Hypertensive encephalopathy

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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.[1] 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.

Historical note[edit]

The first descriptions of the condition date back to the early 1900s. In 1914, Volhard and Fahr distinguished a neurological disorder caused by acute hypertension from a uremic state.[2] 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.[1]

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.[3][4][5]

Clinical features[edit]

Hypertensive encephalopathy is most commonly encountered in young and middle-aged people who suffer from hypertension.[5][6][7] 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.[8][9][10][11] 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.[8] 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, diplopia, 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, Intracerebral haemorrhage, 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.

Pathogenesis[edit]

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.[12][13] According to the autoregulation breakthrough conception, cerebral arterioles are forced to dilate, leading to vasogenic edema.[10]

Cerebral edema can be generalized or focal. Brain ventricles are compressed, cortical gyri flattened.

Diagnostics[edit]

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.

Treatment[edit]

The initial aim of treatment in hypertensive crises is to rapidly lower the diastolic pressure to about 100 to 105 mmHg; this goal should be achieved within two to six hours, with the maximum initial fall in BP not exceeding 25 percent of the presenting value [14][15] . This level of BP control will allow gradual healing of the necrotizing vascular lesions. More aggressive hypotensive therapy is both unnecessary and may reduce the blood pressure below the autoregulatory range, possibly leading to ischemic events (such as stroke or coronary disease)[16][17]

Once the BP is controlled, the patient should be switched to oral therapy, with the diastolic pressure being gradually reduced to 85 to 90 mmHg over two to three months. The initial reduction to a diastolic pressure of approximately 100 mmHg is often associated with a modest worsening of renal function; this change, however, is typically transient as the vascular disease tends to resolve and renal perfusion improves over one to three months.[18] Antihypertensive therapy should not be withheld in this setting unless there has been an excessive reduction in BP. A change in medication, however, is indicated if the decline in renal function is temporally related to therapy with an angiotensin (ACE) converting enzyme inhibitor or angiotensin II receptor blocker, which can interfere with renal autoregulation and produce acute renal failure in patients with bilateral renal artery stenosis. (See "Renal effects of ACE inhibitors in hypertension".)

Several parenteral antihypertensive agents are most often used in the initial treatment of malignant hypertension.[14][15]

●Nitroprusside – an arteriolar and venous dilator, given as an intravenous infusion. Initial dose: 0.25 to 0.5 µg/kg per min; maximum dose: 8 to 10 µg/kg per min. Nitroprusside acts within seconds and has a duration of action of only two to five minutes. Thus, hypotension can be easily reversed by temporarily discontinuing the infusion, providing an advantage over the drugs listed below. However, the potential for cyanide toxicity limits the prolonged use of nitroprusside, particularly in patients with renal insufficiency.[14][15]

●Nicardipine – an arteriolar dilator, given as an intravenous infusion. Initial dose: 5 mg/h; maximum dose: 15 mg/h.[19]

●Clevidipine – a short-acting dihydropyridine calcium channel blocker. It reduces blood pressure without affecting cardiac filling pressures or causing reflex tachycardia. Initial dose: 1 mg/hour; maximum dose: 21 mg/hour.[14][15]

●Labetalol – an alpha- and beta-adrenergic blocker, given as an intravenous bolus or infusion. Bolus: 20 mg initially, followed by 20 to 80 mg every 10 minutes to a total dose of 300 mg. Infusion: 0.5 to 2 mg/min.[14][15]

●Fenoldopam – a peripheral dopamine-1 receptor agonist, given as an intravenous infusion. Initial dose: 0.1 µg/kg per min; the dose is titrated at 15 min intervals, depending upon the blood pressure response.[14][15]

Oral agents — A slower onset of action and an inability to control the degree of BP reduction has limited the use of oral antihypertensive agents in the therapy of hypertensive crises. They may, however, be useful when there is no rapid access to the parenteral medications described above. Both sublingual nifedipine (10 mg) and sublingual captopril (25 mg) can substantially lower the BP within 10 to 30 minutes in many patients.[20] A more rapid response is seen when liquid nifedipine is swallowed. The major risk with these drugs is ischemic symptoms (eg, angina pectoris, myocardial infarction, or stroke) due to an excessive and uncontrolled hypotensive response.[21] Thus, their use should generally be avoided in the treatment of hypertensive crises if more controllable drugs are available.

Prognosis[edit]

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]

References[edit]

  1. ^ a b c Oppenheimer, B S, and Fishberg, A M, Archives of Internal Medicine, 1928, 41, 264.
  2. ^ Volhard F, Fahr T (1914) Die Brittische Nierenkrankheit, Vol. 2 (German). Berlin, Springer 232-265.
  3. ^ Finnerty FA Jr (1972) Hypertensive encephalopathy. Am J Med 52:672-678.
  4. ^ Ram CVS (1978) Hypertensive encephalopathy: recognition and management. Arch Int Med 138: 1851-1853.
  5. ^ a b Dinsdale HB (1983) Hypertensive encephalopathy. Neurol Clin 1: 3-16.
  6. ^ Moyer JH, Miller SI, Tashner AB, Snyder H, Bowman RO(1953) Malignant hypertension and hypertensive encephalopathy. Am J Med 14: 175-183
  7. ^ Chester EM, Agamanolis DP, Banker BQ, Victor M (1978) Hypertensive encephalopathy: a clinicopathologic study of 20 cases. Neurology 28: 928-939.
  8. ^ a b Clarke E, Murphy EA (1956) Neurological manifestations of malignant hypertension. Br Med J 2: 1319-1326.
  9. ^ Ziegler DK, Zosa A, Zileli T (1965) Hypertensive encephalopathy Arch Neurol 12: 472-478.
  10. ^ a b Healton EB, Brust JC, Feinfeld DA, Thomson GE (1982) Hypertensive encephalopathy and the neurological manifestations of malignant hypertension. Neurology 32: 127-132.
  11. ^ Perera GA (1955) Hypertensive vascular disease; description and natural history. J Chronic Dis 1: 33-42.
  12. ^ Strandgaard S, Paulson OB (1989) Cerebral blood flow and its pathophysiology in hypertension. Am J Hypertens 2: 486-492.
  13. ^ 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. ^ a b c d e f Kaplan, NM. Hypertensive crises. In: Kaplan's Clinical Hypertension, 9th ed, Neal, W (Ed), Lippincott, Williams and Wilkins, Baltimore 2006. p.311.
  15. ^ a b c d e f Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet 2000; 356:411.
  16. ^ Ledingham JG, Rajagopalan B. Cerebral complications in the treatment of accelerated hypertension. Q J Med 1979; 48:25.
  17. ^ Haas DC, Streeten DH, Kim RC, et al. Death from cerebral hypoperfusion during nitroprusside treatment of acute angiotensin-dependent hypertension. Am J Med 1983; 75:1071.
  18. ^ Woods JW, Blythe WB. Management of malignant hypertension complicated by renal insufficiency. N Engl J Med 1967; 277:57.
  19. ^ Neutel JM, Smith DH, Wallin D, et al. A comparison of intravenous nicardipine and sodium nitroprusside in the immediate treatment of severe hypertension. Am J Hypertens 1994; 7:623.
  20. ^ Angeli P, Chiesa M, Caregaro L, et al. Comparison of sublingual captopril and nifedipine in immediate treatment of hypertensive emergencies. A randomized, single-blind clinical trial. Arch Intern Med 1991; 151:678.
  21. ^ Grossman E, Messerli FH, Grodzicki T, Kowey P. Should a moratorium be placed on sublingual nifedipine capsules given for hypertensive emergencies and pseudoemergencies? JAMA 1996; 276:1328.