Ogilvie Syndrome - Pathophysiology

Pathophysiology

The exact mechanism behind the acute colonic pseudo-obstruction is not known. The probable explanation is imbalance in the regulation of colonic motor activity by the autonomic nervous system.

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 others.

Acute megacolon can also lead to ischemic necrosis in massively dilated intestinal segments. This is explained by Pascal's principle and Laplaces's law. Pascal's principle states that the pressure within a cylindrical structure is the same, regardless of whether the structure is dilated, and Laplace's law states that the wall tension of a cylinder is equal to the pressure within the cylinder multiplied by the radius. Therefore, a dilated intestinal segment has a greater wall tension than a nondilated segment; if the dilatation and tension are sufficiently great, blood flow may be obstructed and ischemia of the bowel will occur. Ogilivies syndrome may precipitate Volvulus.