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A5193 - Unexplained Lactic Acidosis and Shock Caused by Rare Gastrointestinal Beriberi
Author Block: D. Patel, R. C. Rajmane, A. Yelisetty, H. Patel; NYU Langone Hospital - Brooklyn, Brooklyn, NY, United States.
Introduction:Cardiovascular collapse due to thiamine deficiency, known as Shohsin Beriberi, is reversible but fatal if unrecognized and left untreated. We present a rare case of gastrointestinal beriberi associated with severe lactic acidosis and shock.
Case report:A 68 y/o woman with a history of alcoholism, hypothyroidism and hypertension presented with generalized weakness, decreased oral intake, vomiting and abdominal pain for three days after falling at home. The patient self-medicated with analgesics. She reported consuming large quantities of alcohol during this time with no other oral intake. Vitals at the time of arrival were significant for hypotension and tachycardia. Her mental status started to deteriorate leading to intubation for airway protection.
Blood work was significant for profound metabolic acidosis with a lactate of >20.0 mmol/L (reference range 0.90-1.70 mmol/L). Initially she was admitted to the medical ICU for severe metabolic acidosis presumably due to severe sepsis. Lactic acidosis persisted despite appropriate antibiotics and intravenous hydration over the next 48 hours. Bowel ischemia was ruled out. She was started on high dose intravenous thiamine, which precipitously caused her lactic acidosis to resolve within 24 hours. Patient was subsequently weaned off vasopressors and organ dysfunction resolved.
Discussion:Thiamine is a water-soluble vitamin that plays an essential role in carbohydrate metabolism. Thiamine pyrophosphate, a thiamine derivative, is an important cofactor of pyruvate metabolism to allow entry into citric acid cycle, which is required for mitochondrial synthesis of ATP in carbohydrate metabolism. Thus, in thiamine deficiency, pyruvate metabolism is diverted to lactic acid production. Thiamine deficiency has commonly been associated with cardiac and neurological syndromes, such as beriberi and Wernicke’s encephalopathy respectively.
Thiamine deficiency may occur in patients within 14 days of inadequate intake but rapid recovery within hours is possible after intravenous supplementation. Because serologic assessments of thiamine deficiency are time-consuming, it is not routinely done leading to inadequate identification in critically ill patients. Historically, thiamine deficiency has been frequently associated with neurological and cardiac dysfunction. Our case is unique because the primary symptoms were gastroenterological that rapidly progressed to shock. Heightened suspicion of thiamine deficiency should be suspected in unexplained lactic acidosis or refractory shock in patients with history of chronic malnutrition, alcoholism or long-term parenteral feeding. Survival in Shoshin Beriberi - whether presenting with traditional cardiac or neurologic derangement or in our rare gastroenterological case - is dependent on early recognition and early intravenous supplementation of thiamine.