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Hypertensive encephalopathy is a neurological dysfunction induced by malignant hypertension. The term "hypertensive encephalopathy" was introduced to describe this type of encephalopathy by Oppenheimer and Fishberg in 1928. It describes cerebral conditions, typically reversible, caused by sudden and sustained severe elevation of blood pressure. Hypertensive encephalopathy occurs in eclampsia, acute nephritis and crises in essential hypertension. Symptoms of hypertensive encephalopathy include headache, restlessness, nausea, disturbances of consciousness, seizures, retinal hemorrhage and papilledema. Focal brain lesions may be associated with specific neurological symptoms. These neurological impairments may culminate in a coma. The condition is treated by drugs that decrease blood pressure.
The first descriptions of the condition date back to early 1900s. In 1914, Volhard and Fahr distinguished a neurological disorder caused by acute hypertension from a uremic state. He described this condition a "pseudouremia". The term "hypertensive encephalopathy" was introduced by Oppenheimer and Fishberg in 1928 to describe the case of a patient with acute nephritis, severe hypertension and cerebral symptoms.
In the past, the term "hypertensive encephalopathy" has been applied to a range of neurological problems occurring in hypertensive patients, such as headache, dizziness cerebral hemorrhage and transient ischemic attacks. However, currently this term is narrowed down to a clinical condition produced by elevated blood pressure and which can be reversed by blood pressure reduction.
Hypertensive encephalopathy is most commonly encountered in young and middle-aged people who suffer from hypertension. Overall, the condition is rare even among hypertensive patients. Different clinicians reported that from 0.5 to 15% of patients with malignant hypertension developed hypertensive encephalopathy. With the development of methods for detection and treatment of hypertension, hypertensive encephalopathy has been becoming more rare.
Symptoms of hypertensive encephalopathy typically start to occur 12–48 hours after a sudden and sustained increase in blood pressure. The first manifestation of these symptoms is a severe headache. Headache occurs in greater than 75% of patients. The patient becomes restless. Alterations in consciousness may follow several hours later, which include impaired judgement and memory, confusion, somnolence and stupor. If the condition is not treated, these neurological symptoms may worsen and ultimately turn into a coma. Other symptoms may include increased irritability, vomiting, seizures, twitching and myoclonus of the limbs. Alterations in vision (vision blurring, hemivisual field defects, color blindness, cortical blindness) are common. They occur in 4 out of 11 cases (Jellinek et al. 1964). Hemiparesis and aphasia may also occur, but they are less common. Electroencephalographic examination detects the absence of alpha waves, signifying impaired consciousness. In patients with visual disturbances, slow waves are detected in the occipital areas.
Hypertensive encephalopathy is caused by an increase in blood pressure. Several conditions may evoke blood pressure elevation: acute nephritis, eclampsia, crises in chronic essential hypertension, sudden withdrawal of antihypertensive treatment. Additionally, hypertensive encephalopathy may occur in pheochromocytoma, Cushing's syndrome, renal artery thrombosis.
The impairment of cerebral blood flow that underlies hypertensive encephalopathy is still controversial. Normally, cerebral blood flow is maintained by an autoregulation mechanism that dilate arterioles in response to blood pressure decreases and constricts arterioles in response to blood pressure increases. This autoregulation falters when hypertension becomes excessive. According to the over-regulation conception, brain vessels spasm in response to acute hypertension, which results in cerebral ischemia and cytotoxic edema. According to the autoregulation breakthrough conception, cerebral arterioles are forced to dilate, leading to vasogenic edema.
Cerebral edema can be generalized or focal. Brain ventricles are compressed, cortical gyri flattened.
Diagnostic methods for hypertensive encephalopathy include physical examination, blood pressure measurement, blood sampling, ECG, EEG, chest X-ray, urinalysis, arterial blood gas analysis, cranial CAT scans and MRI. Since decreasing the blood pressure is essential, anti-hypertensive medication is administered without awaiting the results of the laboratory tests.
Acute cases of hyertensive encephalopathy require urgent treatment, preferably in intensive care units where vital signs and electroencephalographic characteristics can be monitored. The first measure is to lower blood pressure with drugs. Blood pressure reduction is monitored to avoid damage from excessive reduction. Excessively reduced blood pressure may result in cerebral infarction, blindness and cardiac ischemia.
Intravenously injected diazoxide is effective in 80% of the patients with hypertensive encephalopathy. It normalizes blood pressure within 3-5 min, and the effect lasts 6–18 hours. One benefit of diazoxide is that it does not cause drowsiness and thus does not affect the patient’s state of consciousness. Reflex tachycardia caused by this drug is the major disadvantage which limits its use in patients with ischemic heart disease. Furosemide injected simultaneously with diazoxide enhances both the antihypertensive effect and its duration.
