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Encephalopathy, Hypertensive
Updated: Nov 17, 2009
Introduction
Background
Hypertension affects more than 60 million Americans. With adequate control, fewer than 1% of patients experience a hypertensive crisis. Hypertensive crisis is classified as hypertensive emergency or hypertensive urgency. Acute or ongoing vital target organ damage, such as damage to the brain, kidney, or heart, in the setting of severe hypertension is considered a hypertensive emergency. It requires a prompt reduction in blood pressure within minutes or hours. The absence of target organ damage in the presence of severe elevation of blood pressure with diastolic blood pressure frequently greater than 120 mm Hg is considered hypertensive urgency, and it requires reduction in blood pressure within 24-48 hours. A continuum exists between the clinical syndrome of hypertensive urgency and emergency; hence, their distinction may not always be clear and precise.1
In 1928, Oppenheimer and Fishberg introduced the term hypertensive encephalopathy 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. 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 the neurologic impairment from an elevated intracranial pressure.
Hypertensive encephalopathy describes the transient migratory neurologic symptoms associated with the malignant hypertensive state in hypertensive emergency. The clinical symptoms usually are reversible with prompt initiation of therapy. In the evaluation of an encephalopathic patient, exclude systemic disorders and various cerebrovascular events that may present with a similar constellation of clinical findings.
Pathophysiology
The clinical manifestations of hypertensive encephalopathy are due to increased cerebral perfusion from the loss of blood-brain barrier integrity, resulting 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 and an intact blood-brain barrier.
In chronically hypertensive individuals, the cerebral autoregulatory range gradually is shifted to higher pressures as an adaptation to chronic elevation of systemic blood pressure. This cerebral autoregulatory response is overwhelmed during a hypertensive emergency in which the acute rise in systemic blood pressure exceeds the individual's cerebral autoregulatory range, resulting in hydrostatic leakage across the capillaries within the central nervous system. With persistent elevation of the systemic blood pressure, arteriolar damage and necrosis occur. The progression of vascular pathology leads to generalized vasodilatation, cerebral edema, and papilledema, which clinically manifest as neurologic deficits and altered mentation in hypertensive encephalopathy.
Frequency
United States
Of the 60 million Americans with hypertension, fewer than 1% of patients develop a hypertensive emergency.
Mortality/Morbidity
The morbidity and mortality associated with hypertensive encephalopathy are related to the degree of target organ damage. Without treatment, the 6-month mortality rate for hypertensive emergencies is 50%, and the 1-year mortality rate approaches 90%.
Race
The frequency of hypertensive encephalopathy corresponds to the occurrence of hypertension in the general population. Hypertension is more prevalent in black people, exceeding the frequency in other ethnic minority groups. The incidence of hypertensive encephalopathy is lowest in white people.
Sex
Hypertension is more prevalent in men than in women.
Age
Hypertensive encephalopathy mostly occurs in middle-aged individuals who have a long-standing history of hypertension.
Clinical
History
Most patients have a history of hypertension. Of those without a prior history of hypertension, place emphasis on past medical history, medication list, and medication compliance. Actively seek drug-induced causes.
- Patients usually have vague neurologic symptoms and may present with symptoms of headache, confusion, visual disturbances, seizures, nausea, and vomiting. Headaches are usually anterior and constant in nature. The onset of symptoms usually occurs over 24-48 hours, with neurologic progression over 24-48 hours.
- Patients also may present with symptoms resulting from other end organ damage. Examples of these symptoms include the following:
- Cardiovascular symptoms of aortic dissection, congestive heart failure, angina, palpitations, irregular heart beat, and dyspnea
- Renal hematuria and acute renal failure
Physical
A thorough and complete neurologic and funduscopic examination is essential in evaluation of patients.
- Funduscopic examination: Grade IV retinal changes are associated with hypertensive encephalopathy,2 including papilledema, hemorrhage, exudates, and cotton-wool spots.
- Neurologic examination reveals transient and migratory neurological nonfocal deficits ranging from nystagmus to weakness and an altered mental status ranging from confusion to coma.
