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Wernicke Encephalopathy Treatment & Management

  • Author: Philip N Salen, MD; Chief Editor: Robert E O'Connor, MD, MPH  more...
 
Updated: Oct 28, 2015
 

Approach Considerations

WE 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.[6]

Prehospital care

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

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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 WE in most alcoholic patients may be as high as greater than 500 mg given once or, preferably, 2 or 3 times daily parenterally. Alcohol also appears to significantly increase the amount of thiamine required to treat the patient successfully compared with individuals in whom thiamine deficiency has a predominantly nutritional cause.[3]

Thiamine has a short half-life so multiple daily administrations may be necessary to replete levels and allow for optimal blood-brain diffusions.[6] Thiamine solution should be fresh, since old solutions may be inactive. Oral preparations have been shown to vary in bioavailability, but in hospital practice, thiamine is usually administered parenterally to patients thought to be at high risk of WKS. Parenteral administration is associated with some risk of anaphylaxis.

Treat all malnourished patients with large doses of parenteral thiamine, particularly if intravenous glucose administration is necessary, even in the absence of symptoms and signs of WE. 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.[7]

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 has the potential for harm, 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 WE 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.[3] After correction of hypomagnesemia in conjunction with thiamine repletion, the blood transketolase activity can return to normal and clearing of the clinical signs of WE may occur.

There is evidence that suggests thiamine treatment brings about rapid resolution of the ataxia and ophthalmoplegia and slow but significant improvement in the severity of nystagmus. The global confusional state also appears to improve rapidly within hours of thiamine treatment, but other issues remain unresolved. Impairment of memory and learning responds more slowly and often incompletely, suggesting a different mechanism of effect.[3]

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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 WE to an inpatient internal medicine or neurology service.

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

Inpatient therapy for infants with thiamine deficiency involves administration of high-dose, parenteral 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.

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Consultations, Monitoring, and Prevention

An internist and/or metabolic specialist can evaluate the encephalopathic patient for metabolic causes of acute mental status abnormalities. Consult a neurologist for further evaluation and treatment of altered mental status or other focal 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 WE should be advised to 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.

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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, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

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

Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Heart Association, Medical Society of Delaware, Society for Academic Emergency Medicine, Wilderness Medical Society, American Medical Association, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Additional Contributors

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, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

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. 2006 Oct. 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. 2005 Feb. 115(2):e233-8. [Medline].

  3. [Guideline] Day E, Bentham PW, Callaghan R, Kuruvilla T, George S. Thiamine for prevention and treatment of Wernicke- Korsakoff Syndrome in people who abuse alcohol (Cochrane Review ). The Cochrane Library. 2013. 7:1-20.

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

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

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

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

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

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

  10. Hung SC, Hung SH, Tarng DC, Yang WC, Chen TW, Huang TP. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. 2001 Nov. 38(5):941-7. [Medline].

  11. 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. 2002 Nov-Dec. 37(6):513-21. [Medline].

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

  13. 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. 1998 Oct. 171(4):1131-7. [Medline].

  14. 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. 2006 Oct. 105(4):847-8. [Medline].

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

  16. Roh JH, Kim JH, Koo Y, Seo WK, Lee JM, Lee YH, et al. Teaching NeuroImage: Diverse MRI signal intensities with Wernicke encephalopathy. Neurology. 2008 Apr 8. 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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