ABSTRACT
Pseudo-obstruction of the colon, characterized by colonic ileus with extreme dilatation of the right colon and cecum in the absence of mechanical obstruction, was first recognized as a clinical entity in 1948. The English surgeon Sir W. Heneage Ogilvie reported two such cases and proposed a pathophysiologic mechanism of the disorder. Previously, the medical literature had only made note of a similar functional occlusion of the small intestine, first described in 1896 as ‘‘spastic ileus’’ (1). In a paper entitled ‘‘Large-Intestine Colic Due to Sympathetic Deprivation,’’ Ogilvie described two patients with colicky abdominal pain, distention, and constipation who, despite normal barium enemas, had symptoms of colonic obstruction, which were so convincing that both were taken to surgery. In the operating room, both patients were found to have normal colons with malignant infiltration of the subdiaphragmatic sympathetic plexus. From this finding, he surmised that interruption of the sympathetic supply to the colon left parasympathetic innervation from sacral nerves unopposed (2). The term ‘‘intestinal pseudo-obstruction’’ was first used to describe this condition in 1958 (3). Current consensus is that colonic ileus caused by malignant infiltration of the celiac plexus as reported by Ogilvie, along with various syndromes described throughout the medical literature including ‘‘idiopathic large-bowel obstruction,’’ ‘‘false colonic obstruction,’’ ‘‘pseudo-obstruction of the colon,’’ ‘‘colonic ileus,’’ ‘‘idiopathic nontoxic megacolon,’’ and ‘‘nonobstructive colonic dilatation’’ are all examples of the broader disorder now referred to as ‘‘acute colonic pseudo-obstruction’’ (ACPO) (1,4-6).
