Introduction
Pain will bring a patient into the doctor’s office. One can even say that the mark of a physician is the ability to differentiate disease processes based upon their pain descriptors. Questions eliciting the quality, time course, location, and associated symptoms of pain complaints may narrow the diagnosis from a vast array of pathologic options. However, what happens when pain becomes only a vague indicator of pathology and not a defining characteristic? How does one treat pain that is no longer an acute presentation of active disease but rather a chronic presence?
By its broadest definition, chronic pelvic pain (CPP) is a noncyclic pain localized to the pelvis and abdomen lasting for greater than 6 months causing functional disability or leading to medical care. Within the US, the estimated prevalence of chronic pelvic pain in the primary care setting ranges from 16% to 39%. Even 10% of all gynecologic referrals are secondary to chronic pelvic pain [1]. Estimations in the UK place the prevalence of CPP equal to that of asthma, back pain, and migraines [2]. Despite the commonality of this disease, about 50% of all CPP have no diagnosed etiology, and 50% of all patients with CPP will remain dissatisfied with their treatment [2,3].
The anatomy of pain lies within the peripheral nerve, which contains four different neuron axons: A-β, A-δ, C-fiber, and sympathetic axons. Of these four, the A-δ and C-fiber axons fire with painful stimuli, and are labeled as primary afferent nociceptors (pain receptors). A-β fibers exist primarily in the skin and respond to light touch and movement, while sympathetic axons are silent nociceptors (i.e. in the presence of inflammatory mediators they may trigger a pain response). The signals sent by nociceptors reach the somatosensory cortex via the spinal nerves where the brain maps the location, intensity, and quality of pain.
Sensitization and convergence contribute to the primary physiologic cause of chronic pain. In the setting of chronic pain, sensitization of the primary afferent nociceptor pathway occurs with constant or prolonged stimulation of receptors in the presence of damaged or inflamed tissue. Because of the constant stimulation, the threshold of neuron activation decreases while the firing frequency of each neuron increases, thus allowing even innocuous stimuli to cause pain. Convergence contributes to the varied localization of chronic pelvic pain, otherwise known as referred pain. Since each peripheral axon contacts many spinal neurons and each spinal neuron receives input from several peripheral axons, localization of pain often relates to the area covered by a spinal neuron rather than the specific stimulate fiber or receptor.
In reviewing the innervation of the pelvis, the complexity of pelvic pain becomes more evident. Stimulation of the reproductive viscera travels through sympathetic nerves that run through the pelvic plexuses to the hypogastric nerves to end on spinal nerves T11 and T12. At the same time, T11 and T12 receive stimulation from the kidneys, ureters, bowel, and skin dermatomes. Pain fibers (a combination of somatic sensory and autonomic nerves) from the cervix and vagina synapse on spinal nerves S2–4. These same spinal nerves also receive information from the rectum and bladder [4]. Thus, the task at hand is to identify and target therapy at the etiology of the stimulation whether it lies in the reproductive, urinary, gastrointestinal or musculoskeletal organs.
Identifying those patients more prone to chronic pelvic pain has been a difficult task given the amorphous nature of pelvic pain. Latthe et al. attempt to list some predisposing factors, which include drug/alcohol abuse, miscarriage, heavy menstrual flow, pelvic inflammatory disease, previous cesarean section, pelvic pathology, abuse, and psychologic co-morbidities [6]. Depending upon the primary complaint, CPP is more often attributed to the urinary or gastrointestinal system, though, 20% of this population will receive a gynecologic diagnosis. Laparoscopic investigation into these 20% of CPP cases reveals that about 33% have endometriosis and 24% have adhesive pathology [2]. A different survey suggests that about 80% of the CPP patients referred to gynecologists may have interstitial cystitis, still most reviews believe inflammatory bowel disease to be a prominent etiologic factor [7]. Pelvic congestion has also been implicated as a cause of CPP. Box 57.1 lists the nongynecologic sources of pelvic pain while Box 57.2 lists common gynecologic etiologies. Here, we will review endometriosis, adhesive pathology, pelvic congestion, interstitial cystitis, and psychosomatic disorders.
Evaluation should begin with a thorough history and physical examination. The site, duration, pattern, quality, intensity, and association with bodily functions or activities add to the differentiation of diagnoses. Physical examination includes a thorough examination of the abdomen and pelvis. Pelvic exam should include inspection of the external genitalia, evaluation of vaginismus, assessment of cervical motion tenderness, notation of uterine mobility/contour/tenderness, enlargement of adnexa with respective tenderness, and finally rectal exam for nodularity/blood/hemorrhoids.
Laboratory testing helpful to the differentiation of possible pathologic processes includes urinalysis, complete blood count, and sedimentation rates. Stool guiaic tests may be helpful in uncovering possible gastrointestinal disorders such as Crohn’s disease or ulcerative colitis. Analysis for sexually transmitted infections with a wet mount and/or urinary chlamydia/gonorrhea tests may also delineate the cause of vague pelvic pain.
Box 57.1 Common causes of pelvic pain not directly associated with the reproductive tract
Appendicitis
Regional enteritis/diverticulitis
Inflammatory bowel disease/syndrome
Urinary tract infection
Renal and bladder calculi
Interstitial cystitis
Mesenteric vascular disease
Rectus hematoma
Aortic aneurysm
Herpes zoster
Porphyria
Sickle cell crisis
Box 57.2 Most common reproductive tract etiologies for pelvic pain
Episodic
Mittelschmerz
Dysmenorrhea
Endometriosis
Adneomyosis
Salpingitis
Ectopic pregnancy
Adnexal torsion
Pelvic venous congestion
Continuous
Adhesions
Pelvic relaxation
Anatomic distortions
(i.e. chronic tubo-ovarian abscess, leiomyomata)