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:
- In the US: 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.
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.
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.
Nitroprusside is frequently used as initial therapy because of its rapid onset and short duration of action. 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 nitroglycerin pose a theoretical risk of intracranial shunting of blood. Thus, an increasing number of authorities are considering labetalol the preferred agent.
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.
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 with suspected coronary artery disease.
| Drug Name | Nitroprusside sodium (Nitropress) -- First-line medication for hypertensive encephalopathy. Decreases systemic vascular resistance via direct dilatation of arterioles and veins. May cause intracerebral shunting of blood, increasing ICP. |
|---|---|
| Adult Dose | 0.5-1 mcg/kg/min IV infusion, titrate to desired BP |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; idiopathic hypertrophic subaortic stenosis, atrial fibrillation or flutter |
| Interactions | None reported |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| 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 causing perfusion to nonventilated areas of the lung |
| Drug Name | 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. |
|---|---|
| Adult Dose | 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 Dose | Not established |
| Contraindications | Documented hypersensitivity; cardiogenic shock, bradycardia, atrioventricular block, uncompensated congestive heart failure; pulmonary edema, reactive airway disease |
| 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 |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| 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 |
| Drug Name | Nitroglycerin (Nitro-Bid) -- Provides arteriolar dilation and venodilation. Used in emergencies involving myocardial ischemia due to the dilatory effects of nitroglycerin on coronary arteries. |
|---|---|
| Adult Dose | 5-300 mcg/min IV infusion, titrate to desired BP |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma, cerebral hemorrhage; closed-angle glaucoma |
| 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) |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Caution in coronary artery disease and low systolic and diastolic blood pressure |
| Drug Name | Trimethaphan camsylate (Arfonad) -- A ganglionic blocking agent primarily used in aortic dissection. Reduces heart rate and left ventricular ejection rate, thus lowering shearing force. |
|---|---|
| Adult Dose | 0.5-10 mg/min IV infusion, titrate to desired BP |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; anemia; cerebral vascular disease; coronary artery disease; glaucoma; hypovolemia; MI; respiratory insufficiency; shock |
| Interactions | Coadministration with anesthetic agents may cause hypotension; trimethaphan may potentiate neuromuscular blocking action of nondepolarizing agents and succinylcholine |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Decreased cardiac output and peripheral vascular resistance may occur, causing orthostatic hypotension; ganglionic blockade causes dry mouth, visual changes, urinary retention, and ileus |
| Drug Name | Hydralazine (Hydrea) -- Direct arteriolar dilator. Limited role because of reflex tachycardia causing increased cardiac oxygen demand. |
|---|---|
| Adult Dose | 5-20 mg IV bolus 0.5-1 mg/min IV infusion |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; mitral valve rheumatic heart disease |
| Interactions | MAOIs and beta-blockers may increase hydralazine toxicity; pharmacologic effects of hydralazine may be decreased by indomethacin |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Hydralazine has been implicated in MI; caution in suspected coronary artery disease |
| Drug Name | 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. |
|---|---|
| Adult Dose | 5-10 mg IV bolus 0.2-5 mg/min IV infusion |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; coronary or cerebral arteriosclerosis; renal impairment |
| Interactions | Concurrent administration of epinephrine or ephedrine may decrease phentolamine effects; ethanol increases phentolamine toxicity |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Caution in tachycardia, peptic ulcer, and gastritis; cerebrovascular occlusions and myocardial infarctions can occur following phentolamine administration |
| Drug Name | 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. |
|---|---|
| Adult Dose | Loading dose: 5-15 mg/h IV Maintenance dose: 3-5 mg/h IV |
| Pediatric Dose | Not established |
| Contraindications | Documented hypersensitivity; severe hypotension; cardiogenic shock; atrial fibrillation; CHF |
| Interactions | H2 blockers may increase bioavailability of nicardipine; coadministration with propranolol or metoprolol may increase cardiac depressant effects on AV conduction |
| Pregnancy | C - Safety for use during pregnancy has not been established. |
| Precautions | Adjust dose in hepatic and renal impairment; may increase frequency and duration of angina attacks |
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