Comments on “Wernicke’s Encephalopathy after Laparoscopic Roux-en-Y Gastric Bypass: A Misdiagnosed Complication”

Abstract

In a recent issue of Obesity Surgery, Iannelli and colleagues reported a case of a 27-year-old woman that developed diplopia, weakness in both upper and lower extremities, urinary incontinence, and memory loss to recent events 10 months after laparoscopic Roux-en-Y gastric bypass for morbid obesity. They established the diagnosis of Wernicke’s encephalopathy (WE) based on clinical manifestations as well as a 12-month follow-up [1]. This case is interesting because it provided general surgeons an insight into the overlooked diagnosis of WE after obesity surgery. However, we have some concerns about the differential diagnoses of this case. WE is defined as the combination of ataxia, ophthalmoplegia, nystagmus, and mental confusion resulting from vitamin B1 deficiency [2]. In their report, the authors did not detect the level of vitamin B1 in the serum. As a result, differential diagnoses should be distinguished from the diagnosis they proposed, i.e. WE. The patient was admitted at a peripheral hospital with severe dehydration and a history of persistent vomiting. We would like to know whether electrolyte disorders exist at that time. Electrolyte disorders such as hypopotassaemia and hyponatremia may present as quadriplegia, absent deep tendon reflexes, and disturbance of consciousness. We agree that thiamine plays a role in carbohydrate metabolism and the administration of glucose and other carbohydrates without thiamine can be dangerous for patients with thiamine deficiency, while extrapontine myelinolysis (EPM) due to rapid correction of severe hyponatremia should also be taken into account since the patient manifested diplopia, weakness in both upper and lower extremities, urinary incontinence, and memory loss to recent events after she was admitted by the authors [3]. Lesions in extrapontine myelinolysis have been increasingly documented, including cerebellum, lateral geniculate body, external and extreme capsules, hippocampus, putamen, cerebral cortex/subcortex, thalamus, and caudate nucleus. Unusual sites for EPM include spinal cord, mamillary bodies, amygdala, columns of the fornix, anterior commissure, optic tract, subthalamic nucleus, etc. The clinical manifestations, as a consequence, vary according to different lesions [4–8]. In WE, MRI may show a symmetrically increased T2 signal in the paraventricular regions of the thalamus, hypothalamus, mamillary bodies, and/or midline cerebellum [9]. However, MRI of this case showed only multiple ranges of subcortical edema in the occipital regions, which not only support the diagnosis of WE but also EPM. In addition, polyneuropathy is not uncommon in patients with vitamin B1 deficiency [10]. The patient was reported to have quadriplegia and absent deep tendon reflexes in knee and ankle joints bilaterally, whereas pathological signs, which are important in differentiating peripheral paralysis from central paralysis, were not reported. In particular, urinary incontinence that the patient presented with may be indicative of spinal cord involvement. K.-J. Zhang :D. Zhang Department of Plastic Surgery, The First Hospital of Jilin University, Changchun, China