Expert Commentary

Chronic pelvic pain: 11 critical questions about causes and care

OBG Manag. 2009 August;21(8):27-40

References

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Not all viscera generate pain, possibly owing to a lack of sensory receptors or appropriate nociceptive stimulus
Visceral pain is not always linked to injury and, therefore, may be functional
Visceral pain frequently results in somatic referral of pain, possibly due to central convergence of visceral and somatic afferents
Visceral pain tends to be diffuse or poorly localized, probably because of the low concentration of nociceptive afferents within viscera (only 2% to 10% of total afferents to the spinal cord originate from visceral nociceptors).⁸

It is not clear whether there are visceral neurons dedicated solely to nociception; it appears that viscera utilize sympathetic and parasympathetic neurons as nociceptors. It also is important to note that the stimuli that activate somatic nociceptors—cutting, crushing, and burning, for example—do not generally cause visceral pain. Visceral nociceptive pain is generated in response to:

distention of a viscous or organ capsule
spasm of visceral muscular fibers
ischemia from vascular disturbances
hemorrhage
neoplasm
inflammation
traction on mesentery.

Another characteristic that distinguishes visceral from somatic nociception: Visceral nociception utilizes a dorsal midline pathway within the central nervous system, in addition to the lateral spinothalamic tract pathway utilized by somatic nociception.

Although this anatomic and mechanistic classification is clinically useful in the diagnostic evaluation of CPP, it is an oversimplification. Most patients—like Sara B., described in the opening case—have multiple anatomic and mechanistic causes of their pain.

7. What are the primary visceral causes of chronic pelvic pain?

A limited number of visceral and somatic diagnoses are backed by level-A evidence as having a causal relationship with CPP (TABLE 2). A few are discussed here.

TABLE 2

Disorders that may cause CPP or make it worse*

Reproductive tract Endometriosis Pelvic inflammatory disease Pelvic congestion syndrome Ovarian remnant syndrome Ovarian retention syndrome (residual ovary syndrome) Gynecologic malignancy (especially late-stage) Tuberculosis salpingitis
Urinary tract Interstitial cystitis Urethral syndrome Bladder malignancy Radiation cystitis
Gastrointestinal tract Irritable bowel syndrome Carcinoma of the colon Constipation Inflammatory bowel disease
Musculoskeletal system Abdominal wall myofascial pain (trigger points) Pelvic floor myalgia (levator ani or piriformis syndrome) Chronic coccygeal pain Faulty or poor posture Neuralgia of iliohypogastric, ilioinguinal, and/or genitofemoral nerves Peripartum pelvic pain syndrome Abdominal cutaneous nerve entrapment in surgical scar
Depression
Somatization disorder
* Disorders with Level-A evidence, i.e., good and consistent scientific evidence of a causal relationship to CPP

Disorders of the reproductive tract

Endometriosis is the most common gynecologic diagnosis in women who have CPP. There is significant epidemiologic evidence that endometriosis causes CPP. There is also strong evidence that endometriosis is a risk factor for CPP.

For example, human and animal experimental data suggest that women who have endometriosis have more episodes of urinary calculosis—and more severe pain—than women who do not have endometriosis.^9,10 They also are more likely to report vaginal pain than are women who do not have endometriosis, and that vaginal pain is more likely to be severe.

Such viscerovisceral interactions may play a significant role in CPP in women and may explain why some women who have a history of endometriosis have persistent pelvic pain after their endometriosis is gone, or even appear to develop other pain syndromes, such as interstitial cystitis.¹¹

Our introductory case illustrates these concepts. Sara B.’s history is classic for endometriosis-associated pelvic pain; that was her original diagnosis. Although her pelvic pain recurred and persisted, a repeat laparoscopy found no endometriosis—but it did reveal evidence of interstitial cystitis and painful bladder syndrome (IC/PBS). Could Sara’s current pain be neuropathic or inflammatory?

Treatment of IC/PBS targets neuropathic and inflammatory pain mechanisms, but this approach has not been fully explored for endometriosis. Might the visceral pain mechanisms be as important as the end-organ diagnoses? Clearly, this area merits further attention in gynecology.

Pelvic inflammatory disease (PID) often causes CPP. Approximately 18% to 35% of all women who have acute PID develop CPP.^12,13 The actual mechanisms by which CPP results from PID are not known, but it seems likely that both inflammatory and neuropathic mechanisms are important. Adhesive disease secondary to PID may also contribute to CPP by generating nociceptive pain. The route of treatment of PID—parenteral or oral antibiotics—does not appear to affect the odds of developing CPP.

Pelvic congestion syndrome is a controversial diagnosis that is uncommon in the United States. However, a well-designed study from Turkey suggests that about 40% of women who consult a gynecologist about CPP may have this syndrome.¹⁴ In Sara’s case, pelvic congestion syndrome was diagnosed after venous dilation and delayed emptying were confirmed by selective ovarian venography (transcervical venography is another option).¹⁵ This approach is recommended.

According to the data, the most effective treatment of pelvic congestion syndrome is a high-dose progestin or gonadotropin-releasing hormone (GnRH) agonist.^14,16 Only observational data back treatment with ovarian venous embolization, which was performed in Sara’s case.⁸