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Authors

Michael D. Levin

Abstract

It is currently believed that the cause of superior mesenteric artery syndrome (SMAS) is compression of the duodenum in the angle between the aorta and superior mesenteric artery (SMA). It is recognized that a decrease in aortomesenteric angle (AMA) <25 and intervascular distance <8 mm, caused by fat loss, is characteristic of SMAS. Based on these statements, surgeons operate on patients with symptoms of dyspepsia only based on a reduction of AMA. This study is devoted to the analysis of the literature, including four own studies on this issue.


Results: Measurement of the length of the constriction in the third part of the duodenum on radiograms from available sources showed that its true length ranged from 2.5 to 4.2 (3.30 _ 0.15) cm and began a few centimetres cranial to the AMA. Therefore, it could not have been caused by compression in the AMA. In terms of length (3.20 _ 0.15 cm) and location, this constriction corresponded to Ochsner’s sphincter, which normally short-term contracts to prevent the penetration of an acid bolus into the jejunum. Conscientious studies have shown that AMA is proportional to BMI, i.e., a decrease in AMA is observed in all thin people. An analysis of 211 cases of SMAS made it possible to differentiate two types of diseases. In 101 patients, the disease occurred acutely 1–53 (8.2 _ 1.9) days after stressful situations, accompanied by a catabolic reaction and hypersecretion of hydrochloric acid. In 110 patients, SMAS developed 3

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