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.

Thiamine deficiency types

Clinical Features
Dry Beriberi with symmetric peripheral neuropathy.
Bariatric beriberi with bilateral wrist drop and peripheral neuropathy after bariatric surgery for morbid obesity.

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

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

Differential Diagnosis

Vitamin deficiencies

High-output heart failure

Evaluation
Chest x-ray showing cardiomegaly with mild pulmonary congestion and pleural effusion in a patient with wet beriberi.
  • 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

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]

  • Thiamine 100mg IV
  • Folate 1mg IV (cheaper PO)
  • Multivitamin 1 tab IV (cheaper PO)
  • Magnesium sulfate 2mg IV
  • Normal saline as needed for hydration

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.
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