Anorexia Nervosa and Superior Mesenteric Artery Syndrome Hitoshi Miyaoka 1 , Sadao Nakamura 1 , Masahiro Asai 1 , Yukihisa Miyazawa 2 , Norio Tada 2 , Shigeaki Sano 3 1Department of Ncuropsychiatry, School of Medicine, Keio University 22nd Dcpartment of Surgery, School of Mcdicine, Teikyo University 3Department of lnternal Medicine, Aoto Hospital, School of Medicine, Jikei University Keyword: Anorexia nervosa , Superior mesenteric artery syndrome , Gastric dilatation , Vascular compression of the duodenum pp.1379-1389
Published Date 1985/12/15
DOI https://doi.org/10.11477/mf.1405204052
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 Superior mesenteric artery syndrome (SMAS) is the condition caused by delay in the passage of intestinal contents beyond the third portion of the duodenum, due to compression of this part against the spine by the superior mesenteric artery. Two subtypes, acute and chronic, are recognized. The acute syndrome occurs in immobilized supine padents who have lost weight rapidly as in a systemic disease. The presenting symptoms which develop suddenly are those of acute obstruction of the small bowel. The chronic SMAS usually occurs in patients of the habitus asthenicus and is characterized by intermittent abdominal pain, bloating, anorexia, nausea and vomiting. Most of the patients learn to limit food intake or may become phobic to eating.

 Anorectic patients who have had a rapid weight loss may develop the acute form of SMAS. Physical symptoms of acute SMAS may be mistaken for psychogenic vomiting in anorexia nervosa (AN) though they are severe complications, which may often lead to death. Chronic SMAS sometimes occurs in anorectic patients and worsens gastrointestinal symptoms of AN itself. Although AN may cause chronic SMAS as its complication, pure chronic SMAS itself may be misdiagnosed as AN because of the similarity of the symptoms of AN and SMAS.

 A 15-year-old girl developed anorexia and amenorrhea 4 months after entrance into a high school. Her weight had fallen from 44kg to 30kg (43.6% below ideal weight) for 6 months. She was diagnosed as AN. One year after the onset of AN she began to complain post prandial nausea, vomiting and intermittent abdominal pain. Two years after the onset acute gastric dilatation developed. Her weight was 39kg (36.1% below ideal weight). A barium meal X-ray examination and abdominal ultrasonography revealed obstruction of the third portion of the duodenum at the level of the superior mesenteric artery. The diagnosis of arterio-mesenteric occlusion of the duodenum (superior mesenteric artery syndrome) was confirmed. An operation (translocation of the duodenum) was performed. Over 7 months postoperatively she gained 10 kg and recovered to her premorbid body weight. Two years and 8 months after the operation she weighed 60kg (12.8% above ideal weight) and has been free of the symptoms of AN.

 In this case the authors speculate that rapid loss of weight resulting from AN caused chronic SMAS as a complication of AN when postprandial gastrointestinal symptoms became worse. Acute deterioration of SMAS occurred and acute gastric dilatation developed. Disappearance of AN symptoms after the surgical operation can be related to the fact that AN is often recovered after surgical procedures such as laparotomy, tonsilectomy and appendectomy SMAS needs to be considered in the diagnosis and treatment for AN in that : 1) acute SMAS is a severe complication of AN but its symptoms may be often misdiagnosed as psychogenic, 2) chronic SMAS resulting from emaciation in AN worsensgastrointestinal symptoms of AN itself, and 3) pure chronic SMAS may be misdiagnosed as AN because of the similarity of the symptoms.

Copyright © 1985, Igaku-Shoin Ltd. All rights reserved.


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