SAT175 Noninsulinoma Pancreatogenous Hypoglycemia Syndrome As A Complication Of Nissen Fundoplication

Disclosure: R. Rinn: None. S. Lacount: None. J. Muuse: None. Hypoglycemia is a common condition that is typically diagnosed with Whipple’s Triad (hypoglycemic symptoms, low blood glucose, resolution of symptoms with treatment). It is important to recognize and treat early as it has the potential for lethal outcomes. Dumping syndrome is a rare presentation after Nissen’s fundoplication and predominantly reported in children. Here we present a case of an adult with persistent postprandial hypoglycemia after Nissen Fundoplication. A 79-year-old male with a recent Nissen’s fundoplication presented with repeated episodes of extreme fatigue and diaphoresis after eating. Other complaints included weakness and significant weight loss. Finger stick glucose on multiple checks were found to be in 40s. He was hospitalized and underwent extensive workup with Endocrinology and Gastroenterology. Important labs revealed elevated insulin 10.2, C-peptide level at 7.3 and pro-insulin at 27.7, negative insulin antibodies, a normal Insulin like growth factor (IGF-1) at 74, Beta-hydroxybutyrate level 0.1, and a negative screen for sulfonylureas. He was discharged home on a low carbohydrate diet but continued having repeated Whipple’s triad positive hypoglycemic episodes. In terms of imaging, CT of the abdomen did not reveal a mass, other localization studies were deferred since the episodes were mostly post-prandial concerning for NIPHS than insulinoma. For management, he had minimal response to octreotide and verapamil. His symptoms are currently being managed on acarbose and diazoxide with dietary modifications consisting of high protein and limited complex carbohydrates. Postprandial hypoglycemia as a complication of Nissen’s fundoplication is thought to be secondary to dumping syndrome (DS). DS is divided into two stages- early/osmotic stage and late/ hypoglycemic stage. Both types are caused by a large amount of gastric contents emptying into the duodenum, resulting in vasomotor symptoms from changes in blood pressure, pulse and glucose levels, as well as gastrointestinal symptoms. Glucagon like peptide-1 is responsible for the second phase and the levels are directly related to gastric emptying and inversely related to plasma glucose concentration. Accelerated gastric emptying causes increased GLP-1 levels leading to exaggerated insulin response resulting in rebound severe hypoglycemia. It is important to realize that diet plays an important role in symptom management. After Nissen’s fundoplication, a decrease occurs in the storage capacity of the fundus and gastric distensibility, which causes increased gastric motility with rapid emptying. Dietary modifications include reduction of carbohydrate intake and supplementation of dietary fibers with meals greatly help relieve symptoms associated with dumping syndrome in addition to drug therapy. Presentation: Saturday, June 17, 2023