Colonic Diverticula - Causes of Development

Intestinal diverticula can be congenital and acquired. Congenital ones arise due to a local developmental defect. The causes and mechanism of development of acquired diverticula remain unclear. It is believed that 2 groups of factors are responsible for their occurrence: factors that increase intraintestinal pressure (constipation, flatulence, systematic use of laxatives, intestinal stenosis, etc.) and those that cause weakening of the intestinal wall (avitaminosis, dystrophy, inflammation, ischemia, congestion in the portal vein system, abdominal trauma, fatty degeneration of the intestinal muscle, congenital insufficiency of the intestinal wall).

The following data support the role of increased intraintestinal pressure in the development of pseudodiverticula.

In patients with diverticula in the sigmoid colon, the frequency and amplitude of pressure waves increases after eating, administration of proserin, morphine significantly more than in the control group, especially in areas with diverticula. In diverticulosis, hypertrophy of the intestinal muscle is often determined, which indicates increased motor activity of the intestine. The results of X-ray cinematographic research, combined with simultaneous determination of intraintestinal pressure, show that segmental contractions of the intestine lead to the formation of high-pressure zones and the appearance of diverticula that were not detected during the resting period.

The following facts indicate the importance of the relative weakness of the intestinal wall: more frequent occurrence of diverticula in the colon, where the longitudinal muscles do not form a continuous layer, but are grouped into 3 bands of the colon; occurrence of diverticula mainly in places where blood vessels pass, in areas of the intestine with insufficient resistance; more frequent diverticulosis in elderly and senile individuals; reports of colon diverticula in children and adolescents with Marfan syndrome, Ehlers-Danlos syndrome, when there is a collagen deficiency, with scleroderma, often accompanied by a violation of the structure of the intestinal wall; frequent combination of colon diverticulosis with other diseases caused by a decrease in tissue resistance (hernias, varicose veins of the legs, visceroptosis).

It is currently accepted that the pathogenetic significance is due to dietary features. Diverticular disease of the colon is more common in areas where refined foods are consumed than in regions where plant-based foods predominate, and is less common in vegetarians than in residents of the same country who eat normally.

There are various theories of the pathogenesis of acquired diverticula: the theory of congenital predisposition, vascular, mesenchymal, mechanical, or pulsion. The last one is the most widespread, according to which, with increased activity of the intestinal muscles, excessive and frequent segmentation of the intestine develops, which leads to the creation of high intraintestinal pressure in some areas of the intestine. Under its influence, prolapse of the mucous membrane through the intestinal wall occurs, most often through tunnels formed by blood vessels. Apparently, the mechanism of diverticula formation is complex, and the causes of the disease are represented by a combination of factors, and not the action of any one.

The magnitude of intraluminal pressure and the degree of resistance of the intestinal wall are independent factors. The different share 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 accepted that the leading factor in the development of diverticulitis is a disruption in the evacuation of contents from the diverticulum. Stasis of contents in the diverticulum, which contributes to damage to its mucous membrane, and the addition of infection from the intestinal contents cause inflammation. Of great importance is the state of the intestinal microflora, which, according to H. Haenal, is a potential danger. Bacteriological examination of feces in 80% of patients with uncomplicated diverticular disease and in all patients with chronic diverticulitis reveals profound qualitative changes in the microflora and quantitative shifts in the ratio of various groups of microorganisms. In diverticulitis, the changes are more pronounced.

Diverticulitis can also be caused by local circulatory disorders, chemical, toxic factors. Some believe that hematogenous, lymphogenous pathways of infection penetration into the diverticulum wall are possible. The inflammatory process from the intestinal wall can spread to the diverticulum. Having started in the diverticulum, the inflammation in turn can spread to the intestinal wall, mesentery, which is facilitated by the thin wall of the false diverticulum.

When inflammatory phenomena develop in the diverticulum, either an exudative (purulent) process often predominates, which can be reversible to some extent, or a fibroplastic process with a tendency to shrink. In both cases, partial or complete stenosis of the intestine can occur. In the first case, a more rapid course of the disease is observed, in the second, the possibility of reverse development is limited.

According to the nature of the course, acute and chronic diverticulitis are distinguished. Acute diverticulitis in the pathological anatomical sense is rare and mainly in true diverticula. The diagnosis of acute diverticulitis is often mistakenly made in chronic diverticulitis.

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

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