- Include careful vascular examination to evaluate for vasculopathy because radiologic examinations might not acutely identify ischemic stroke.
- Other target organ damage that may be found includes the following:
- Cardiovascular - S3, elevated neck veins, peripheral edema, murmurs, abdominal pulsations, and diminished pulses
- Renal - Acute renal failure, pulmonary edema, and peripheral edema
- Pulmonary - Pulmonary edema, rales, and wheezes
Causes
The most common cause of hypertensive encephalopathy is abrupt blood pressure elevation in the chronically hypertensive patient. Other conditions predisposing a patient to elevated blood pressure can cause the same clinical situation.
- Chronic renal parenchymal disease
- Acute glomerulonephritis
- Renovascular hypertension
- Withdrawal from hypertensive agents (eg, clonidine)
- Encephalitis, meningitis
- Pheochromocytoma
- Sympathomimetic agents (eg, cocaine, amphetamines, phencyclidine [PCP], lysergic acid diethylamide [LSD])
- Eclampsia and preeclampsia
- Head trauma
- Collagen vascular disease
- Autonomic hyperactivity
- Vasculitis
- Ingestion of tyramine-containing foods or tricyclic antidepressants in combination with monoamine oxidase inhibitors (MAOIs)
Differential Diagnoses
| Eclampsia | Subarachnoid Hemorrhage |
| Encephalopathy, Hepatic | Subdural Hematoma |
| Encephalopathy, Uremic | |
| Head Trauma | |
| Pheochromocytoma |
Other Problems to Be Considered
Acute CNS event
Acute thrombotic stroke
Cerebral embolus
CNS mass lesions
Encephalitis
Intracranial hemorrhage
Renal failure
Workup
Laboratory Studies
- Hypertensive encephalopathy is a diagnosis of exclusion; evaluate other etiologies as indicated clinically in the workup. Evaluation includes determining the extent of hypertensive damage and excluding intracranial processes. Laboratory and radiologic studies should not take the place of a careful history and physical examination, which includes a complete neurological and funduscopic examination.
- CBC count: Obtain a CBC count to determine whether microangiopathic hemolytic anemia is present.
- Urinalysis, BUN, and creatinine: With hypertensive nephropathy, an elevated creatinine with hematuria and casts may be present.
- Cardiac enzymes: Exclude myocardial ischemia with cardiac enzymes.
- Urine toxicology screen: This study is important in excluding drug-induced hypertensive encephalopathy.
Imaging Studies
- Consider a head CT scan to evaluate the presence of stroke, hemorrhage, or intracranial masses.
- Obtain chest radiographs to evaluate for possible complications of hypertensive encephalopathy, including aspiration due to altered mentation. Chest radiographs can also be used to evaluate for other conditions, eg, acute pulmonary edema and aortic dissection.
Other Tests
Perform electrocardiogram to evaluate for the presence of cardiac ischemia.
Treatment
Medical Care
In patients without hypertension, cerebral autoregulation preserves a relatively constant cerebral blood flow at a range of mean arterial blood pressures of 60-90 mm Hg. In chronically hypertensive patients, autoregulation is altered and shifted upward to maintain a relatively constant cerebral blood flow at a higher mean arterial blood pressure range.
- When initiating therapy, the baseline blood pressure must be considered to avoid excessive blood pressure lowering and prevent cerebral ischemia. Lowering the mean arterial pressure by 25% and the diastolic blood pressure to 100-110 mm Hg usually is a safe maneuver because of the pressure autoregulatory cerebral blood flow range.
- Acute monitoring in an intensive care unit with arterial blood pressure monitoring is required for adequate titration of pharmacologic agents and monitoring of end organ function.
Medication
Pharmacologic agents selected for use in hypertensive encephalopathy should have few or no CNS adverse effects. Avoid agents such as clonidine, reserpine, and methyldopa. Although the clinical impact has not been determined, diazoxide is avoided because of the impact of decreased cerebral blood flow. If neurological deterioration worsens with therapy, reconsider the extent of blood pressure lowering or consider alternate diagnoses.
