Thiamine depletion causing neurological complications during nutritional restoration.
Critical depletion of thiamine (vitamin B1) in severely malnourished patients that becomes symptomatic during refeeding when carbohydrate metabolism increases dramatically. Can cause Wernicke encephalopathy.
Severe malnutrition causes thiamine depletion even when serum levels appear normal because thiamine stores are depleted while laboratory values remain in normal range. When feeding is reintroduced, glucose metabolism increases sharply, creating acute thiamine demand that cannot be met by depleted stores. This causes Wernicke encephalopathy, characterized by confusion, ophthalmoplegia, and ataxia—a medical emergency with risk of permanent neurological damage. Prevention requires thiamine supplementation (100 mg daily for 3-5 days, then maintenance) given BEFORE or WITH initial nutritional support in all severely malnourished patients.
Prevents Wernicke encephalopathy and permanent neurological damage by restoring thiamine stores prior to and during nutritional restoration in malnourished patients.
Give thiamine 100 mg parenterally or orally for 3-5 days BEFORE or immediately WITH first feeding in severely malnourished patients. Continue oral supplementation 10-100 mg daily during refeeding. Ensure thiamine is given before glucose-containing IV solutions to prevent Wernicke encephalopathy.
Thiamine supplementation before feeding is essential to prevent Wernicke encephalopathy in severely malnourished patients undergoing nutritional restoration.
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