Wernicke's encephalopathy in a patient with gastric carcinoma: a diagnosis not to miss

Abstract

We describe a case of a patient who presented with a 20-day history of vomiting, generalised weakness and loss of appetite and a 2-day history of altered sensorium. On examination, he was grossly emaciated and there were no palpable lymph nodes. Central nervous system examination revealed nystagmus with bilateral lateral recti palsy and abdominal examination showed mild hepatomegaly. MRI of the brain showed bilateral and symmetrical hypertense signal changes in T2-weighted and fluid-attenuated inversion recovery sequences with diffusion restriction in the paramedian ventromedial thalamus. These findings were compatible with Wernicke's encephalopathy. He was started on thiamine supplementation with which neurological signs improved. An ultrasound of the abdomen showed mild hepatomegaly with multiple hyperechoic lesions and wall thickening of the pyloric antrum. Upper gastroduodenoscopy showed ulcerative lesions involving the antrum, pylorus and duodenum. Biopsy revealed moderately differentiated adenocarcinoma. The patient underwent palliative gastrojejunostomy and was clinically better at discharge. It is important to consider Wernicke encephalopathy in patients with gastric cancer who have acute neurological symptoms.

Nonalcoholic Wernicke’s encephalopathy: a retrospective study of 17 cases

“…Therefore, areas of the brain with high energy metabolism may be damaged because of excess accumulation of toxic intermediates, which is caused by thiamine deficiency. 6 Therefore, thiamine is crucial for health.…”

“…However, diagnostic delays were common in our study, which is consistent with the literature. 6 The possible causes of a delay in diagnosis and treatment include doctors' lack of awareness of WE, delayed referral to a higher center, and late consultation with a neurologist. Because there is no specific routine laboratory test for diagnosing WE, the initial diagnosis of WE remains based on clinical findings.…”

“…Measuring blood thiamine concentrations or erythrocyte transketolase activity may be useful for diagnosing WE. 6 The limitations of blood tests are that they are costly and timeconsuming. However, because the prognosis of WE is favorable in patients who are diagnosed and treated early, early diagnosis and timely administration of thiamine is important.…”

“…Thiamine is an important co-enzyme for the pyruvate dehydrogenase complex, transketolase a-ketoglutarate, and the dehydrogenase complex, which are involved in glucose degradation and thus energy metabolism. 6,7 Moreover, a deficiency of these enzymes caused by thiamine deficiency results in increased anaerobic fermentation and even lactic acidosis, causing permanent brain cell damage and ultimately death. 8 We report our experience of patients with nonalcoholic WE in our hospital during the last 5 years.…”

“…5 Sometimes these lesions are found in the cerebellum, cranial nerve nuclei, and cerebral cortex. 6 If the clinical triad of abnormal mental symptoms, dystaxia, and eye symptoms 3 are not apparent in nonalcoholic patients with WE, MRI may confirm a diagnosis because of its high specificity. However, MRI has low sensitivity and could thus potentially delay treatment and should not be considered a major tool.…”