Hypertensive Encephalopathy Treatment & Management
- Author: Irawan Susanto, MD, FACP; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more...
In patients without hypertension, cerebral autoregulation preserves a relatively constant cerebral blood flow (CBF) at a mean arterial pressure (MAP) range of 60-90 mm Hg. In chronically hypertensive patients, autoregulation is altered and shifted upward to maintain a relatively constant CBF at a higher MAP range.
When therapy is initiated, it is important to consider the baseline blood pressure in order to avoid excessive blood pressure reduction and prevent cerebral ischemia. It is usually safe to reduce MAP by 25% and to lower the diastolic blood pressure to 100-110 mm Hg.
Acute monitoring in an intensive care unit (ICU) with arterial blood pressure monitoring is required for adequate titration of pharmacologic agents and monitoring of end-organ function. Potential complications of medical therapy (eg, overzealous reduction in blood pressure and adverse effects or toxicity of pharmacologic therapy) must be watched for.
Deterioration of clinical status despite therapy warrants immediate and further investigation into other possible etiologies or reevaluation of therapy for worsening hypertensive encephalopathy.
Pharmacologic agents selected for use in hypertensive encephalopathy should have few or no adverse effects on the central nervous system (CNS). Avoid agents such as clonidine, reserpine, and methyldopa. Although the clinical impact of diazoxide has not been determined, this agent is avoided because of the impact of decreased CBF. An increasing number of authorities are considering labetalol, nicardipine, and esmolol as preferred initial agents.
Nicardipine is a second-generation dihydropyridine-derivative calcium channel blocker, which has high vascular selectivity and strong cerebral and coronary vasodilatory activity. It has been shown to increase stroke volume and coronary blood flow.
Labetalol provides a steady consistent drop in blood pressure without compromising CBF. It is frequently used as initial therapy. Because of its nonselective beta-blocking properties, labetalol should be avoided in severe reactive airway disease and cardiogenic shock.
Nitroglycerin has been used to provide a rapid reduction in elevated 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 sodium and hydralazine pose a theoretical risk of intracranial shunting of blood. Accordingly, these agents should be avoided in patients suspected of having increased intracranial pressure (ICP), because the potential intracerebral shunting of blood can increase the ICP. Hydralazine has a limited role in this setting, owing to reflex tachycardia, and it should not be used in patients with suspected coronary artery disease (CAD). Diuretics should also not be used in these patients unless there is clear evidence of volume overload. This is due to pressure natriuresis that occurs and leaves these patients volume depleted. Volume repletion by itself can sometimes lower the blood pressure.
If neurologic deterioration worsens with therapy, it is necessary to reconsider the extent of blood pressure reduction or to consider alternate diagnoses.
Acute Inpatient Monitoring
Acute inpatient ICU 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, evaluation the progression of a neurologic insult, watch for overzealous reduction of blood pressure, or assess a possible alternative cause 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 alternative therapy with agents that do not require close monitoring until a monitored situation becomes available.
Recommend lifestyle modifications, including weight reduction to decrease the patient’s body mass index (BMI) to less than 27, moderation of alcohol and sodium intake, increasing physical activity, and avoidance of tobacco products.
Discharge patients on antihypertensives that were effective in maintaining an adequate blood pressure range during hospitalization. Emphasize the importance of adhering to antihypertensive therapy and scheduling reassessment at regular intervals to modify failing regimens.
Because hypertension is a chronic problem, regularly reassessment is vital. 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 a more effective treatment plan, document prior hypertensive medication regimens that have failed.
Aggarwal M. Hypertensive crisis: hypertensive emergencies and urgencies. Cardiol Clin. 2006. 24:135-46. [Medline].
Bales A. Hypertensive crisis. How to tell if it's an emergency or an urgency. Postgrad Med. 1999 May 1. 105(5):119-26, 130. [Medline].
Immink RV, van den Born BJ, van Montfrans GA, Koopmans RP, Karemaker JM, van Lieshout JJ. Impaired cerebral autoregulation in patients with malignant hypertension. Circulation. 2004 Oct 12. 110(15):2241-5. [Medline].
Schwartz RB, Jones KM, Kalina P, et al. Hypertensive encephalopathy: findings on CT, MR imaging, and SPECT imaging in 14 cases. AJR Am J Roentgenol. 1992 Aug. 159(2):379-83. [Medline].
Grossman E, Messerli FH. High blood pressure. A side effect of drugs, poisons, and food. Arch Intern Med. 1995 Mar 13. 155(5):450-60. [Medline].
Frohlich E.D. Target organ involvement in hypertension: a realistic promise of prevention and reversal. Med Clin North Am. 2004. 88:1-9. [Medline].
Amraoui F, van Montfrans GA, van den Born BJ. Value of retinal examination in hypertensive encephalopathy. J Hum Hypertens. 2009 Oct 29. [Medline].
Ahmed ME, Walker JM, Beevers DG, Beevers M. Lack of difference between malignant and accelerated hypertension. Br Med J (Clin Res Ed). 1986 Jan 25. 292(6515):235-7. [Medline]. [Full Text].
Lambert CR, Hill JA, Nichols WW, Feldman RL, Pepine CJ. Coronary and systemic hemodynamic effects of nicardipine. Am J Cardiol. 1985 Mar 1. 55(6):652-6. [Medline].
Gavras H, Brunner HB, Vaughan ED, Laragh JH. Angiotensin-sodium interaction in blood pressure maintenance of renal hypertensive and normotensive rats. Science. 1973 Jun 29. 180(4093):1369-71. [Medline].