A 54-year-old Caucasian female presented to the clinic with epigastric pain and bloating after meals. Seven months ago she underwent a laparoscopic Nissen fundoplication for refractory gastroesophageal reflux disease in her native country. Her reflux symptoms started 2 years ago which included severe heartburn, retrosternal crampy pains as well globus sensation. She was initially treated with PPIs for a period of 4 months with only minimal improvement of her symptoms. She underwent laparoscopic Nissen Fundoplication with unremarkable hospital course and was discharged home in the stable condition on the third postoperative day. Shortly after her surgery she left her country and traveled to Los Angeles, only to find herself in an urgent care clinic few days later where she was evaluated for her daily bloating episodes lasting 2-3 hours, inability to belch, and intermittent nausea. After thorough evaluation, which included laboratory work and abdominal X-ray, it was concluded that her complaints were most likely related to a normal post-Nissen fundopication symptoms. She was reassured and subsequently discharged home. However, she continued to have similar symptoms and several weeks later she represented to a local hospital with severe abdominal pain and fevers of 101 F. Her laboratory work revealed elevated WBC 18 000 cells/muL (normal, 4500-10 500 cells/muL). She had sinus tachycardia with the systolic blood pressure of 90 and abdominal examination consisting of generalized peritonitis. She was taken emergently to the operating room for exploratory laparotomy. Intraoperative findings revealed an acute gastric linear tear on the anterior portion of the body of the stomach, 10 centimeters distal to the intact fundoplication wrap. The gastric tear appeared traumatic in origin without any other gastric pathology. Two-layer primary closure of the defect was performed. She remained stable during her hospital stay and was discharged home on 5th postoperative day tolerating regular diet. Two months after her second surgery, she represented again to the emergency department with severe epigastric pain radiating to the back. She was diagnosed with acute pancreatitis on the basis of her symptoms and laboratory values of amylase and lipase 800 UL (normal 60-180 U/L) and 1200 U/L (normal <190 U/L), respectively. Ultrasound and endoscopic retrograde cholangiopancreatography on the admission revealed no evidence of gallstones or choledocholithiasis. Her pancreatitis responded to conservative treatment and she was subsequently discharged home 6 days after her admission with complete resolution of symptoms.
 During her surgical follow-up visit she continued to complain of postprandial pain with an early satiety and episodic nausea. She appeared weak and malnourished. She noted a 20 lbs weight loss since her initial antireflux procedure. Her abdomen was slightly distended with hyperactive bowel sounds. She had moderate epigastric pain during palpation. She was admitted to the hospital for a work-up of her ongoing symptoms and as well as for poor nutritional status. Her work-up included plain abdominal films, which demonstrated air in a dilated stomach and duodenum with an abrupt vertical cut off and no evidence of air in the small intestine distal to the 3rd portion of the duodenum (Figure 1). Upper Gastrointestinal series obtained subsequently revealed contrast in the dilated duodenum with an abrupt cut off at the level of the superior mesenteric artery pedicle in a supine position (Figure 2). Obstruction was relieved once patient was placed in the prone position (Figure 3). Based on her clinical signs as well as classic radiological findings, a diagnosis of superior mesenteric artery syndrome was made. Patient was taken to the operating room where she underwent duodenojejunostomy. Her postoperative hospital course was uneventful. She was tolerating regular diet and was subsequently discharged home on the 5th postoperative day. Patient remains asymptomatic at one year followup.