Wernicke Encephalopathy Medication

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

Medication Summary

The cornerstone of therapy for prevention or treatment of Wernicke encephalopathy in most alcoholic patients is thiamine until the patient resumes a normal diet. Administer daily oral thiamine (100 mg) on a long-term, outpatient basis.

As previously stated, 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.

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Nutrients

Class Summary

The primary objective is to replenish vitamin B-1 stores. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol/L of phosphate per day appear necessary to achieve optimum metabolic balance.

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Thiamine

 

Begin thiamine administration prior to treating the patient with intravenous glucose solutions. Glucose infusions may precipitate Wernicke disease or acute cardiovascular beriberi in a previously unaffected patient or cause rapid worsening of an early form of the disease.

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Magnesium sulfate

 

Magnesium is a cofactor in a number of enzyme systems; it is also involved in neurochemical transmission and muscular excitability. Persons with long-term alcoholism and patients who are malnourished usually have inadequate magnesium stores.

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Potassium acid phosphate (K-Phos)

 

Potassium is essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion, through gastrointestinal loss, or because of low intake. Patients with chronic alcoholism and those who are malnourished usually have inadequate nutrient stores. Potassium depletion sufficient to cause a 1-mEq/L drop in serum potassium requires a loss of about 100-200 mEq of potassium from the total body store.

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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

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  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].

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  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].

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  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].

 
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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.
 
 
 
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