Pelvic adhesive disease is a pathological formation of fibrous connective tissue bands (adhesions, films) between the visceral peritoneum of the pelvic organs (uterus, tubes, ovaries, bladder, intestines) and the parietal peritoneum.
The process leads to the impairment of anatomical mobility of the organs and the distortion of their topography.
Adhesion formation is a universal protective response of the peritoneum to injury. In cases of inflammation (tuberculosis, chlamydia), ischemia, mechanical trauma (surgery), or endometriosis, mesothelial cells secrete an inflammatory exudate rich in fibrinogen. Under the action of thrombin, it is converted into fibrin, which “glues” surfaces together, localizing the focus of the lesion.
Normally, fibrin should be lysed by enzymes (plasminogen activators) within 3–5 days. If fibrinolysis is suppressed due to ischemia or infection, fibroblasts migrate into the fibrin matrix, synthesizing collagen, and new blood vessels grow (neoangiogenesis). A dense, vascularized scar is formed.
Adhesions cause mechanical occlusion (obstruction) and deformation of the fallopian tubes, impairing the capture of the oocyte by the fimbriae, which is the primary cause of tubo-peritoneal infertility. Rigid fixation of the organs limits their physiological displacement during the filling of the bladder or intestines, causing chronic pelvic pain and deep dyspareunia. In severe cases (“frozen pelvis” syndrome), strangulation bowel obstruction may occur.
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