Diverticulitis

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35 Diverticulitis

Pathophysiology

Diverticulosis

Diverticula are thought to arise from defects in the muscularis layer of the intestines (Fig. 35.1) and are related to abnormalities in muscle tone and increased intraluminal pressure; saclike protrusions eventually form at points of weakness. If stool is caught in these sacs, it becomes inspissated and hardened and causes abrasions of the mucosa that lead to inflammation, although the same end result can occur from pressure differentials alone without the presence of trapped fecal material.

Diverticula generally form at a site of focal weakness in the wall of the bowel, such as the location of blood vessel penetration (vasa recta). The mucosal and submucosal layers herniate through the muscular layer of the intestine, with only a covering of serosa remaining. This leads to an inherent weakness in the diverticular sac relative to the normal bowel. Only thinned layers of mucosa protect blood vessels, which are subject to stretching and thinning of their media, thereby predisposing to weakness and rupture of the vascular tissue.

The left side of the colon is the most common site for diverticulosis in patients with westernized diets and lifestyle. Right-sided diverticula occur more frequently in certain Asian populations. Right-sided diverticula have a higher rate of hemorrhage because of anatomic differences in their development.3 Small bowel diverticula occur most commonly in the duodenum, where they are predominantly asymptomatic. About 20% of small bowel diverticula occur in the jejunum or ileum; complications develop in these diverticula at rates three times greater than in duodenal diverticula.4

A low-fiber diet and constipation may contribute to the development of diverticular disease. High-fiber diets that prevent constipation clearly lead to fewer relapses of diverticulitis and less frequent complications. Lack of physical activity and advanced age are both believed to increase the incidence of the disease. Men and women are affected equally.

Diverticulitis

Diverticulitis arises from the initial microperforation of a diverticulum (Table 35.1).5 The process starts with blockage of the colonic opening of the diverticulum or by direct contact with food and fecal particles lodged in the affected portion of the bowel. Increased intraluminal or direct local pressure causes erosion of the diverticular wall, which leads to inflammatory changes, focal necrosis, and eventually perforation. The process is generally mild and limited by local pericolic fat and mesentery. Virtually all cases of diverticulitis involve perforation of the intestines, with the course of the resultant illness determined by the extent of this perforation. Complicated diverticulitis refers to regional spread of the inflammatory process by the formation of larger abscesses, a fistula with adjacent organs, or peritonitis (Fig. 35.2).1,5 Patients with purulent peritonitis have a mortality rate of 6%, which rises to 35% when fecal soilage of the peritoneal cavity occurs. Patients with diverticular disease occasionally have segmental colitis of the sigmoid colon, probably from fecal stasis or localized ischemia. The effects can be mild or may resemble those of inflammatory bowel disease.1

Table 35.1 Classification of the Severity of Colonic Diverticulitis

STAGE DEFINITION
1 Small, confined pericolic abscesses
2 Larger purulent collections
3 Generalized suppurative peritonitis
4 Fecal peritonitis

Adapted from Hinchey EG, Schaal PGH, Richards GK. Treatment of perforated diverticular disease of the colon. Adv Surg 1978;12:85-109.