AME case reports · 2026
Fulminant cardiovascular collapse after acute pancreatitis: a case report of non-alcoholic Shoshin beriberi and literature review.
Клинический случайСтатьяНазвание и аннотация: Перевод в очереди
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Xie Xin, Deng Liehua, Zhao Jia, Sun Xiaocong, Liu Lizhen, Pan Xiaoyan, Zhang Yuanli
Аннотация
BACKGROUND: Shoshin beriberi-fulminant cardiogenic shock caused by thiamine deficiency-is rare in adults and is rarely reported after acute pancreatitis has been treated with long‑term parenteral nutrition (PN). Timely thiamine administration is curative, but the diagnosis is often delayed, and patients may perish before metabolic therapy takes effect.
CASE DESCRIPTION: A previously healthy 25-year-old man developed refractory shock 2 months into PN for necrotizing pancreatitis. His lactate concentration was 17.4 mmol·L-1, and echocardiography revealed global hypokinesis (left ventricular ejection fraction, LVEF, of 15%). Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was started within 90 min. Diplopia plus severe malnutrition raised suspicion of thiamine deficiency, and high-dose intravenous (i.v.) thiamine (200 mg, q8h) was started empirically on day 2. The lactate concentration normalized, and the LVEF increased to 25% within 96 h. ECMO was removed on day 8, and the LVEF fully recovered (to 55%) by day 10. The pretreatment serum thiamine concentration was later confirmed to be low (40 nmol·L-1). Brain magnetic resonance imaging (MRI) demonstrated typical Wernicke's lesions. The patient was discharged to rehabilitation on day 29 and remained asymptomatic at the 3-month follow-up.
CONCLUSIONS: By demonstrating that VA-ECMO can preserve end-organ perfusion until high-dose thiamine reverses fulminant beriberi, this adult case extends the clinical spectrum of thiamine deficiency shock. In practice, diagnosis hinges on a high index of suspicion and simple bedside cues, including prolonged poor intake or PN without vitamin supplementation, otherwise unexplained hyperlactatemia, and subtle neurological signs, such as diplopia, prompting early empirical intravenous thiamine treatment.
CASE DESCRIPTION: A previously healthy 25-year-old man developed refractory shock 2 months into PN for necrotizing pancreatitis. His lactate concentration was 17.4 mmol·L-1, and echocardiography revealed global hypokinesis (left ventricular ejection fraction, LVEF, of 15%). Venoarterial extracorporeal membrane oxygenation (VA-ECMO) was started within 90 min. Diplopia plus severe malnutrition raised suspicion of thiamine deficiency, and high-dose intravenous (i.v.) thiamine (200 mg, q8h) was started empirically on day 2. The lactate concentration normalized, and the LVEF increased to 25% within 96 h. ECMO was removed on day 8, and the LVEF fully recovered (to 55%) by day 10. The pretreatment serum thiamine concentration was later confirmed to be low (40 nmol·L-1). Brain magnetic resonance imaging (MRI) demonstrated typical Wernicke's lesions. The patient was discharged to rehabilitation on day 29 and remained asymptomatic at the 3-month follow-up.
CONCLUSIONS: By demonstrating that VA-ECMO can preserve end-organ perfusion until high-dose thiamine reverses fulminant beriberi, this adult case extends the clinical spectrum of thiamine deficiency shock. In practice, diagnosis hinges on a high index of suspicion and simple bedside cues, including prolonged poor intake or PN without vitamin supplementation, otherwise unexplained hyperlactatemia, and subtle neurological signs, such as diplopia, prompting early empirical intravenous thiamine treatment.