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
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-bariatric surgery
- 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)
- Vitamin B3 deficiency (Pellagra)
- Vitamin B9 deficiency (Folate)
- Vitamin B7 deficiency (Biotin)
- Vitamin B12 deficiency
- Vitamin C deficiency (Scurvy)
- Vitamin D deficiency (Rickets)
- Vitamin E deficiency
- Vitamin K deficiency
- Zinc deficiency
High-output heart failure
- Hyperthyroidism
- Beriberi
- High-output heart failure from AV fistula
- AVM
- Paget disease
- Anemia
- Pregnancy
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)
- 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]
- 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
- 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