Superior Mesenteric Artery Syndrome: An Unusual Cause of Small Bowel Obstruction

Abstract

Superior mesenteric artery (SMA) syndrome is an uncommon cause of duodenal outlet obstruction due to acquired anatomical defects. Often, weight loss precedes obstruction, causing narrowing of the fat pad between the SMA and aorta leading to intestinal compression, usually the 3rd part of the duodenum. SMA syndrome should be considered in patients with rapid weight loss, narrowed vascular angles on imaging, and no other obvious cause of small bowel obstruction (SBO). Our patient is a 51 year-old female with a past medical history of end stage renal disease and hepatitis C. She presented with a recent 30-pound weight loss and complaints of diffuse abdominal pain associated with nausea and vomiting undigested food. The pain was described as constant, pressure-like, increased by oral intake and relieved by left lateral decubitus positioning. A CT scan demonstrated an angle between the SMA and aorta measuring 21 degrees, an aortomesenteric (fat-pad) distance of less than 8 mm and duodenal dilation proximally. A nasogastric tube was placed and symptomatic relief was achieved. Total parental nutrition followed by a nasojejunal feeding tube resulted in weight gain and a subsequent ability to tolerate soft foods prior to discharge. Initially described in 1842, SMA syndrome has prevalence between 0.013 and 0.3%. A high level of suspicion should be maintained in patients with symptoms of obstruction in the setting of rapid weight loss or recent spinal surgery. Diagnosis is based on history and radiographic evidence of obstruction involving the 3rd portion of the duodenum. Computer tomography angiography or magnetic resonance angiography is required to identify vascular measurements of angulation and aortomesenteric distance. The angle between the SMA and aorta is typically 38-65 degrees and the aortomesenteric distance is normally 10-28 mm. In SMA syndrome, both parameters are reduced to 25 degrees (most sensitive measurement) and 2-8 mm respectively. Initial treatment involves correction of electrolyte abnormalities, symptomatic relief including gastric decompression and reconstitution of nutrition and weight. In cases refractory to conservative management or symptoms persisting beyond 3-4 weeks, surgical intervention should be considered. Available options include laparoscopic procedures such as duodenojejunostomy and gastrojejunostomy, or open such as Strong's procedure.Figure 1Figure 2