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What causes acute cholecystitis?
Last reviewed: 17.10.2021
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The leading role in the development of acute cholecystitis in children belongs to infection (E. Coli, Staphylococcus aureus, Streptococcus, Proteus, Enterococcus, typhoid bacillus). The pathogenetic role of enzymes and proenzymes of the pancreas, entering the bile ducts and the gallbladder and provoking acute fermentative cholecystitis, is investigated.
How does acute cholecystitis develop in children?
Infection can penetrate into the bile duct and gall bladder in various ways:
- ascending path - microorganisms enter the biliary tract from the duodenum through the outlet of the large duodenal papilla. The casting of duodenal contents is facilitated by the deficiency of the sphincter of Oddi with simultaneous intraduodenal hypertension;
- descending (hematogenous) pathway - the infection is entered in the biliary tract from any organ along a large range of blood circulation;
- The lymphogenous path is caused by the fact that the gallbladder and the bile ducts are connected by lymphatic vessels to other organs of the digestive tract. Intestinal bacilli, proteus, enterococci and other representatives of opportunistic microflora with nonspecific or inflammatory changes in the intestinal mucosa under conditions of increased permeability of the intestinal barrier are able to penetrate the biliary tract by lymphogenous and hematogenous pathways, as well as per continuitatem.
In the pathogenesis of acute inflammation and necrotic changes in the wall of the gallbladder, the importance of increasing intravesical pressure is attached. The causes of the disorder are diverse, but the main one is a violation of the outflow of bile from the gallbladder due to the hypertonicity of the sphincter of Oddi, spasm of the sphincter of the cystic duct (Lutkens), obstruction by lumps of mucus or microliths.
Of great importance in the launching of pathological processes is lysolecithin, convertible from lecithin bile phospholipase A, released when traumatizing the mucous membrane of the gallbladder.
In the pathogenesis of acute cholecystitis, a significant role is played by the increased synthesis of prostaglandins E and F la. Due to hypertension, the blood supply to the mucous membrane of the gallbladder decreases, which contributes to the disruption of the natural barrier for microorganisms. Infection, predominantly anaerobic (75%), increases inflammatory exudation in the lumen of the gallbladder, increasing intravesical pressure and aggravating the damage to the mucous membrane of the organ.