Prostaglandin E and F2α production from explants of petechial lesions present in mild, low-stage disease was found to be significantly greater than from the explants of powder-burn or black lesions, which are more common in patients with higher-stage endometriosis. Prostaglandin and cytokine production may account for severe pain in some patients with mild disease. More importantly, endometriotic implants acquire a vascular and nerve supply that may contribute to peripheral and central nervous system sensitization and persistence of pain even after surgical therapy (82–84).
Endometriosis-related pain syndrome is a new and evolving concept that is defined as pain that does not respond adequately to appropriate medical and surgical therapy, especially in the setting of minimal or mild disease. In this situation, neural plasticity results from central sensitization, hypothetically initiated by the peripheral inﬂammatory insult (83). The disease is no longer just the endometriosis, but is fostered by the alterations in the peripheral and CNS. Endometriosis-related pain syndrome is often co-existent or “co-morbid” with other chronic conditions such as bladder pain syndrome/interstitial cystitis (BPS/IC), irritable bowel syndrome (IBS), myofascial pain, fibromyalgia and vulvodynia, and anxiety disorders. These disorders need to be managed concurrently.
Adhesions Adhesions noted at the time of laparoscopy may be in the same general region of the abdomen as the source of the pelvic pain; however, neither the specific location (i.e., adnexa structures, parietal, visceral peritoneum, or bowel) nor density of the adhesions correlates consistently with the presence of pain symptoms (85,86). In one nonrandomized, noncontrolled study of adhesion lysis, a subgroup of women with anxiety, depression, multiple somatic symptoms, and social and occupational disruption responded poorly to adhesiolysis. The group without these characteristics had significant improvement in pain (87). Prospective randomized controlled trials do not support adhesiolysis for women with CPP. A randomized controlled trial of laparoscopic adhesiolysis showed an improvement in both the groups (i.e., laparoscopy with and laparoscopy without lysis of adhesions), suggesting a large placebo effect (88–90). One randomized controlled trial that did not consistently demonstrate a significant long-term reduction in pain did find some improvement if the adhesions were dense and involved the small bowel (91).
Most women with adhesions had a prior surgical procedure with possible injury to abdominal wall nerves, such as the iliohypogastric or ilioinguinal nerves, and those are more likely to be the cause of the pain. The abdominal wall must be carefully evaluated for myofascial or nerve injury, or entrapment, as the source of pain before assuming that adhesions contribute to the genesis of pain.
Diagnostic laparoscopy is recommended if GI, GU, and myofascial and neuropathic causes are ruled out or treated and the results of the psychological evaluation are negative. Minilaparoscopy using local anesthesia and conscious sedation is used to perform “conscious pain mapping,” whereby specific adhesions are tweaked and pelvic pain response is recorded (92). In an observational study of 50 women using local anesthesia, manipulation of appendiceal and pelvic adhesions contributed to pelvic pain. However, lysis of these adhesions did not improve outcomes over traditional laparoscopic therapy (2,11).