symptoms are:

  • Cardiovascular symptoms of aortic dissection, congestive heart failure, angina pectoris, palpitations, irregular heartbeat, or dyspnea
  • Renal hematuria and acute renal failure


Pharmacological therapy

Pharmacological agents in hypertensive encephalopathy should have little or no adverse effect on the central nervous system (CNS).

Agents such as clonidine, reserpine, and methyldopa should be avoided. Although the clinical impact of diazoxide has not been determined, this agent is avoided due to the effects of decreased FEBIC. Many health authorities consider esmolol, labetalol, and nicardipine as preferred initial agents.

Nicardipine is a calcium channel blocker dihydropyridine-derived second generation, which has high vascular selectivity and vigorous coronary and cerebral vasodilator activity. It has been shown to increase systolic volume and coronary blood flow.

Labetalol provides a constant fall consistent in blood pressure without compromising the CBF. It is often used as an initial treatment. Due to its non-selective beta-blocker properties, labetalol should be avoided in severe reactive airway disease and cardiogenic shock.

Nitroglycerin has been used to reduce high blood pressure that complicates myocardial ischemia rapidly. The reduction of blood pressure can be severe and can cause more complications due to the vasodilatory effects in individuals.

Hydralazine and sodium nitroprusside represent a theoretical risk of intracranial blood diversion. Consequently, these agents should be avoided in patients suspected of having increased intracranial pressure (ICP) because the intracerebral deviation potential of blood may increase ICP.

Hydralazine has a limited role in this setting due to tachycardia and should not be used in patients with suspected coronary artery disease (CAD). Diuretics should also not be used in these patients unless there is clear evidence of volume overload.

This is due to the pressure natriuresis that occurs and leaves these patients with an exhausting volume. The volume depletion by itself can sometimes lower blood pressure.

If neurological deterioration worsens with therapy, it is necessary to reconsider the measure of blood pressure reduction or consider alternative diagnoses.

Laboratory studies

Hypertensive encephalopathy is a diagnosis of exclusion; other potential causes of the symptoms should be evaluated in an intense diagnostic study as indicated by the clinical results. The evaluation includes determining the degree of hypertensive damage and excluding the intracranial processes.

Obtain a complete blood count (CBC) to determine if microangiopathic hemolytic anemia is present.

Perform a urine and blood test to measure urea nitrogen (BUN) and creatinine; with hypertensive nephropathy, an elevated creatinine with hematuria and molds may be present. Cardiac enzyme studies are ordered to exclude myocardial ischemia. A urine toxicology test is performed to help exclude drug-induced hypertensive encephalopathy.

Consider computed tomography (CT) of the head to look for evidence of stroke, bleeding or intracranial masses.

Chest radiographs are obtained to evaluate the possible complications of hypertensive encephalopathy, including aspiration due to alterations of the sensorium.

Chest x-rays can also evaluate other conditions, such as acute pulmonary edema and aortic dissection. Electrocardiography (ECG) is performed to assess the presence of cardiac ischemia.