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Thiamine has a key role in the regulation of cell metabolism. Thiamine is considered as an important co-factor for crucial enzymes in carbohydrate metabolism to preserve brain health. Severe deficiency of thiamine is impaired to mitochondrial function and metabolic system in brain. The mechanisms are disruption of blood brain barrier, inducing inflammation, and degeneration in the neurological system probably due to increased oxidative stress and lactic acidosis. Its deficiency induces types of beriberi, characterized by neuropathy, Wernicke’s encephalopathy (WE), and heart failure. Although delay in the treatment of thiamine deficiency can be life-threatening, early supplementation shows a quick beneficial effect. Thiamine deficiency has reported among the critically ill patients with major stress, especially those who were under surgery, and receive parenteral nutrition.1 Many patients with neurological presentations of thiamine deficiency have missed because there is often no history of alcohol abuse or malnutrition accompanied by a lack of reliable diagnostic test. Diagnosis of WE is according to the classical triad of acute confusion, ophthalmoplegia and ataxia. Misdiagnosis of WE can lead to a chronic mental dysfunction known as Korsakoff’s syndrome in 85% of survivors.2 The stress of major surgeries such as coronary artery bypass grafts or gastric surgeries with malabsorption conditions may deplete some essential biochemical substrates such as thiamine, and consequently induce WE in a chronic condition.3,4 A 49-year-old woman with a history of diabetes mellitus, hypothyroidism, mitral valve prolapse, and surgery about 18 years ago was referred to our emergency department.

Wernicke’s encephalopathy as a presentation of severe thiamine deficiency after cardiac valve surgery: A case report and narrative review