CHAPTER 11: Pelvic Pain

Pain in the lower abdomen and pelvis is a common complaint. But, pain is subjective and often ambiguous, and thus, difficult to diagnose and treat. To assist, clinicians ideally understand the mechanisms underlying human pain perception, which involves complex physical, biochemical, emotional, and social interactions. Providers are obligated to search for organic sources of pain, but equally important, avoid overtreatment of a condition that is minor or short lived.

Pain is a protective mechanism meant to warn of an immediate threat and to prompt withdrawal from noxious stimuli. Pain is usually followed by an emotional response and inevitable behavioral consequences. These are often as important as the pain itself. The mere threat of pain may elicit emotional responses even in the absence of actual injury.

When categorized, pain may be considered somatic or visceral depending on the type of afferent nerve fibers involved. Additionally, pain is described by the physiologic steps that produce it and can be defined as inflammatory or neuropathic (Kehlet, 2006). Both categorizations are helpful for diagnosis and treatment.

Somatic or Visceral Pain

Somatic pain stems from nerve afferents of the somatic nervous system, which innervates the parietal peritoneum, skin, muscles, and subcutaneous tissues. Somatic pain is typically sharp and localized. It is found on either the right or left within dermatomes that correspond to the innervation of involved tissues (Fig. 11-1).

In contrast, visceral pain stems from afferent fibers of the autonomic nervous system, which transmits information from the viscera and visceral peritoneum. Noxious stimuli typically include stretching, distention, ischemia, necrosis, or spasm of abdominal organs. The visceral afferent fibers that transfer these stimuli are sparse. Thus, the resulting diffuse sensory input leads to pain that is often described as a generalized, dull ache.

Visceral pain often localizes to the midline because visceral innervation of abdominal organs is usually bilateral (Flasar, 2006). As another attribute, visceral afferents follow a segmental distribution, and visceral pain is typically localized by the brain’s sensory cortex to an approximate spinal cord level that is determined by the embryologic origin of the involved organ. For example, pathology in midgut organs, such as the small bowel, appendix, and caecum, causes perceived periumbilical pain. In contrast, disease in hindgut organs, such as the colon and intraperitoneal portions of the genitourinary tract, causes midline pain in the suprapubic or hypogastric area (Gallagher, 2004).

Visceral afferent fibers are poorly myelinated, and action potentials can easily spread from them to adjacent somatic nerves. As a result, visceral pain may at times be referred to dermatomes that correspond to these adjacent somatic nerve fibers (Giamberardino, 2003). In addition, both peripheral somatic and visceral nerves often synapse in the spinal cord at the same dorsal horn neurons. These neurons, in turn, relay sensory information to the brain. The cortex recognizes the signal as coming from the same dermatome regardless of its visceral or somatic nerve origin. This phenomenon is termed viscerosomatic convergence and makes it difficult for a patient to distinguish internal organ pain from abdominal wall or pelvic floor pain (Fig. 11-2) (Perry, 2003).

Viscerosomatic convergence explains the dermatomal distribution of some visceral pain. In contrast, direct intraspinal neuronal reflexes permit transmission of visceral nociceptive input to other pelvic viscera (viscerovisceral reflex), to muscle (visceromuscular reflex), and to skin (viscerocutaneous reflex). These intraspinal reflexes may explain why patients with endometriosis or interstitial cystitis manifest other pain syndromes such as vestibulitis, pelvic floor myalgia, or irritable bowel syndrome (IBS). Thus, unless the underlying chronic visceral pain source is identified and properly treated, referred pain and secondary pain syndromes may not be successfully eliminated (Perry, 2000).

Inflammatory Pain

With acute pain, noxious stimuli such as a knife cut, burn, or crush injury activate sensory pain receptors, more formally termed nociceptors. Action potentials travel from the periphery to dorsal horn neurons in the spinal cord. Here, reflex arcs may lead to immediate muscle contraction, which removes and protects the body from harm. Additionally, within the spinal cord, sensory information is augmented or dampened and may then be transmitted to the brain. In the cortex, it is recognized as pain (Janicki, 2003). After an acute stimulus is eliminated, nociceptor activity quickly diminishes.

