Case report of superior mesenteric artery syndrome that developed in a lean type 2 diabetes patient and was associated with rapid body weight loss after sodium-glucose cotransporter 2 inhibitor administration.

A 58-year-old women who was diagnosed with type 2 diabetes 20 years earlier had been treated with antidiabetic medicines since she was aged 40 years. After sodium-glucose cotransporter 2 inhibitors administration, her bodyweight rapidly decreased from 40 to 30 kg over a period of 3 weeks. She had abdominal symptoms, including nausea, especially after a meal. On admission, physical examinations and laboratory data showed euglycemic ketoacidosis, dehydration and low insulin secretion levels. Additionally, abdominal contrast computed tomography showed the finding of superior mesenteric artery syndrome. This case urges caution, including rapid excessive bodyweight loss and euglycemic ketoacidosis, on the use of sodium-glucose cotransporter 2 for lean diabetes patients.

Superior mesenteric artery syndrome in a burn patient.

Weight loss resulting from the hypermetabolic response to burn injury is not unusual and is often unavoidable. The loss of retroperitoneal fat has been postulated as a major factor in the cause of the uncommon complication of superior mesenteric artery syndrome. This syndrome is frequently treated nonoperatively with aggressive nutrition support. Nasojejunal feeding past the point of obstruction should be considered as the primary method of nutrition support. Alternatively, total parenteral nutrition or a combination of enteral and parenteral feeding may be necessary to meet nutritional needs until the duodenal obstruction resolves. This case study describes the nutrition management of a burn patient who developed superior mesenteric artery syndrome.