Labetalol provides a steady consistent drop in blood pressure without compromising cerebral blood flow. Labetalol is frequently used as initial therapy. Because of nonselective beta-blocking properties, it should be avoided in severe reactive airways disease and cardiogenic shock.
Nitroglycerin has been used to provide a rapid reduction in blood pressure complicating myocardial ischemia. The reduction in blood pressure may be severe and can cause further complications due to venodilatory effects in volume-contracted individuals. Nitroprusside and hydralazine pose a theoretical risk of intracranial shunting of blood. Thus, these agents should be avoided in patients suspected of having increased intracranial pressure (ICP) because they may cause intracerebral shunting of blood, which increases ICP. An increasing number of authorities are considering labetalol, nifedipine, and esmolol as the preferred initial agent.
Trimethaphan camsylate is used to reduce the shearing force in the presence of aortic dissection. Hydralazine has a limited role, owing to reflex tachycardia, and it should not be used in patients with suspected coronary artery disease.
Antihypertensive Agent
These agents are used to reduce blood pressure.
Labetalol (Normodyne)
Competitive and selective alpha1-blocker and nonselective beta-blocker with predominantly beta effects at low doses. Onset of action is 5 min, with half-life of 5.5 h. Provides a steady, consistent drop in BP without compromising cerebral blood flow.
Dosing
Adult
20 mg IV bolus, then 20-80 mg IV bolus q10min; not to exceed 300 mg; 2 mg/min IV infusion alternatively, titrate to desired BP; not to exceed 300 mg
Pediatric
Not established
Interactions
Labetalol decreases the effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase labetalol blood levels; glutethimide may decrease labetalol effects by inducing microsomal enzymes
Contraindications
Documented hypersensitivity; cardiogenic shock, bradycardia, atrioventricular block, uncompensated congestive heart failure; pulmonary edema, reactive airway disease
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in impaired hepatic function; discontinue therapy if signs of liver dysfunction are present; in elderly patients, a lower response rate and higher incidence of toxicity may be observed
Nicardipine (Cardene)
Calcium channel blocker. Potent rapid onset of action, ease of titration, and lack of toxic metabolites. Effective but limited reported experience in hypertensive encephalopathy.
Dosing
Adult
Loading dose: 5-15 mg/h IV
Maintenance dose: 3-5 mg/h IV
Pediatric
Not established
Interactions
H2 blockers may increase bioavailability of nicardipine; coadministration with propranolol or metoprolol may increase cardiac depressant effects on AV conduction
Contraindications
Documented hypersensitivity; severe hypotension; cardiogenic shock; atrial fibrillation; CHF
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Adjust dose in hepatic and renal impairment; may increase frequency and duration of angina attacks
Esmolol (Brevibloc)
Ultra — short-acting agent that selectively blocks beta 1 receptors with little or no effect on beta 2 receptor types. Particularly useful in patients with elevated arterial pressure, especially if surgery is planned. Shown to reduce episodes of chest pain and clinical cardiac events compared with placebo. Can be discontinued abruptly if necessary.
Useful in patients at risk for experiencing complications from beta-blockade; particularly those with reactive airway disease, mild-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.
Dosing
Adult
Loading dose: 250-500 mcg/kg infused over 1 min
Maintenance infusion: 50 mcg/kg/min over 4 min
If adequate effect not observed within 5 min, repeat loading dose and follow with maintenance infusion using increments of 50 mcg/kg/min (for 4 min); regimen may be repeated up to 4 times if necessary
As desired BP approached, skip loading infusion and reduce dose increments in maintenance infusion from 50 mcg/kg/min to 25 mcg/kg/min; may increase interval between titration steps from 5-10 min
Pediatric
Not established
Interactions
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Contraindications
Documented hypersensitivity; uncompensated congestive heart failure, bradycardia, cardiogenic shock, and A-V conduction abnormalities
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm may worsen when medication is abruptly withdrawn; withdraw drug slowly and monitor patient closely
Nitroprusside sodium (Nitropress)
Decreases systemic vascular resistance via direct dilatation of arterioles and veins. Should be avoided in patients suspected of having increased ICP. May cause intracerebral shunting of blood, increasing ICP.
