Wernicke-Korsakoff syndrome: Difference between revisions

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===Vitamin Prophylaxis for Alcoholics===
===Vitamin Prophylaxis for Alcoholics===
*For the majority of chronic alcoholics, you should not administer a banana bag (thiamine 100 mg + magnesium 2-4 g + folate 1 mg + multivitamin; all in 1L NS or D5W)<ref>Krishel, S, et al. Intravenous Vitamins for Alcoholics in the Emergency Department: A Rreview. The Journal of Emergency Medicine. 1998; 16(3):419–424.</ref><ref>Li, SF, et al. Vitamin deficiencies in acutely intoxicated patients in the ED. The American Journal of Emergency Medicine. 2008; 26(7):792–795.</ref>
*For the majority of chronic alcoholics, you should not administer a banana bag (thiamine 100 mg + magnesium 2-4 g + folate 1mg + multivitamin; all in 1L NS or D5W)<ref>Krishel, S, et al. Intravenous Vitamins for Alcoholics in the Emergency Department: A Rreview. The Journal of Emergency Medicine. 1998; 16(3):419–424.</ref><ref>Li, SF, et al. Vitamin deficiencies in acutely intoxicated patients in the ED. The American Journal of Emergency Medicine. 2008; 26(7):792–795.</ref>
**At risk for thiamine deficiency but no symptoms: thiamine 100 mg PO q day
**At risk for thiamine deficiency but no symptoms: thiamine 100 mg PO q day
**Give multivitamin; patient at risk for other vitamin deficiencies
**Give multivitamin; patient at risk for other vitamin deficiencies

Revision as of 01:10, 21 July 2016

Background

  • Wernicke’s Encephalopathy (WE): ACUTE neuro/cardiovascular symptoms caused by thiamine deficiency
  • Korsakoff’s Psychosis (KP): CHRONIC neurologic symptoms caused by thiamine deficiency
  • Wernicke-Korsakoff Syndrome (WKS): presence of WE + KP simultaneously

Epidemiology

  • Only 20% identified before death, failure of dx leads to 20% mortality and 75% permanent damage

Pathophysiology

  • Brain lesions/atrophy occurs: mamillary bodies (nearly all cases), thalamus, periaqueductal gray matter, 3rd/4th ventricle, cerebellum, frontal lobe
  • Thiamine is a cofactor for enzymes required in:
    • krebs cycle
    • Pentose phosphate pathway
    • Alpha-ketoglutarate dehydrogenase, pyruvate dehydrogenase.
  • Because thiamine is an important cofactor in critical pathways for energy production, deficiency results in lactic acidosis and alteration of brain metabolism.
  • Thiamine is also important for lipid metabolism and may affect myelin sheath formation. This may explain peripheral neuropathy symptoms in dry beriberi.

Causes

  • Anything that causes thiamine (vitamin B1) deficiency: poor dietary intake, malabsorption, increased metabolic requirement
    • Chronic alcoholism, dieting/fasting/starvation, anorexia, vomiting/diarrhea, unbalanced TPN, GI surgery, malignancy, dialysis, AIDS, IBD, pancreatitis, liver disease, thyrotoxicosis

Clinical Features

Wernicke’s Encephalopathy

  • Classic triad: encephalopathy, oculomotor dysfunction, gait ataxia
  • werNICke mnemonic:
    • N: Nystagmus/ophthalmoplegia. Ocular findings may also include bilateral 6th nerve palsy, conjugate gaze palsy, pupillary abnormality, retinal hemorrhage, ptosis.
    • I: Incoordination/ataxia
    • C: Confusion/memory impairment
  • Other sx: hypotension, tachycardia, ECG abnormalities, DOE, CHF sx, hypothermia, coma, dry/wet Beriberi

Korsakoff’s Psychosis

  • Sx: anterograde/retrograde amnesia, confabulation, confusion, apathy

Wernicke-Korsakoff Syndrome

  • Sx: combination of WE and KP

Differential Diagnosis

Ethanol related disease processes

Vitamin deficiencies

Diagnosis

WE/KP/WKS = clinical diagnoses.

Wernicke's Encephalopathy diagnosis requires at least 2 out of the following 4 clinical criteria:

  1. Nutritional deficiency
  2. Ocular findings (ophthalmoplegia, nystagmus)
  3. Ataxia
  4. Mental status change

Management

If you suspect WE/KP/WKS then treat it! Diagnosis is clinical and difficult to confirm, treatment is simple/inexpensive/effective, there is little risk to treatment, and the risk of morbidity/mortality from not treating is high

  • Suspected WE/KP/WKS: thiamine 500 mg IV over 30 min TID x 2 days, then 500 mg IV/IM q day for 5 days, then 100 mg PO q day until patient no longer at risk
    • Give magnesium; hypomagnesemic state may be resistant to thiamine administration
    • Treatment can take days to weeks to work if at all (despite accurate diagnosis)
    • Give thiamine BEFORE glucose in patients requiring glucose who are at risk for thiamine deficiency; glucose without thiamine can precipitate/worsen WE by driving thiamine intracellularly

Vitamin Prophylaxis for Alcoholics

  • For the majority of chronic alcoholics, you should not administer a banana bag (thiamine 100 mg + magnesium 2-4 g + folate 1mg + multivitamin; all in 1L NS or D5W)[1][2]
    • At risk for thiamine deficiency but no symptoms: thiamine 100 mg PO q day
    • Give multivitamin; patient at risk for other vitamin deficiencies

See Also

References

  1. Donnino, Michael, et al. “Myths and misconceptions of wernicke’s encephalopathy: what every emergency physician should know.” Annals of emergency medicine. 2007. Vol 50, no 6. Pages 715-721.
  2. Sechi, GianPietro; Serra, Alessandro. “Wernicke’s encephalopathy: new clnical settings and recent advances in diagnosis and management.” Neurology. Vol 6, May 2007. Pages 442-455
  1. Krishel, S, et al. Intravenous Vitamins for Alcoholics in the Emergency Department: A Rreview. The Journal of Emergency Medicine. 1998; 16(3):419–424.
  2. Li, SF, et al. Vitamin deficiencies in acutely intoxicated patients in the ED. The American Journal of Emergency Medicine. 2008; 26(7):792–795.

Video

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