Ogilvie syndrome is the acute dilatation of the colon in the absence of any mechanical obstruction in severely ill patients.

Acute colonic pseudo-obstruction is characterized by massive dilatation of the cecum (diameter > 10 cm) and right colon on abdominal X-ray.[2][3] It is a type of megacolon, sometimes referred to as "acute megacolon," to distinguish it from toxic megacolon.

The exact mechanism is not known. The probable explanation is imbalance in the regulation of colonic motor activity by the autonomic nervous system.[1] It has been postulated that reactivation of varicella zoster virus (which causes chickenpox and shingles) in the enteric ganglia may be a cause of Ogilvie syndrome.[10]

Acute megacolon develops because of abnormal intestinal motility. Normal colonic motility requires integration of myogenic, neural, and hormonal influences. The enteric nervous system is independent but is connected to the central nervous system by sympathetic and parasympathetic nerves. The targets of the enteric neurons are muscle cells, secretory cells, endocrine cells, microvasculature, and inflammatory cells. The neurons in the enteric plexuses are stimulated by a food bolus, which both distends the gut and stimulates the mucosal surface, leading to the release of factors that stimulate interneurons. The stimulated interneurons transmit excitatory signals proximally, which cause contraction and inhibitory signals distally, and these in turn cause relaxation. These signals are transmitted by the neurotransmitters acetylcholine and serotonin, among other