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Hypertensive Encephalopathy

  • Author: Irawan Susanto, MD, FACP; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM  more...
 
Updated: Apr 14, 2015
 

Background

The term hypertensive encephalopathy was introduced in 1928 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, as follows:

  • 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 neurologic impairment from an elevated intracranial pressure (ICP)

With adequate control of hypertension, less than 1% of patients experience a hypertensive crisis. A hypertensive crisis is classified as either a hypertensive emergency or a hypertensive urgency,[1] as follows:

  • Acute or ongoing vital target organ damage (eg, damage to the brain, kidney, or heart) in the setting of severe hypertension is considered a hypertensive emergency; a prompt reduction in blood pressure is required within minutes or hours
  • The absence of target organ damage in the presence of a severe elevation in blood pressure (with diastolic blood pressure frequently exceeding 120 mm Hg) is considered a hypertensive urgency; a reduction in blood pressure is required within 24-48 hours

A continuum exists between the clinical syndromes of hypertensive urgency and emergency; hence, the distinction between the 2 syndromes may not always be clear and precise in practice.[2]

Hypertensive encephalopathy refers to the transient migratory neurologic symptoms that are associated with the malignant hypertensive state in a hypertensive emergency. The clinical symptoms are usually reversible with prompt initiation of therapy. In the evaluation of an encephalopathic patient, it is vital to exclude systemic disorders and various cerebrovascular events that may present with a similar constellation of clinical findings.

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Pathophysiology

The clinical manifestations of hypertensive encephalopathy are due to increased cerebral perfusion from the loss of blood-brain barrier integrity, which results 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 (CBF) and an intact blood-brain barrier.

In chronically hypertensive individuals, the cerebral autoregulatory range is gradually shifted to higher pressures as an adaptation to the chronic elevation of systemic blood pressure.[3] This adaptive 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 (CNS). Brain MRI scans have shown a pattern of typically posterior (occipital greater than frontal) brain edema that is reversible. This usually is termed reversible posterior leukoencephalopathy or posterior reversible encephalopathy syndrome (PRES).[4]

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 are clinically manifested as neurologic deficits and altered mentation in hypertensive encephalopathy.

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Etiology

The most common cause of hypertensive encephalopathy is abrupt blood pressure elevation in a chronically hypertensive patient. Other conditions that can predispose a patient to elevated blood pressure and cause the same clinical situation include the following:

  • Chronic renal parenchymal disease
  • Acute glomerulonephritis
  • Renovascular hypertension
  • Withdrawal from hypertensive agents (eg, clonidine)
  • Encephalitis, meningitis
  • Pheochromocytoma, renin-secreting tumors
  • Sympathomimetic agents (eg, cocaine, amphetamines, phencyclidine [PCP], and lysergic acid diethylamide [LSD])
  • Eclampsia and preeclampsia
  • Head trauma, cerebral infarction
  • Collagen vascular disease
  • Autonomic hyperactivity
  • Vasculitis
  • Ingestion of tyramine-containing foods or tricyclic antidepressants in combination with monoamine oxidase inhibitors (MAOIs)
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Epidemiology and Prognosis

Of the 60 million Americans with hypertension, less than 1% develop a hypertensive emergency. The morbidity and mortality associated with hypertensive encephalopathy are related to the degree of target-organ damage. Without treatment, the 6-month mortality for hypertensive emergencies is 50%, and the 1-year mortality approaches 90%.

Hypertensive encephalopathy mostly occurs in middle-aged individuals who have a long-standing history of hypertension. Hypertension in general is more prevalent in men than in women. The frequency of hypertensive encephalopathy in various ethnic groups corresponds to the frequency 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.

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Patient Education

Refer patients to a dietitian to reduce the risk of vascular and hypertensive disease. Encourage lifestyle modifications, including smoking cessation, increasing exercise, moderation of alcohol, and avoidance of tobacco.

Educate patients about medication adherence and compliance, and strongly emphasize the need for medical compliance. Explain the effects of uncontrolled hypertension, including the complications of persistent hypertension. Inform patients about signs of acute target-organ damage, including visual changes, persistent headaches, and neurological changes.

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Contributor Information and Disclosures
Author

Irawan Susanto, MD, FACP Clinical Professor of Medicine, Director of Pulmonary Consultation and Procedures, Divisions of Interventional Pulmonology and Critical Care, University of California, Los Angeles, David Geffen School of Medicine

Irawan Susanto, MD, FACP is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM Professor of Critical Care Medicine, Bioengineering, Cardiovascular Disease, Clinical and Translational Science and Anesthesiology, Vice-Chair of Academic Affairs, Department of Critical Care Medicine, University of Pittsburgh Medical Center, University of Pittsburgh School of Medicine

Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM is a member of the following medical societies: American College of Chest Physicians, Association of University Anesthetists, European Society of Intensive Care Medicine, American College of Critical Care Medicine, American Heart Association, American Thoracic Society, Shock Society, Society of Critical Care Medicine

Disclosure: Received income in an amount equal to or greater than $250 from: Masimo<br/>Received honoraria from LiDCO Ltd for consulting; Received intellectual property rights from iNTELOMED for board membership; Received honoraria from Edwards Lifesciences for consulting; Received honoraria from Masimo, Inc for board membership.

Additional Contributors

Najia Huda, MD Assistant Professor, Wayne State University School of Medicine; Director of MICU, Division of Pulmonary and Critical Care, Detroit Receiving Hospital

Najia Huda, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Ryan C Chang, MD Consulting Staff, Department of Internal Medicine, Divisions of Pulmonary and Critical Care, Kaiser Permanente San Francisco

Ryan C Chang, MD is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Oleh Wasyl Hnatiuk, MD Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences

Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

References
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  2. 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].

  3. 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].

  4. 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].

  5. 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].

  6. Frohlich E.D. Target organ involvement in hypertension: a realistic promise of prevention and reversal. Med Clin North Am. 2004. 88:1-9. [Medline].

  7. Amraoui F, van Montfrans GA, van den Born BJ. Value of retinal examination in hypertensive encephalopathy. J Hum Hypertens. 2009 Oct 29. [Medline].

  8. 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].

  9. 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].

  10. 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].

 
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Papilledema. Note the swelling of the optic disc, with blurred margins.
Hypertensive retinopathy. Note the flame-shaped hemorrhages, soft exudates, and early disc blurring.
 
 
 
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