Hypertensive Encephalopathy

Author: Irawan Susanto, MD, FACP; Chief Editor: Michael R Pinsky, MD, CM, Dr(hc), FCCP, MCCM
Updated: Apr 14, 2015

Updated: Apr 14, 2015


Epidemiology and Prognosis
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The term hypertensive encephalopathy was introduced in 1928 to describe the encephalopathic findings
associated with the accelerated malignant phase of hypertension. The terms accelerated and malignant
were used to describe the retinal findings associated with hypertension, as follows:

Accelerated hypertension is associated with group 3 Keith-Wagener-Barker retinopathy, which is
characterized by retinal hemorrhages and exudates on funduscopic examination

Malignant hypertension is associated with group 4 Keith-Wagener-Barker retinopathy, which is
characterized by the presence of papilledema, heralding neurologic impairment from an elevated
intracranial pressure (ICP)
With adequate control of hypertension, less than 1% of patients experience a hypertensive crisis. A
hypertensive crisis is classified as either a hypertensive emergency or a hypertensive urgency,[1] as follows:

Acute or ongoing vital target organ damage (eg, damage to the brain, kidney, or heart) in the
setting of severe hypertension is considered a hypertensive emergency; a prompt reduction in blood
pressure is required within minutes or hours

The absence of target organ damage in the presence of a severe elevation in blood pressure (with
diastolic blood pressure frequently exceeding 120 mm Hg) is considered a hypertensive urgency; a
reduction in blood pressure is required within 24-48 hours
A continuum exists between the clinical syndromes of hypertensive urgency and emergency; hence, the
distinction between the 2 syndromes may not always be clear and precise in practice. [2]
Hypertensive encephalopathy refers to the transient migratory neurologic symptoms that are associated
with the malignant hypertensive state in a hypertensive emergency. The clinical symptoms are usually
reversible with prompt initiation of therapy. In the evaluation of an encephalopathic patient, it is vital to
exclude systemic disorders and various cerebrovascular events that may present with a similar
constellation of clinical findings.

The clinical manifestations of hypertensive encephalopathy are due to increased cerebral perfusion from
the loss of blood-brain barrier integrity, which results in exudation of fluid into the brain. In normotensive
individuals, an increase in systemic blood pressure over a certain range (ie, 60-125 mm Hg) induces
cerebral arteriolar vasoconstriction, thereby preserving a constant cerebral blood flow (CBF) and an intact
blood-brain barrier.
In chronically hypertensive individuals, the cerebral autoregulatory range is gradually shifted to higher
pressures as an adaptation to the chronic elevation of systemic blood pressure. [3] This adaptive response is

