Beriberi

Background

  • Dry Beriberi: neuro symptoms caused by thiamine deficiency
  • Wet Beriberi: cardiac symptoms caused by thiamine deficiency
  • Infantile Beriberi: neuro/cardiac symptoms caused by thiamine deficiency in <1 year old infant

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

Pathophysiology

  • 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.

Clinical Features

Dry Beriberi

  • Symmetrical peripheral neuropathy (motor and sensory) mostly distal extremities

Wet Beriberi

  • CHF, high output heart failure, cardiomegaly, peripheral edema, tachycardia, DOE/PND/orthopnea
  • Can include neuropathy seen in Dry Beriberi

Infantile Beriberi

  • CHF, cardiomegaly, tachycardia, cyanosis, dyspnea, weight loss, marasmus, vomiting, loud cry, nystagmus, seizure

Bariatric Beriberi

  • Occurs 1-3 months post-op
  • Causes are multifactorial, including low nutritional intake, poor baseline nutrition, persistent vomiting, malabsorption

Differential Diagnosis

Vitamin deficiencies

Evaluation

  • Clinical diagnosis

Management

If you suspect Beriberi 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

  1. Thiamine 50-100mg IV/IM q day x 7-14 days, then 10mg PO q day until complete recovery
  2. Magnesium; hypomagnesemic state may be resistant to thiamine administration
  3. Multivitamin (at risk for other vitamin deficiencies)
  • 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

Disposition

Prevention

Vitamin Prophylaxis for Chronic alcoholics

  • At risk for thiamine deficiency, but no symptoms: thiamine 100mg PO q day
  • Give multivitamin PO; patient at risk for other vitamin deficiencies

Banana bag

The majority of chronic alcoholics do NOT require a banana bag[1][2]

Disposition

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 Review. 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.