One of the unfortunate consequences of man's assumption of the erect posture is a sharp decrease in the angle formed between the aorta and the root of the mesentery, the latter containing the superior mesenteric artery. The third part of the duodenum crosses the aorta just beneath the origin of the superior mesenteric artery, thus tending to become wedged in this angle. This constitutes a precarious anatomical situation. Obstruction of the duodenum due to compression by the mesenteric root as a chronic intermittent condition is a well recognized syndrome (1–3). Similar compression of the duodenum as an acute transient phenomenon, secondary to local and more remote inflammation, appears either not to have been described or, in many cases, to have been erroneously attributed to duodenal atony. The selected cases to be reported here illustrate the varied clinical causes of duodenal compression, on the one hand, and the possibility of a unifying concept of mechanism, on the other. Appreciation of this concept makes the recognition of the phenomenon of considerable diagnostic value. This is especially to be stressed in relation to acute pancreatitis, which often presents an elusive clinical and radiological problem. In the investigation of obscure causes of any acute abdominal situation, a deliberate search for the phenomenon may be rewarding. Illustrative Case Reports Acute Pancreatitis Case I: A. B., 52-year-old male, was admitted in February 1960, eighteen hours after the onset of a constant aching epigastric pain. Similar less severe episodes had occurred five or six times yearly since 1958. In 1959 the upper gastrointestinal tract was radiologically normal. In 1949 cholecystectomy had been performed for cholecystitis. On this admission the low fever and epigastric tenderness, unaccompanied by guarding, slowly disappeared over the first four days. There was one episode of vomiting. The laboratory changes considered indicative of pancreatitis included: a serum amylase level of 853 Somogyi units on admission (normal 40–120) declining to 308 on the third day and 88 by the twelfth day; leucine-amino-peptidase elevation to 944 Klett units (normal below 200), dropping to 368 by the fifteenth day; a transient rise in serum bilirubin (3.5 mg. per cent); a drop in prothrombin to 45 per cent, considered responsible for occult blood in the stools, which disappeared by the eighth day; polymorphonuclear leukocytosis (91 per cent of 10,000 white blood cells, declining to 5,200 in ten days). The electrocardiogram was normal. Radiologically the stomach and duodenum had appeared normal fourteen months earlier. The plain abdominal films made on admission showed gastric and duodenal distention. Upper gastrointestinal examination on the following day (Fig. 1) revealed a sharp demarcation of the duodenal distention near the midline; it was not relieved by putting the patient into the knee-chest crouch position.