[5] Patients usually have vague neurologic symptoms and may present with symptoms of headache. and strongly emphasize the need for medical compliance. and lysergic acid diethylamide [LSD]) Eclampsia and preeclampsia Head trauma. Other conditions that can predispose a patient to elevated blood pressure and cause the same clinical situation include the following:              Chronic renal parenchymal disease Acute glomerulonephritis Renovascular hypertension Withdrawal from hypertensive agents (eg. Patient Education Refer patients to a dietitian to reduce the risk of vascular and hypertensive disease. and the 1year mortality approaches 90%. Encourage lifestyle modifications. the 6-month mortality for hypertensive emergencies is 50%. cerebral edema. in which the acute rise in systemic blood pressure exceeds the individual’s cerebral autoregulatory range. nausea. amphetamines. arteriolar damage and necrosis occur. and papilledema. for example. resulting in hydrostatic leakage across the capillaries within the central nervous system (CNS). including smoking cessation. less than 1% develop a hypertensive emergency. Hypertension in general is more prevalent in men than in women. and vomiting. Actively seek drug-induced causes. In patients who do not have a prior history of hypertension. Educate patients about medication adherence and compliance. which are clinically manifested as neurologic deficits and altered mentation in hypertensive encephalopathy.overwhelmed during a hypertensive emergency. Most patients with hypertensive encephalopathy have a history of hypertension. sympathomimetic agents and illicit drugs such as cocaine. place emphasis on the past medical history. Inform patients about signs of acute target-organ damage. Headaches are usually anterior and . moderation of alcohol. visual disturbances. Brain MRI scans have shown a pattern of typically posterior (occipital greater than frontal) brain edema that is reversible. The morbidity and mortality associated with hypertensive encephalopathy are related to the degree of targetorgan damage. meningitis Pheochromocytoma. persistent headaches. The progression of vascular pathology leads to generalized vasodilatation. The incidence of hypertensive encephalopathy is lowest in white people. Explain the effects of uncontrolled hypertension. renin-secreting tumors Sympathomimetic agents (eg. [4] With persistent elevation of the systemic blood pressure. confusion. increasing exercise. clonidine) Encephalitis. and neurological changes. exceeding the frequency in other ethnic minority groups. Without treatment. cocaine. phencyclidine [PCP]. Hypertension is more prevalent in black people. the medication list. The frequency of hypertensive encephalopathy in various ethnic groups corresponds to the frequency of hypertension in the general population. seizures. Etiology The most common cause of hypertensive encephalopathy is abrupt blood pressure elevation in a chronically hypertensive patient. cerebral infarction Collagen vascular disease Autonomic hyperactivity Vasculitis Ingestion of tyramine-containing foods or tricyclic antidepressants in combination with monoamine oxidase inhibitors (MAOIs) Epidemiology and Prognosis Of the 60 million Americans with hypertension. including the complications of persistent hypertension. This usually is termed reversible posterior leukoencephalopathy or posterior reversible encephalopathy syndrome (PRES). including visual changes. and medication compliance. and avoidance of tobacco. Hypertensive encephalopathy mostly occurs in middle-aged individuals who have a long-standing history of hypertension.

soft exudates. hemorrhage. with neurologic progression over 24-48 hours. Hypertensive retinopathy. with blurred margins. Neurologic examination reveals transient and migratory neurologic nonfocal deficits ranging from nystagmus to weakness and an altered mental status ranging from confusion to coma. [8] Papilledema. and early disc blurring. and cotton-wool spots (see the images below). exudates.angina. Note the swelling of the optic disc. grade IV retinal changes are associated with hypertensive encephalopathy. [6] Examples of these symptoms include the following:   Cardiovascular symptoms of aortic dissection. palpitations. .[7] including papilledema. Although papilledema is usually considered a more severe finding. The onset of symptoms usually occurs over 24-48 hours. Note the flameshaped hemorrhages. Patients also may present with symptoms resulting from other end-organ damage. On ophthalmoscopy.constant in nature. it actually does not confer worse survival than hemorrhages and exudates alone. or dyspnea Renal hematuria and acute renal failure Physical Examination A thorough and complete neurologic and ophthalmoscopic (funduscopic) examination is essential in the evaluation of patients. congestive heart failure. irregular heartbeat.

abdominal pulsations. radiologic examinations might not acutely identify ischemic stroke. murmurs. elevated neck veins. include a careful vascular examination to evaluate for vasculopathy.In addition. rales. Complications of hypertension include the following:         Coma Death Stroke Nephropathy Myocardial ischemia or infarction Nephropathy Retinopathy Peripheral vascular disease Diagnostic Considerations Hypertensive encephalopathy is a diagnosis of exclusion. and other potentially life-threatening causes must be considered in the assessment of a patient with neurologic deficits. which can progress to death.S3. In addition to the conditions listed in the differential diagnosis. and wheezes Complications Complications of hypertensive encephalopathy result in neurologic deficits from hemorrhage and strokes.Acute renal failure. peripheral edema. pulmonary edema.Pulmonary edema. and diminished pulses Renal . Other target-organ damage that may be found includes the following:    Cardiovascular . and peripheral edema Pulmonary . other problems to be considered include the following:        Acute central nervous system (CNS) event Acute thrombotic stroke Cerebral embolus CNS mass lesion Encephalitis Intracranial hemorrhage Renal failure Differential Diagnoses  Eclampsia  Head Trauma  Hepatic Encephalopathy  Pheochromocytoma  Subarachnoid Hemorrhage Surgery  Subdural Hematoma Surgery .

