Wernickeʼs Encephalopathy Following Roux-en-Y Gastric Bypass Complicated by Gastrojejunal Stenosis and Small Bowel Obstruction: 2016 ACG Presidential Poster Award

Abstract

A 28 year-old woman was admitted to our hospital with 3 weeks of abdominal pain, nausea, and vomiting. At another facility, she had undergone Roux-en-Y gastric bypass 3 months prior for morbid obesity, followed by laparoscopic cholecystectomy one week prior for presumed chronic cholecystitis. The patient suffered from multiple daily episodes of nausea and vomiting, resulting in a 95 pound weight loss since her bariatric surgery. The cholecystectomy did not improve her symptoms. Neurologic examination was remarkable for horizontal rotary nystagmus, patellar and ankle areflexia, impaired pin-prick and temperature sensation of anterior aspects of the chest and abdomen, as well as distal legs and feet, impaired vibration sense in both feet, and wide-based ataxic gait. Empiric high dose intravenous thiamine repletion was immediately begun; whole blood thiamine level was later confirmed to be low. An upper GI series/small bowel follow-through did not reveal an obstruction initially, though CT scan showed a distended and fluid-filled gastric remnant and proximal small bowel, with possible transition point near the jejunojejunal anastomosis. EGD, however, demonstrated a normal appearing jejunojejunal anastomosis, but a mild gastrojejunal stenosis, which was successfully dilated. The patient rapidly improved following the dilation and with aggressive thiamine repletion. However, she was re-admitted three weeks later with recurrence of pain, nausea, and vomiting. CT now showed an evolving small bowel obstruction, prompting exploratory laparotomy with lysis of an adhesive band causing obstruction of the common channel. A feeding gastrostomy tube was also placed. Her neurological signs and symptoms have since improved and she is no longer requiring tube feeds. This case illustrates the importance of prompt attention to the development of any central or peripheral neurologic manifestations following bariatric surgery. This is especially important for thiamine deficiency, as Wernicke's encephalopathy only rarely presents with the classical triad of altered mental status, ocular motility abnormalities, and ataxia. If Wernicke's encephalopathy is suspected, it should be treated urgently, as confirmatory laboratory results would result in delays during which neurologic damage may progress. Additionally, although gastric bypass itself can predispose to thiamine deficiency, an underlying etiology, such as complications of surgery, should be sought and addressed.Figure 1Figure 2Figure 3