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Wernicke Encephalopathy: Treatment & Medication

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 Medical School; Research Director, Emergency Medicine Education, Saint Luke's Hospital
Contributor Information and Disclosures

Updated: Jan 13, 2009

Treatment

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.

Emergency Department Care

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.

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, twice or thrice daily parenterally. With a short half-life, multiple daily administrations may be necessary to replete levels and allow for optimal blood-brain diffusions.1  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 in a thiamine-deficient state exacerbates the process of cell death by providing more substrate for biochemical pathways that lack sufficient amounts of coenzymes.2
  • 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 the neurologic damage.6
  • 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 may occur.

Consultations

  • Consult a neurologist for further evaluation and treatment of altered mental status or other neurologic deficit.
  • A psychiatrist may be helpful in evaluating comorbid psychiatric conditions.

Medication

The cornerstone of therapy for prevention or treatment of Wernicke encephalopathy in most alcoholic patients is thiamine until the patient resumes a normal diet.

Nutrients

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.


Thiamine (Thiamilate)

Begin thiamine administration prior to treating with IV 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.

Adult

100-200 mg IV; followed by 50-100 mg/bid up to 5 times/d IV

Pediatric

50 mg IV; followed by 10-25 mg/d IV/IM

Documented hypersensitivity

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sensitivity reactions can occur (intradermal test dose recommended in suspected sensitivity); deaths have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy following glucose administration may occur in patients who are thiamine deficient; administer before or with dextrose-containing fluids in suspected thiamine deficiency


Magnesium sulfate

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

Adult

2-4 g IV mixed with initial IV fluid bolus; followed by 1-4 g IV q4h prn
Alternatively: 1-4 g/h continuous infusion

Pediatric

25-50 mg/kg/dose IV q4-6h mixed with initial fluid bolus for 3-4 h; not to exceed single dose of 2 g; also may be administered and repeated if hypomagnesemia persists

Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade seen with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine

Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

May alter cardiac conduction leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when electrolyte is administered parenterally; caution when administering, since may produce significant hypertension or asystole; in overdose, 10% calcium gluconate solution 10-20 mL IV can be administered as antidote for clinically significant hypermagnesemia

More on Wernicke Encephalopathy

Overview: Wernicke Encephalopathy
Differential Diagnoses & Workup: Wernicke Encephalopathy
Treatment & Medication: Wernicke Encephalopathy
Follow-up: Wernicke Encephalopathy
References

References

  1. 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].

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

  3. 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].

  4. 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].

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

  6. 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].

  7. 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].

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

  9. 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].

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

  11. Blass JP, Gibson GE. Abnormality of a thiamine-requiring enzyme in patients with Wernicke-Korsakoff syndrome. N Engl J Med. Dec 22 1977;297(25):1367-70. [Medline].

  12. Henry GL. Coma and altered states of consciousness. In: Emergency Medicine. 4th ed. 1996:225-233.

  13. Hoffman RS. Thiamine hydrochloride. In: Goldfrank's Toxicologic Emergencies. 5th ed. 1994:825-6.

  14. Hung SC, Hung SH, Tarng DC, et al. Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients. Am J Kidney Dis. Nov 2001;38(5):941-7. [Medline].

  15. Marx JA. The varied faces of Wernicke's encephalopathy. J Emerg Med. 1985;3(5):411-3. [Medline].

  16. Reuler JB, Girard DE, Cooney TG. Current concepts. Wernicke's encephalopathy. N Engl J Med. Apr 18 1985;312(16):1035-9. [Medline].

  17. Victor M. Persistent altered mentation due to ethanol. Neurol Clin. Aug 1993;11(3):639-61. [Medline].

  18. Willett WC, Stampfer MJ. Clinical practice. What vitamins should I be taking, doctor?. N Engl J Med. Dec 20 2001;345(25):1819-24. [Medline].

Further Reading

Keywords

Wernicke encephalopathy, Wernicke's encephalopathy, Wernicke-Korsakoff syndrome, thiamine deficiency, vitamin B-1 deficiency, Wernicke's disease, Wernicke-Korsakoff psychosis, mental confusion, ataxia, ophthalmoplegia, Korsakoff's amnestic syndrome, Korsakoff amnestic syndrome, memory loss, confabulation, vitamin B deficiencies, alcoholism, malnutrition, AIDS

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 Medical School; Research Director, Emergency Medicine Education, Saint 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.

Medical Editor

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 Health Sciences Center
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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

J Stephen Huff, MD, Associate Professor, Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia Health Sciences Center
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.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
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 Employment

 
 
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