or intracranial masses. it is important to consider the baseline blood pressure in order to avoid excessive blood pressure reduction and prevent cerebral ischemia. When therapy is initiated. Obtain a complete blood count (CBC) to determine whether microangiopathic hemolytic anemia is present. Evaluation includes determining the extent of hypertensive damage and excluding intracranial processes. It is usually safe to reduce MAP by 25% and to lower the diastolic blood pressure to 100-110 mm Hg. Avoid agents such as clonidine. such as acute pulmonary edema and aortic dissection. overzealous reduction in blood pressure and adverse effects or toxicity of pharmacologic therapy) must be watched for. other potential causes of the symptoms must be evaluated in the workup as indicated by the clinical findings. Acute monitoring in an intensive care unit (ICU) with arterial blood pressure monitoring is required for adequate titration of pharmacologic agents and monitoring of end-organ function. an elevated creatinine with hematuria and casts may be present. Order cardiac enzyme studies to exclude myocardial ischemia. cerebral autoregulation preserves a relatively constant cerebral blood flow (CBF) at a mean arterial pressure (MAP) range of 60-90 mm Hg. An increasing number of authorities are considering labetalol. nicardipine. . Uremic Encephalopathy  Laboratory Studies   Hypertensive encephalopathy is a diagnosis of exclusion. and ECG    Consider computed tomography (CT) of the head to look for indications of stroke. Approach Considerations In patients without hypertension. In chronically hypertensive patients. Perform a urine toxicology screen to help exclude drug-induced hypertensive encephalopathy. and esmolol as preferred initial agents. Chest radiographs can also be used to evaluate for other conditions. Potential complications of medical therapy (eg. Deterioration of clinical status despite therapy warrants immediate and further investigation into other possible etiologies or reevaluation of therapy for worsening hypertensive encephalopathy. Pharmacologic Therapy Pharmacologic agents selected for use in hypertensive encephalopathy should have few or no adverse effects on the central nervous system (CNS). Plain Radiography. Laboratory and radiologic studies do not take the place of a careful history and physical examination (see Presentation). hemorrhage. and methyldopa. reserpine. Perform electrocardiography (ECG) to evaluate for the presence of cardiac ischemia. autoregulation is altered and shifted upward to maintain a relatively constant CBF at a higher MAP range. and measure blood urea nitrogen (BUN) and creatinine levels. with hypertensive nephropathy. Perform a urinalysis. Obtain chest radiographs to evaluate for possible complications of hypertensive encephalopathy. Although the clinical impact of diazoxide has not been determined. including aspiration due to altered mentation. this agent is avoided because of the impact of decreased CBF.  CT.

The reduction in blood pressure may be severe and can cause further complications due to venodilatory effects in volume-contracted individuals. it is necessary to reconsider the extent of blood pressure reduction or to consider alternate diagnoses. Nitroglycerin has been used to provide a rapid reduction in elevated blood pressure complicating myocardial ischemia. Acute Inpatient Monitoring Acute inpatient ICU monitoring with arterial blood pressure monitoring is required for adequate titration of pharmacologic agents. watch for overzealous reduction of blood pressure.[9] Labetalol provides a steady consistent drop in blood pressure without compromising CBF. Diuretics should also not be used in these patients unless there is clear evidence of volume overload. initiate alternative therapy with agents that do not require close monitoring until a monitored situation becomes available. Because of its nonselective beta-blocking properties. Emphasize the importance of adhering to . or assess a possible alternative cause of the clinical presentation. This is due to pressure natriuresis that occurs and leaves these patients volume depleted. increasing physical activity. Hydralazine has a limited role in this setting. Discharge patients on antihypertensives that were effective in maintaining an adequate blood pressure range during hospitalization. It is frequently used as initial therapy. Accordingly. which has high vascular selectivity and strong cerebral and coronary vasodilatory activity. these agents should be avoided in patients suspected of having increased intracranial pressure (ICP). owing to reflex tachycardia. labetalol should be avoided in severe reactive airway disease and cardiogenic shock. Nitroprusside sodium and hydralazine pose a theoretical risk of intracranial shunting of blood. because the potential intracerebral shunting of blood can increase the ICP. Volume repletion by itself can sometimes lower the blood pressure. If invasive monitoring is not immediately available. and avoidance of tobacco products. moderation of alcohol and sodium intake. including weight reduction to decrease the patient’s body mass index (BMI) to less than 27. evaluation the progression of a neurologic insult.[10] If neurologic deterioration worsens with therapy. Quickly and effectively treat severe hypertension to avoid progression to coma and death. and it should not be used in patients with suspected coronary artery disease (CAD). It has been shown to increase stroke volume and coronary blood flow.Nicardipine is a second-generation dihydropyridine-derivative calcium channel blocker. Routinely perform neurologic reassessment to monitor signs of deterioration due to inadequate treatment. Prevention Recommend lifestyle modifications.

