Shoshin beriberi with severe lactic acidosis and haemodynamic collapse due to long-term diuretic therapy.

A patient on long-term diuretic treatment for pulmonary arterial hypertension presented with acute haemodynamic instability and profound high anion gap metabolic acidosis. Investigations showed severe lactic acidosis with no evidence of sepsis, hypoxia, diabetic ketoacidosis, acute pulmonary embolism or mesenteric ischaemia. Despite fluid resuscitation, vasopressor support and ventilatory support, the metabolic derangement persisted. Since she was on prolonged diuretic use and no other cause was identified, thiamine deficiency was suspected. Empirical intravenous thiamine administration led to rapid and sustained improvement in acid-base status and haemodynamics, allowing tapering of vasopressors. This case highlights thiamine deficiency as an under-recognised but readily reversible cause of severe lactic acidosis and cardiovascular collapse, particularly in patients receiving chronic diuretic therapy.