Encephalopathy, Hypertensive

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, 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)

Source : http://emedicine.medscape.com/article/166129-overview