Endometriosis Pathologic Physiology

It is generally agreed that pelvic pain occurs premenstrually in endometriosis patients. Because of this, pain from endometriosis is thought to be due to stimulation from estrogen and progesterone during the menstrual cycle; the tissue of the implant is stimulated to grow in much the same way as is the endometrium. The implants enlarge and may undergo secretory change and bleeding; however, the fibrotic tissues surrounding the implants prevent the expansion and escape of hemorrhagic fluid that occurs in the uterus. With subsequent cycles, this process repeats itself. Pain is produced by pressure and inflammation within and around the lesion, by traction on adhesions associated with the lesions, by the number of implants and their proximity to nerves and other sensitive structures, and by the mass effect of large lesions. Although this sequence of events explains why premenstrual pelvic pain can occur in endometriosis, it is incomplete, because many patients with extensive endometriosis have no pain. It is a common observation that the occurrence and severity of pain from endometriosis bear little relationship to the amount and distribution of the disease. Severe pain in patients with endometriosis is associated with deeply infiltrating lesions, and it is thought that the degree of pain is perhaps determined by the depth of invasion.

Endometriosis