Pathophysiology of diverticulitis - Essay Example

The exact pathogenesis of diverticulitis is yet unknown (Hobson and Roberts, 2004). An insight into the structural changes in the diverticular disease has been found through studies on various postmortem and surgical specimens (Sheth et al, 2008). Initially, gastroenterologists proposed that a fecolith obstructing an abscessed diverticulum led to diverticulitis. However, in 1976, Sethbhakdi reported that studies on resected sigmoid diverticulitis specimens failed to support fecolith based pathogenesis theory.

Infact, according to the author, these studies found perforation of the fundus of the diverticulum associated with pericolic or peridiverticular inflammmation in the resected specimens (Sethbhakdi, 1976). Also, 30 percent of the specimens showed no features of inflammation, but showed thickening of the intestinal wall (Sethbhakdi, 1976). The thickened and contracted colon part is known as mychosis. Mychosis was initially thought to be due to muscular hypertrophy. But now, it is understood to be due to elastin deposition and shortening of the bowel.

Elastin deposition is thought to be due to increased uptake of a specific substance called proline from the Western diets (Sheth et al, 2008). . Smaller perforations get covered by the pericolic fat. However, larger perforations can lead to other complications like abscess formation, rupture of intestine, fistula formation and peritonitis (Crowe et al, 2011). Fistulas can occur with other adjacent organs or with skin. The most common fistulas in men are colorectal fistulas. Fistulas are uncommon in women (Crowe et al, 2011).

In population from the Western countries, the diverticula, especially in the colonic regions are "pseudo diverticula" because, the diverticula involve only the mucosal layer and submucosal layer and not the muscular and serosal layers (Sheth et al, 2008). There is whopping evidence that such pseudodiverticuli occur because of diets that are low in fibre. Among Asian population, the diverticuli are true diverticula (Sheth et al, 2008). They involve all the layers of the intestine and they are mainly seen in the proximal colonic region, unlike pseudo diverticuli which are seen in the distal colon, mainly the sigmoid colon (Sheth et al, 2008).

Decreased dietary fiber leads to low-volume stools which alter the motility of colon, causing increased luminal pressures. Such high pressures occur when the sigmoid colon undergoes a process called segmentation during smooth muscle contraction. Segmentation leads to distinct compartments of the sigmoid colon. When the stool volume is low, segmentation is exaggerated and the elevated intrasegmental pressures are transmitted across the colonic wall leading to the development of diverticula (Sheth et al, 2008).

Typically diverticuli occur at weak points in the intestinal wall like points where vasa recti penetrate the smooth muscle of the intestine (Sheth et al,