Antihypertensive medications used in this setting include labetalol.antihypertensive therapy and scheduling reassessment at regular intervals to modify failing regimens. and the half-life is 5. nicardipine. Long-Term Monitoring Because hypertension is a chronic problem. Other Class Summary Antihypertensive agents are used to reduce blood pressure. is easy to titrate. Adequate control of hypertension is essential in preventing the progression of target-organ disease. document prior hypertensive medication regimens that have failed. . The onset of action is 5 minutes. Labetalol produces a steady. consistent drop in blood pressure without compromising cerebral blood flow (CBF). phentolamine. View full drug information Labetalol (Trandate) Labetalol is a competitive and selective alpha1 blocker and a nonselective beta-blocker that has predominantly beta effects at low doses. and hydralazine. but the reported experience is limited. Antihypertensive. Esmolol has been shown to reduce episodes of chest pain and clinical cardiac events in comparison with placebo. High blood pressure has been associated with a rapid rate of cognitive decline and an increased risk of cardiac and neurologic events. nitroglycerin. esmolol. regularly reassessment is vital. especially if surgery is planned. It can be discontinued abruptly if necessary. View full drug information Nicardipine (Cardene) Nicardipine is a calcium channel blocker that has a potent and rapid onset of action.5 hours. It appears to be effective in hypertensive encephalopathy. nitroprusside sodium. View full drug information Esmolol (Brevibloc) Esmolol is an ultrashort-acting agent that selectively blocks beta1 receptors but has little or no effect on beta2 receptor types. It is particularly useful in patients with elevated arterial pressure. To guide the formulation of a more effective treatment plan. and lacks toxic metabolites. Medication Summary Pharmacologic agents selected for use in hypertensive encephalopathy should have few or no adverse effects on the central nervous system (CNS).

Nitrostat) Nitroglycerin provides arteriolar dilation and venodilation. Minitran. reducing the hypertension that results from catecholamine effects on the alphareceptors. View full drug information Hydralazine Hydralazine is a direct arteriolar dilator. mild-to-moderate left ventricular dysfunction. or peripheral vascular disease. It may cause intracerebral shunting of blood. View full drug information Phentolamine (Oraverse) Phentolamine is an alpha1.and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action. View full drug information Nitroprusside sodium (Nitropress) Nitroprusside sodium decreases systemic vascular resistance by causing direct dilatation of arterioles and veins.Esmolol is useful in patients at risk for experiencing complications from beta blockade. It should be avoided in patients suspected of having increased ICP. Nitro-Dur. thereby increasing ICP. It is used in emergencies involving myocardial ischemia because of its dilatory effects on coronary arteries. It should be avoided in patients suspected of having increased ICP . View full drug information Nitroglycerin (Nitro-Bid. particularly those with reactive airway disease. Its short half-life (8 minutes) allows easy titration to the desired effect and quick discontinuance if necessary. It plays a limited role in this setting because of reflex tachycardia causing increased cardiac oxygen demand.