Dosing
Adult
0.5-1 mcg/kg/min IV infusion, titrate to desired BP
Pediatric
Not established
Interactions
None reported
Contraindications
Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis, atrial fibrillation or flutter
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Potential for cyanide toxicity occurs with prolonged infusion (>72 h) and high infusion rate (>3 mcg/kg/min); suspect hyperreflexia, worsening mental status, and toxicity in the presence of metabolic acidosis; treatment for cyanide toxicity includes amyl nitrate, thiosulfate, and hydroxocobalamin; dialysis may be necessary for thiocyanate toxicity; hypoxia by inhibition of hypoxia-induced vasoconstriction in the pulmonary vasculature causes perfusion to nonventilated areas of the lung
Trimethaphan camsylate (Arfonad)
A ganglionic blocking agent primarily used in aortic dissection. Reduces heart rate and left ventricular ejection rate, thus lowering shearing force.
Dosing
Adult
0.5-10 mg/min IV infusion, titrate to desired BP
Pediatric
Not established
Interactions
Coadministration with anesthetic agents may cause hypotension; trimethaphan may potentiate neuromuscular blocking action of nondepolarizing agents and succinylcholine
Contraindications
Documented hypersensitivity; anemia; cerebral vascular disease; coronary artery disease; glaucoma; hypovolemia; MI; respiratory insufficiency; shock
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Decreased cardiac output and peripheral vascular resistance may occur, causing orthostatic hypotension; ganglionic blockade causes dry mouth, visual changes, urinary retention, and ileus
Phentolamine (Regitine)
Alpha1- and alpha2-adrenergic blocking agent that blocks circulating epinephrine and norepinephrine action, reducing hypertension that results from catecholamine effects on the alpha receptors.
Dosing
Adult
5-10 mg IV bolus
0.2-5 mg/min IV infusion
Pediatric
Not established
Interactions
Concurrent administration of epinephrine or ephedrine may decrease phentolamine effects; ethanol increases phentolamine toxicity
Contraindications
Documented hypersensitivity; coronary or cerebral arteriosclerosis; renal impairment
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in tachycardia, peptic ulcer, and gastritis; cerebrovascular occlusions and myocardial infarctions can occur following phentolamine administration
Nitroglycerin (Nitro-Bid)
Provides arteriolar dilation and venodilation. Used in emergencies involving myocardial ischemia due to the dilatory effects of nitroglycerin on coronary arteries.
Dosing
Adult
5-300 mcg/min IV infusion, titrate to desired BP
Pediatric
Not established
Interactions
Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of calcium channel blockers (dose adjustment of either agent may be necessary)
Contraindications
Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma, cerebral hemorrhage; closed-angle glaucoma
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in coronary artery disease and low systolic and diastolic blood pressure
Hydralazine (Hydrea)
Direct arteriolar dilator. Limited role because of reflex tachycardia causing increased cardiac oxygen demand. Should be avoided in patients suspected of having increased intracranial pressure.
Dosing
Adult
5-20 mg IV bolus
0.5-1 mg/min IV infusion
Pediatric
Not established
Interactions
MAOIs and beta-blockers may increase hydralazine toxicity; pharmacologic effects of hydralazine may be decreased by indomethacin
Contraindications
Documented hypersensitivity; mitral valve rheumatic heart disease
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hydralazine has been implicated in MI; caution in suspected coronary artery disease
Follow-up
Further Inpatient Care
- Acute inpatient intensive care unit monitoring with arterial blood pressure monitoring is required for adequate titration of pharmacologic agents. Routinely perform neurologic reassessment to monitor signs of deterioration due to inadequate treatment, progression of neurologic insult, overzealous reduction in blood pressure, or alternate etiology of the clinical presentation.
