Wernicke Encephalopathy Treatment & Management

  • Author: Philip N Salen, MD; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Sep 23, 2011
 

Approach Considerations

Wernicke encephalopathy must be viewed as a medical emergency, even if other, competing diagnoses of CNS processes are being considered. Because the condition is potentially reversible, institution of treatment is indicated in patients exhibiting any combination of symptoms and signs, particularly if the patient is in a high-risk population. Onset of the disease may be acute, subacute, or chronic. Administration of thiamine improves the patient’s condition to some degree in almost all cases; however, persistent neurologic dysfunction is common.[5]

Prehospital care

Because patients with Wernicke encephalopathy present with altered mental status in the prehospital setting, focus prehospital care on stabilizing the airway, ensuring oxygenation, and maintaining blood pressure and euvolemia.

Next

Emergency Department Care

Although as little as 2 mg of thiamine may be enough to reverse symptoms, the dose of thiamine required to prevent or treat Wernicke encephalopathy in most alcoholic patients may be as high as greater than 500 mg given once or, preferably, 2 or 3 times daily parenterally. With a short half-life, multiple daily administrations may be necessary to replete levels and allow for optimal blood-brain diffusions.[5] Thiamine solution should be fresh, since old solutions may be inactive. Ataxia and acute confusional state may resolve dramatically, although improvement may not be noted for days or months.

Treat all poorly nourished patients with large doses of parenteral thiamine, particularly if intravenous glucose administration is necessary, even in the absence of symptoms and signs of Wernicke encephalopathy. Administering dextrose to an individual in a thiamine-deficient state exacerbates the process of cell death by providing more substrate for biochemical pathways that lack sufficient amounts of coenzymes.[6]

Start thiamine prior to or concurrently with treatment of intravenous glucose solutions, and continue until the patient resumes a normal diet. The administration of dextrose or other carbohydrates in this setting can be hazardous, because glucose oxidation is a thiamine-intensive process that may drive the last reserves of circulating vitamin B-1 toward the intracellular compartment, thereby aggravating neurologic damage.[2]

Patients with Wernicke encephalopathy are likely hypomagnesemic and should be treated empirically with parenteral magnesium sulfate, as they may be unresponsive to parenteral thiamine in the presence of hypomagnesemia. After correction of hypomagnesemia in conjunction with thiamine repletion, the blood transketolase activity can return to normal and clearing of the clinical signs of Wernicke encephalopathy may occur.

Previous
Next

Inpatient and Outpatient Care

Inpatient care

Depending on mental status and the ability to protect his or her airway, admit a patient with suspected or confirmed Wernicke encephalopathy to an internal medicine or neurology service.

Admission ensures that the patient receives continued intravenous thiamine and magnesium administration, observation for possible development of Korsakoff psychosis, and evaluation for possible cardiovascular beriberi.

Inpatient therapy for infants with thiamine deficiency involves administration of high-dose thiamine 50 mg/day for 2 weeks.[2]

Outpatient care

Patients who are malnourished, whether from alcohol or other causes, should continue to receive thiamine supplementation on an outpatient basis.

Previous
Next

Consultations, Monitoring, and Prevention

Consult a neurologist for further evaluation and treatment of altered mental status or other neurologic deficits. A psychiatrist may be helpful in evaluating comorbid psychiatric conditions. Refer patients with alcoholism to alcohol-cessation programs and monitor them for signs of alcohol withdrawal.

Patients who have been treated for Wernicke encephalopathy should avoid alcohol consumption and other behaviors that predispose to thiamine deficiency.

In the United States, many foods (but not alcoholic beverages) are supplemented with multiple vitamins and minerals. Some health policy experts have hypothesized that fortifying alcoholic beverages with thiamine would lower healthcare costs.

Previous
Proceed to Medication
 
 
Contributor Information and Disclosures
Author

Philip N Salen, MD  Clinical Professor, Department of Emergency Medicine, PA Program, DeSales University; Adjunct Clinical Associate Professor, Department of Emergency Medicine, Temple University School of Medicine; Research Director, Emergency Medicine Education, St Luke's Hospital

Philip N Salen, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Peter MC DeBlieux, MD  Professor of Clinical Medicine and Pediatrics, Section of Pulmonary and Critical Care Medicine, Program Director, Department of Emergency Medicine, Louisiana State University School of Medicine in New Orleans

Peter MC DeBlieux, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Radiological Society of North America, and Society of Critical Care Medicine

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 Salary Employment

J Stephen Huff, MD  Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

References
  1. Attard O, Dietemann JL, Diemunsch P, Pottecher T, Meyer A, Calon BL. Wernicke encephalopathy: a complication of parenteral nutrition diagnosed by magnetic resonance imaging. Anesthesiology. Oct 2006;105(4):847-8. [Medline].

  2. Fattal-Valevski A, Kesler A, Sela BA, et al. Outbreak of life-threatening thiamine deficiency in infants in Israel caused by a defective soy-based formula. Pediatrics. Feb 2005;115(2):e233-8. [Medline].

  3. Donnino M. Gastrointestinal beriberi: a previously unrecognized syndrome. Ann Intern Med. Dec 7 2004;141(11):898-9. [Medline].

  4. Donnino MW, Miller J, Garcia AJ, et al. Distinctive acid-base pattern in Wernicke's encephalopathy. Ann Emerg Med. Dec 2007;50(6):722-5. [Medline].

  5. Donnino MW, Vega J, Miller J, et al. Myths and misconceptions of Wernicke's encephalopathy: what every emergency physician should know. Ann Emerg Med. Dec 2007;50(6):715-21. [Medline].

  6. Buscaglia J, Faris J. Unsteady, unfocused, and unable to hear. Am J Med. Nov 2005;118(11):1215-7. [Medline].

  7. Decker MJ, Isaacman DJ. A common cause of altered mental status occurring at an uncommon age. Pediatr Emerg Care. Apr 2000;16(2):94-6. [Medline].

  8. Aasheim ET. Wernicke encephalopathy after bariatric surgery: a systematic review. Ann Surg. Nov 2008;248(5):714-20. [Medline].

  9. Thomson AD, Cook CC, Touquet R, et al. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke's encephalopathy in the accident and Emergency Department. Alcohol Alcohol. Nov-Dec 2002;37(6):513-21. [Medline].

  10. Azim W, Walker R. Wernicke's encephalopathy: a frequently missed problem. Hosp Med. Jun 2003;64(6):326-7. [Medline].

  11. Antunez E, Estruch R, Cardenal C, et al. Usefulness of CT and MR imaging in the diagnosis of acute Wernicke's encephalopathy. AJR Am J Roentgenol. Oct 1998;171(4):1131-7. [Medline].

  12. Kaineg B, Hudgins PA. Images in clinical medicine. Wernicke's encephalopathy. N Engl J Med. May 12 2005;352(19):e18. [Medline].

  13. Roh JH, Kim JH, Koo Y, Seo WK, Lee JM, Lee YH, et al. Teaching NeuroImage: Diverse MRI signal intensities with Wernicke encephalopathy. Neurology. Apr 8 2008;70(15):e48. [Medline].

Previous
Next
 
This MRI shows typical high signal intensities (SIs) in the medial thalamus (A), periaqueductal gray (B), mamillary bodies (C), cerebellar vermis (B, C, D), and paravermian superior cerebellum (D). All the lesions represent high SIs on the DWI (E–H). The ADC images of the cerebellar vermis (K, L) and paravermian superior cerebellum (L) show low SIs (arrowheads), whereas other described areas (I, J) show iso-SIs (arrows). Image courtesy of Neurology. Apr 8 2008;70(15):e48.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2012 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.