Hydralazine is also administered intravenously or intramuscularly to reduce the blood pressure. Its action is similar to that of diazoxide, but less consistent.
Another class of drugs that are used to reduce blood pressure in hypertensive encephalopathy are ganglionic blocking agents: pentolinium and trimethaphan. These agents have rapid effect, and they do not cause drowsiness. However, they may have side effects, such as bowel and bladder atony. These drugs, with the exception of labetalol, are not used if hypertensive encephalopathy is associated with prepartal eclampsia because they may harm the fetus.
Reserpine, methyldopa and clonidine are less applicable to hypertensive emergency because their effect starts slowly (in 2–3 hours after administration) and they affect the patient's consciousness.
Oral antihypertensive drugs are administered after the patient recovers from the most severe symptoms, and intravenous injections are no longer necessary.
In addition to antihypertensive drugs, anticonvulsant drugs, such as phenytoin, may be given to the patient with seizures. However, typically anti-hypertensive medication is sufficient for treatment of neurological symptoms.
Patients with hypertensive encephalopathy who are promptly treated usually recover without deficit. However, if treatment is not administered, the condition can lead to death.
- ↑ 1.0 1.1 1.2 Oppenheimer, B S, and Fishberg, A M, Archives of Internal Medicine, 1928, 41, 264.
- ↑ Volhard F, Fahr T (1914) Die Brittische Nierenkrankheit, Vol. 2 (German). Berlin, Springer 232-265.
- ↑ Finnerty FA Jr (1972) Hypertensive encephalopathy. Am J Med 52:672-678.
- ↑ Ram CVS (1978) Hypertensive encephalopathy: recognition and management. Arch Int Med 138: 1851-1853.
- ↑ 5.0 5.1 Dinsdale HB (1983) Hypertensive encephalopathy. Neurol Clin 1: 3-16.
- ↑ Moyer JH, Miller SI, Tashner AB, Snyder H, Bowman RO(1953) Malignant hypertension and hypertensive encephalopathy. Am J Med 14: 175-183
- ↑ Chester EM, Agamanolis DP, Banker BQ, Victor M (1978) Hypertensive encephalopathy: a clinicopathologic study of 20 cases. Neurology 28: 928-939.
- ↑ 8.0 8.1 Clarke E, Murphy EA (1956) Neurological manifestations of malignant hypertension. Br Med J 2: 1319-1326.
- ↑ Ziegler DK, Zosa A, Zileli T (1965) Hypertensive encephalopathy Arch Neurol 12: 472-478.
- ↑ 10.0 10.1 Healton EB, Brust JC, Feinfeld DA, Thomson GE (1982) Hypertensive encephalopathy and the neurological manifestations of malignant hypertension. Neurology 32: 127-132.
- ↑ Perera GA (1955) Hypertensive vascular disease; description and natural history. J Chronic Dis 1: 33-42.
- ↑ Strandgaard S, Paulson OB (1989) Cerebral blood flow and its pathophysiology in hypertension. Am J Hypertens 2: 486-492.
- ↑ Tamaki K, Sadoshima S, Baumbach GL, Iadecola C, Reis DJ, Heistad DD (1984) Evidence that disruption of the blood–brain barrier precedes reduction in cerebral blood flow in hypertensive encephalopathy. Hypertension 6: I75-81.
- ↑ 14.0 14.1 Ledingham JG (1983) Management of hypertensive crises. Hypertension 5: III114-119.
- ↑ 15.0 15.1 15.2 15.3 15.4 Vidt DG (1986) Current concepts in treatment of hypertensive emergencies. Am Heart J 111: 220-225.
- ↑ Graham DI (1975) Ischaemic brain damage of cerebral perfusion failure type after treatment of severe hypertension. Br Med J 4: 739.
- ↑ Ledingham JG, Rajagopalan B (1979) Cerebral complications in the treatment of accelerated hypertension. Q J Med 48: 25-41.
- ↑ Cove DH, Seddon M, Fletcher RF, Dukes DC (1979) Blindness after treatment for malignant hypertension. Br Med J 2: 245-246.
- ↑ Kanada SA, Kanada DJ, Hutchinson RA, Wu D (1976) Angina-like syndrome with diazoxide therapy for hypertensive crisis. Ann Intern Med 84: 696-699.
- ↑ Humphrey DC, et al. (1969) Management of severe hypertension with intravenous injections of diazoxide. Am J Cardiol 24:870-875,1969
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