A102-21 Critical Illness and Fetal Loss From Thiamine Deficiency: Wernicke’s Encephalopathy Secondary to Hyperemesis Gravidarum

Abstract Introduction Thiamine deficiency is an often overlooked but reversible cause of metabolic encephalopathy in critically ill patients. Pregnant women with prolonged hyperemesis gravidarum (HG) are especially vulnerable to rapid depletion of thiamine reserves because of increased metabolic demand and reduced intake. The resulting Wernicke’s encephalopathy (WE) can progress to multiorgan failure, and in severe cases fetal demise hence early recognition and prompt repletion are lifesaving. Case Description A 22-year-old primigravida at 18 weeks’ gestation was admitted with acute confusion, horizontal nystagmus, and generalized weakness after several weeks of persistent vomiting. She was tachycardic (HR 113), hypotensive, and encephalopathic (AO × 2). Laboratory results showed hypokalemia (K 3.0 mmol/L), hypernatremia (Na 151 mmol/L), AKI (BUN 42 mg/dL, Cr 2.18 mg/dL), transaminitis (AST 144 U/L, ALT 54 U/L), hyperbilirubinemia (5.4 mg/dL), and lactic acidosis (4.0 mmol/L). An ultrasound revealed a missed abortion, likely from systemic hypoperfusion. CT head was unremarkable, and EEG showed diffuse slowing. MRI brain with and without contrast demonstrated findings diagnostic of Wernicke Encephalopathy(WE). She received high dose intravenous thiamine and isotonic fluids in the ICU, with marked improvement in mentation within 48 hours. After returning to baseline mentation, she underwent dilation and evacuation and was discharged neurologically intact. Discussion This case bridges obstetric and critical-care medicine by illustrating how a single, preventable micronutrient deficiency produced a multi-organ critical illness. Wernicke’s encephalopathy in pregnancy is uncommon but carries maternal mortality up to 5 % and fetal loss exceeding 45 % when treatment is delayed (Oudman et al). Unlike typical reports of WE limited to neurologic findings, this patient presented with hepatic injury, renal failure, and severe electrolyte derangements, mimicking sepsis and acute liver disease. The diagnosis hinged on early MRI recognition of mammillary body and thalamic lesions before the full clinical triad emerged, allowing timely therapy and neurologic recovery.Its uniqueness lies in the fetal loss secondary to maternal thiamine deficiency, underscoring the devastating effect of a reversible disorder. Despite multiple emergency visits for dehydration, thiamine status was never assessed thereby revealing a persistent gap between obstetric and critical-care practice. A simple, inexpensive vitamin could have prevented this cascade of neurologic and fetal injury.This case reframes thiamine deficiency as a critical-care emergency rather than a nutritional curiosity. Empiric thiamine replacement should be standard for any pregnant or critically ill patient with persistent vomiting, malnutrition, or unexplained encephalopathy. Incorporating thiamine assessment into early ICU and prenatal protocols could avert irreversible maternal injury and preventable fetal death. This abstract is funded by: None