During week 4 of foetal development, the embryonic gut, consisting of a straight endodermal tube, develops vascular pedicles to be divided into the foregut, midgut and hindgut based on the anatomical blood supply. The midgut is supplied by the superior mesenteric

artery (SMA) and by the fifth week of embryonic life, it begins Selleckchem Depsipeptide a process of rapid elongation and outgrows the capacity of the abdominal cavity. This leads to a temporary physiological herniation into the umbilical cord at about the sixth week of life with return to the abdominal cavity about 4 to 6 weeks later. During this period, the midgut Afatinib undergoes a 270 degree counterclockwise rotation around the SMA axis. This process leads to the formation of the duodenal C-loop, placing it behind the SMA in

a retroperitoneal position and emerging at the ligament of Treitz. The progressive reduction of the physiological midgut herniation commences at about week 10 of embryonic development. The duodeno-jejunal flexure (DJF) and jejunum to reduce first and lie to the left. The distal small bowel then follows and lies progressively to the right of the abdominal cavity. The descent of the caecum from its higher position in the right upper quadrant forms the latter part this website of this complex rotational development; it becomes positioned in the right lower abdomen. The ascending colon then assumes a retroperitoneal position, also on the right side. The base of the small bowel

mesentery subsequently fuses with the posterior peritoneum in a diagonal fashion, from the ligament of Treitz at the DJF to the caecum, completing the whole process at about the eleventh week of foetal development [1, 4–6]. The failure of the normal physiological rotation of the midgut leads to various degrees of anomaly including the entire small bowel remaining on the right side of the abdomen, the caecum, appendix and colon on the left and an absent ligament of Treitz. In addition, the small bowel mesentery may develop a narrow vertical attachment and the peritoneal fibrous bands fixing the duodenum and caecum to the abdominal wall may persist. These congenital bands extend from the right lateral abdominal wall, across the duodenum and attach to the undescended caecum and are known as Ladd’s bands [2, 4, 6, 7]. Ladd’s bands compress the duodenum and can potentially cause duodenal L-gulonolactone oxidase obstruction. The malrotation of the gut and abnormal location of the caecum produces a narrow superior mesenteric vascular pedicle, as opposed to the normally broadbased small bowel mesentery. This narrow SMA takeoff and lack of posterior peritoneal fusion predispose to subsequent midgut volvulus and obstruction with potential vascular catastrophe [7, 8]. Midgut malrotation in adults presents in numerous ways and the symptoms are non-specific. The clinical diagnosis in adolescents and adults is difficult because it is rarely considered on clinical grounds.