- Quickly and effectively treat severe hypertension to avoid progression to coma and death. If invasive monitoring is not immediately available, initiate alternate therapy with agents that do not require close monitoring until a monitored situation becomes available.
Further Outpatient Care
- Regularly reassess hypertension because it is a chronic problem. Adequate control of hypertension is essential in preventing the progression of target organ disease.
- High blood pressure has been associated with a rapid rate of cognitive decline and an increased risk of cardiac and neurologic events.
- To guide the formulation of an effective treatment plan, document prior hypertensive medication regimes that have failed.
Inpatient & Outpatient Medications
- Discharge patients on antihypertensives that were effective in maintaining an adequate blood pressure range during hospitalization.
Deterrence/Prevention
- Recommend lifestyle modifications, including weight reduction to decrease body mass index (BMI) to less than 27, moderation of alcohol and sodium intake, increasing physical activity, and avoidance of tobacco products.
- Patients should adhere to antihypertensive therapy and schedule reassessment at regular intervals to modify failing regimens.
Complications
- 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/infarction
- Nephropathy
- Retinopathy
- Peripheral vascular disease
Prognosis
The morbidity and mortality associated with hypertensive encephalopathy are related to the degree of target organ damage. Without treatment, the 6-month mortality rate for hypertensive emergencies is 50%, and the 1-year mortality rate approaches 90%.
Patient Education
- Refer patients to a dietitian to reduce the risk of vascular and hypertensive disease.
- Encourage lifestyle modifications, including smoking cessation, increasing exercise, moderation of alcohol, and avoidance of tobacco.
- Educate patients about medication adherence and compliance and enforce the need for medical compliance. Educate patients regarding the effects of uncontrolled hypertension, including the complications of persistent hypertension. Inform patients about signs of acute target organ damage, including visual changes, persistent headaches, and neurological changes.
Miscellaneous
Medicolegal Pitfalls
- Hypertensive encephalopathy is a diagnosis of exclusion, and other potentially life-threatening etiologies must be considered in assessing a patient with neurologic deficits.
- Deterioration of clinical status despite therapy warrants immediate and further investigation into other possible etiologies or reevaluation of therapy for worsening hypertensive encephalopathy.
- Monitor complications of medical therapy (eg, overzealous reduction in blood pressure, adverse effects or toxicity of pharmacological therapy).
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Keywords
hypertension, encephalopathy, hypertensive encephalopathy, hypertensive crisis, hypertensive emergency, hypertensive urgency, accelerated hypertension, malignant hypertension, arteriolar damage, necrosis, atherosclerosis
Contributor Information and Disclosures
Author
Ryan C Chang, MD, Consulting Staff, Department of Internal Medicine, Divisions of Pulmonary and Critical Care, Kaiser Permanente San Francisco
Ryan C Chang, MD is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society
Disclosure: Nothing to disclose.
Coauthor(s)
Irawan Susanto, MD, Director of Pulmonary Consultation and Procedures, Associate Professor, Department of Internal Medicine, Divisions of Pulmonary and Critical Care, University of California at Los Angeles School of Medicine
Irawan Susanto, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine
Disclosure: Nothing to disclose.
Medical Editor
Oleh Wasyl Hnatiuk, MD, Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences
Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
CME Editor
Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.
Chief Editor
Michael R Pinsky, MD, CM, FCCP, FCCM, Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease and Anesthesiology, Vice-Chair, Academic Affairs, University of Pittsburgh School of Medicine, University of Pittsburgh Medical Center
Michael R Pinsky, MD, CM, FCCP, FCCM is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Association of University Anesthetists, Shock Society, and Society of Critical Care Medicine
Disclosure: LiDCO Ltd Honoraria Consulting; iNTELOMED Intellectual property rights Board membership; Edwards Lifesciences Honoraria Consulting; Applied Physiology, Ltd Honoraria Consulting; Cheetah Medical Consulting fee Consulting
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