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Beriberi
From WikEM
Contents
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
- Vitamin A deficiency
- Vitamin B deficiencies
- Vitamin B1 deficiency (Thiamine)
- Beriberi
- Wernicke-Korsakoff syndrome
- Vitamin B3 deficiency (Pellagra)
- Vitamin B9 deficiency (Folate)
- Vitamin B7 deficiency (Biotin)
- Vitamin B12 deficiency
- Vitamin B1 deficiency (Thiamine)
- Vitamin C deficiency (Scurvy)
- Vitamin D deficiency (Rickets)
- Vitamin E deficiency
- Vitamin K deficiency
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
- Thiamine 50-100mg IV/IM q day x 7-14 days, then 10mg PO q day until complete recovery
- Magnesium; hypomagnesemic state may be resistant to thiamine administration
- Multivitamin (at risk for other vitamin deficiencies)
- For chronic alcoholics consider banana bag: thiamine 100mg + magnesium 2-4 g + folate 1mg + multivitamin; all in 1L NS or D5W
- 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
See Also
References
- 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.
- 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