Wernicke Encephalopathy after Restrictive Bariatric Surgery

Due to persistent nausea and vomiting, a peripherally inserted central catheter was placed on hospital day 7 in anticipation of initiation of total parenteral nutrition. Discussion Micronutrient deficiency due to malabsorption is a well-described phenomenon in postoperative bariatric surgical patients.1 However, clinical deficiency is generally associated with malabsorbitive procedures rather than restrictive bariatric procedures.2 Notably, the risk of developing clinically significant micronutrient deficiencies after LSG has been thought to be so low that routine monitoring is not practiced.3 In 2014, Stroh reported 255 cases of bariatric beriberi.4 Of these 255 cases, 254 were diagnosed after Roux-en-Y gastric bypass.4 In these patients, thiamine deficiency developed between one and three months after surgery.4 The authors hypothesized that the cause of thiamine deficiency was due to a number of factors including (though not limited to) poor preoperative nutritional status, surgical excision of segments of the small intestine required for thiamine absorption, poor postoperative nutritional intake, and recurrent postoperative emesis.4 Thiamine is a water-soluble vitamin that is primarily absorbed in the duodenum and proximal jejunum via carrier-mediated active transport.5 Because thiamine is an essential nutrient, is water soluble, and has a limited intracellular reserve (approximately 30 mg), constant supplementation is critical.6 Thiamine diphosphate, the biologically active form of thiamine, acts as a cofactor for the enzymes pyruvate dehydrogenase, a-ketoglutarate dehydrogenase, transketolase, and branched-chain a-ketoacid dehydrogenase, all of which are involved in carbohydrate and amino acid metabolism.7 Thiamine also assists in the regulation and activation of sodium and potassium ion movement in nerve and muscle cells.4 Thiamine deficiency impairs metabolism and function of astrocytes responsible for maintaining the integrity and functionality of surrounding neurons.7 The result of this metabolic dysfunction leads to intra- and extracellular edema, neuronal loss, microhemorrhage, and proliferation of microglial cells involved in scar formation.8 These changes tend to occur in the mammillary bodies, the paraventricular periaqueductal gray matter, the medial thalami, and other structures around the third ventricle.9 Symptomatically, thiamine deficiency manifests as Wernicke encephalopathy (WE).