CHRONIC PELVIC PAIN

Practice Committee, American Society for Reprodutive Medicine. Treatment of pelvic pain associated with edometriosis. Fertil Steril. 2006;86:S156–S160.

Varma R, Sinha D, Gupta JK. Non-contraceptive uses of levonorgestrel-releasing hormone system—a systematic enquiry and overview. Eur J Obstet Gynecol Reprod Biol. 2006;125:9–28.

Because endometriosis involves the ectopic presence of endometrium in the pelvis or beyond, medical and surgical treatments have traditionally targeted the implants. However, American Fertility Society staging of the disease, based on a fundamentally oncologic model (volume and distribution), is poorly predictive of the 2 major clinical morbidities of endometriosis: pain and infertility. Hence, the mechanisms of pain remain obscure.

Three aspects of endometriosis deserve comment here:

• Successful treatment with a gonadotropin-releasing hormone (GnRH) agonist does not necessarily mean endometriosis is present
  
• The levonorgestrel-releasing intrauterine system (LNG-IUS) eases pain, suggesting uterine involvement
  
• Surrounding organ systems appear to contribute to the disease.
  

Is a presumptive diagnosis accurate?

When treatment of pelvic pain with first-line agents such as NSAIDs or oral contraceptives fails, it is common practice to make a presumptive diagnosis of endometriosis and administer a GnRH agonist. If pain is relieved, it is assumed that endometriosis was the cause, but data do not support this conclusion. In the study most often cited in support of preemptive GnRH-agonist treatment without laparoscopic diagnosis,⁵ women with and without endometriosis experienced pain relief with equal frequency. The ASRM concluded in its recent guideline that relief of pelvic pain in response to a GnRH agonist does not make the diagnosis of endometriosis. This agent interrupts the hypothalamic–pituitary–ovarian axis, causing hypoestrogenism and amenorrhea, and may alter pain by

• reducing contractility of intestinal muscle
  
• eliminating the physiologic perimenstrual rise in pain sensitivity
  
• quieting uterine contractions.
  

Evidence suggests a uterine link

According to Varma and colleagues, the easing of endometriosis-related pain with the LNG-IUS suggests that the uterus itself—as opposed to the peritoneal implants—plays an important role. (Women with chronic pelvic pain, with or without endometriosis, have increased nerve-fiber density in the lower uterine segment.⁶) Therefore, the benefits of progestins may be at least partly attributable to their quieting effect on uterine contractility, in addition to their direct impact on endometriosis implants, and therapies thought to target implants may relieve pain in part through their impact on the uterus.

In a randomized trial, the LNG-IUS relieved endometriosis-related pain as effectively as depot leuprolide.⁷ Given that this device may remain in place for 5 years, it offers substantial benefit.

What interstitial cystitis may reveal about endometriosis

Clinical evidence suggests that endometriosis and disorders of surrounding visceral systems (eg, interstitial cystitis and irritable bowel syndrome) share some morbidities. Assuming these associations are validated by epidemiologic investigations, the common denominator may be vulnerability to inflammation (or a deficit in counterinflammatory systems), nonspecific stress responses to the primary illness, genetically determined deficits in neuromodulation of nociceptive signals reaching the spinal chord,⁴ and other mechanisms awaiting discovery.

How myofascial tissue contributes to pelvic pain

Tu FF, As-Sanie S, Steege JF. Prevalence of pelvic musculoskeletal disorders in a female chronic pelvic pain clinic. J Reprod Med. 2006;51:185–189.

More than 20 years ago, Lipscomb and colleagues⁸ identified pelvic floor dysfunction as an important component of pelvic pain in women, and Slocumb⁹ described abdominal wall trigger points as another. We continue to gain appreciation of myofascial contributions to pelvic pain, although systematic study is lacking.

Tu and colleagues retrospectively studied the records of 987 women who presented to a chronic pelvic pain clinic for evaluation. Single-digit, intravaginal palpation revealed tenderness in the levator ani and piriformis muscles in 22% and 14% of women, respectively. Tenderness at these sites was associated with a higher total number of pain sites, previous surgery for pelvic pain, higher scores on the Beck Depression Inventory and McGill Pain Inventory, and worsening pain with bowel movements.

Muscles that are tender to palpation may, on occasion, be the prime movers in a pain syndrome, but my experience suggests that muscle problems often develop secondary to some other condition. For example, a woman with endometriosis may, over time, develop pelvic floor dysfunction as an important part of her dyspareunia, as a reaction to the tenderness in the posterior cul-de-sac. In a similar manner, muscle dysfunction may follow in the wake of pelvic infection or uterine enlargement, or after gynecologic surgery.

Suboptimal response to generally effective treatments is a common clue to the presence of myofascial and other factors. In this circumstance, rather than escalating treatment (eg, by operating repeatedly to treat endometriosis), the gynecologist should broaden the clinical inquiry by palpating the pelvic muscle groups during physical examination.