Colon diverticula: causes of development

Intestinal diverticula can be congenital and acquired. Congenital diseases arise from a local developmental defect. The causes and mechanism of development of acquired diverticula remain unexplained. It is believed that 2 groups of factors are responsible for their occurrence: factors that increase intestinal pressure (constipation, flatulence, the systematic use of laxatives, intestinal stenosis, etc.) and induce intestinal wall weakness (beriberi, degeneration, inflammation, ischemia, stasis in the portal system veins, abdominal trauma, fatty degeneration of the intestinal muscle, congenital insufficiency of the intestinal wall).

The following data testify to the role of increased intestinal pressure in the development of pseudodiverticules.

In patients with diverticula in the sigmoid colon, the frequency and amplitude of pressure waves increase after eating, the intake of proserine, morphine is significantly greater than in the control group, especially in areas with diverticula. With diverticulosis, hypertrophy of the intestinal muscle is often determined, which indicates an increased motor activity of the intestine. The results of the X-ray film examination combined with the simultaneous determination of intra-intestinal pressure show that segmental contractions of the gut lead to the formation of high-pressure zones and the appearance of diverticula that did not appear during the rest period.

The following facts speak of the significance of the relative weakness of the intestinal wall: the more frequent appearance of diverticula in the large intestine, where the longitudinal muscles form not a continuous layer but are grouped into 3 bands of the colon; the appearance of diverticula mainly in the areas of passage of blood vessels, areas of the bowel with insufficient resistance; more frequent lesion of diverticulosis in elderly and senile individuals; reports of diverticulum of the colon in children and boys with Marfan, Ehlers-Danlos syndromes when there is a deficiency of collagen, with scleroderma often accompanied by a violation of the intestinal wall structure; a frequent combination of diverticulosis of the large intestine with other diseases caused by a decrease in the resistance of tissues (hernia, varicose veins of the legs, visceroptosis).

At present, it is accepted that nutrition features are pathogenetic. There is a large prevalence of diverticular disease of the colon where refined food is used, in comparison with regions where vegetable products predominate, its frequency is lower in vegetarians compared to those who usually eat in the same country.

There are various theories of the pathogenesis of acquired diverticula: the theory of congenital predisposition, vascular, mesenchymal, mechanical, or pulsatile. The most widespread was the latter, according to which, with increased activity of the intestinal musculature, excessive and frequent segmentation of the intestine develops, which leads to the formation of high intestinal pressure in some parts of the intestine. Under its influence, mucosal prolapse arises through the intestinal wall, most often through tunnels formed by blood vessels. Apparently, the mechanism of formation of diverticula is complex, and the causes of the disease are represented by a combination of factors, rather than by the action of any one.

The magnitude of intraluminal pressure and the degree of resistance of the intestinal wall are independent factors. A different proportion of their participation in the development of diverticula determines the heterogeneity of the disease not only in relation to etiopathogenesis, but also in manifestations, in its course, in the choice of treatment.

It is generally believed that the leading factor in the occurrence of diverticulitis is a violation of the evacuation of the contents from the diverticulum. The stasis of the contents in the diverticulum, which contributes to damage to the mucous membrane, and the attachment of infection from the intestinal contents cause inflammation. Important is the state of the intestinal microflora, which, according to N. Haenal, is a potential hazard. At bacteriological study of feces in 80% of patients with uncomplicated diverticular disease and in all patients with chronic diverticulitis, profound qualitative changes in microflora and quantitative shifts in the ratio of different groups of microorganisms are determined. With diverticulitis changes are more pronounced.

The cause of diverticulitis can be local circulatory disorders, chemical, toxic factors. Some believe that a hematogenous, lymphogenous way of infection can enter the wall of the diverticulum. Inflammatory process from the intestinal wall can spread to the diverticulum. Beginning in the diverticulum, the inflammation in turn can go to the intestinal wall, the mesentery, which contributes to the thin wall of the false diverticulum.

With the development of inflammatory phenomena in the diverticulum, either exudative (purulent) process, which may be more or less reversible, or fibroplastic with a tendency to wrinkling, often prevails. In both cases, partial or complete intestinal stenosis may occur. In the first case, a more turbulent course of the disease is observed, in the second case, the possibility of reverse development is limited.

The nature of the flow distinguish between acute and chronic diverticulitis. Acute diverticulitis in the pathological and anatomical sense is rare and mainly in true diverticula. The diagnosis of acute diverticulitis is mistakenly placed more often with chronic diverticulitis.

In most cases, diverticulitis develops in patients with multiple diverticula. Most often it appears in the sigmoid and descending gut, in the places of favorite localization of diverticula.

[1], [2], [3], [4], [5], [6]