P06 | Development of wet beriberi with prolonged Qtc and severe LVEF in a Wernicke’s encephalopathy patient

C. Ambrosi, L. Bettazzoni, F. Gravina, C. Bertoldi, M. Domenicali | Università degli Studi di Bologna, Italy

Background: Severe thiamine deficiency, generally associated with alcohol-related disorders and malnutrition, can cause cognitive impairment (Wernicke’s encephalopathy, WE), peripheral neuropathy (dry beriberi) or heart failure (wet beriberi).
Case report: A 65-years-old woman with a history of hypertension, alcohol abuse and poor nutrional intake was brought to the ED for confusion. On admission she was afebrile, asymptomatic for angor and hemodynamically stable, she had mild lower extremity edema and mild bibasal crakles. Neurological evaluation revealed ataxia and oculomotor abnormalities. Lab exams were remarkable for: Mg 1.5 mg/dL, K 3.2 mg/dL, lactic acidosis (lac 6 mMol/L) and mildly elevated TnT (80-70-76 ng/L). Urine tox screen was negative for illicit substances. CT of the head was negative. WE was suspected and empiric treatment with high dosage IV thiamine was started. At EKG monitoring progressive prolongation of QTc (650 msec) and inverted T waves were detected. TTE revealed global LV hypokinesis with severely reduced EF (25%). On suspicion of wet beriberi IV thiamine was continued along with electrolytes supplementation. In 24 h a drastic improvement in symptoms, lactic acidosis and LV systolic function (45%) was observed, therefore coronarography was omitted.
Conclusions: Acute heart failure with lactic acidosis in patients with WE is highly suggestive of wet beriberi. Severe forms can lead to reduced LVEF. QTc prolongation is observed in thiamine deficiency, so EKG monitoring should be considered in WE. Positive response to thiamine supports the diagnosis.