If tissues are injured, then inflammation usually follows. Body fluids, along with inflammatory proteins and cells, are called to the injury site to limit tissue damage. Because cells and most inflammatory proteins are too large to cross normal endothelium, vasodilation and increased capillary permeability are required features of this response. Chemical mediators of this process are prostaglandins, which are released from the damaged tissue, and cytokines, which are produced in white blood cells and endothelial cells. Cytokines include interleukins, tissue necrosis factors, and interferons. These sensitizing mediators are released into affected tissues and lower the conduction threshold of nociceptors. This is termed peripheral sensitization. Similarly, neurons within the spinal cord and/or brain display increased excitability, termed central sensitization. As a result, within inflamed tissues, the perception of pain is increased relative to the strength of the external stimulus (Kehlet, 2006). Normally, as inflammation decreases and healing ensues, the increased sensitivity to stimuli and thus the perception of pain subsides.

Neuropathic Pain

In some individuals, sustained noxious stimuli can lead to persistent central sensitization and to a permanent loss of neuronal inhibition. As a result, a decreased threshold to painful stimuli remains despite resolution of the inciting stimuli (Butrick, 2003). This persistence characterizes neuropathic pain, which is felt to underlie many chronic pain syndromes. During central sensitization, neurons within spinal cord levels above or below those initially affected may eventually become involved. This phenomenon results in chronic pain that may be referred across several spinal cord levels. In addition, some evidence suggests that chronic pain states are also associated with regional brain morphology changes in regions known to regulate pain. This has been described as maladaptive central nervous system (CNS) plasticity in response to prolonged nociceptive input (As-Sanie, 2012). The concept of neuropathic pain helps explain in part why many patients with chronic pain have discomfort disproportionately greater than the amount of coexistent disease found.

Thus, in assessing patients with chronic pain, a clinician may find an ongoing inflammatory condition. In these cases, inflammatory pain dominates, and treatment is directed at resolving the underlying inflammatory condition. However, for many patients, evaluation may reveal no or minimal current pathology. In these cases, pain is neuropathic, and treatment thus focuses on management of pain symptoms themselves.

The definition of acute lower abdominal pain and pelvic pain varies based on duration, but in general, discomfort is present less than 7 days. The sources of acute lower abdominal and pelvic pain are extensive, and a thorough history and physical examination can aid in narrowing the list (Table 11-1). With acute pain, a timely and accurate diagnosis is the goal and ensures the best medical outcome. Thus, although history and examination are described separately here, in clinical settings they often are performed almost simultaneously for optimal results.

History

In addition to a thorough medical and surgical history, a verbal description of the pain and its associated factors is essential. For example, duration can be informative, and pain with abrupt onset may be more often associated with organ torsion, rupture, or ischemia. The nature of pain may add value. Patients with acute pathology involving pelvic viscera may describe visceral pain that is midline, diffuse, dull, achy, or cramping. One example is the midline periumbilical pain of early appendicitis.

Patients may repeatedly shift or roll to one side to find a comfortable position.

The underlying pelvic pathology may extend from the viscera to inflame the adjacent parietal peritoneum. In these cases, sharp somatic pain is described, which is localized, often unilateral, and focused to a specific corresponding dermatome. Again using appendicitis as an example, the classic migration of pain to the site of peritoneal irritation in the right lower quadrant illustrates acute somatic pain. In other instances, sharp, localized pain may originate, not from the parietal peritoneum, but from pathology in specific muscles or in isolated areas of skin or subcutaneous tissues. In either instance, with somatic pain, patients classically rest motionless to avoid movement of the affected peritoneum, muscle, or skin.

Colicky pain may reflect bowel obstructed by adhesion, neoplasia, stool, or hernia. It can also stem from increased bowel peristalsis in those with irritable or inflammatory bowel disease or infectious gastroenteritis. Alternatively, colic may follow forceful uterine contractions with the passage of products of conception, pedunculated submucous leiomyomas, or endometrial polyps. Last, stones in the lower urinary tract may cause spasms of pain as they are passed.

Associated symptoms may also direct diagnosis. For example, absence of dysuria, hematuria, frequency, or urgency will exclude urinary pathology in most instances. Gynecologic causes are often associated with vaginal bleeding, vaginal discharge, dyspareunia, or amenorrhea. Alternatively, exclusion of diarrhea, constipation, or gastrointestinal bleeding lowers the probability of gastrointestinal (GI) disease.

Vomiting complaints, however, are less informative, although the temporal relationship of vomiting to the pain may be helpful. In the acute surgical abdomen, if vomiting occurs, it usually follows as a response to pain and results from vagal stimulation. This vomiting is typically severe and develops without nausea. For example, vomiting has been found in approximately 75 percent of adnexal torsion cases (Descargues, 2001; Huchon, 2010). Thus, the acute onset of unilateral pain that is severe and associated with a tender adnexal mass in a patient with vomiting alerts one to the increased probability of adnexal torsion. Conversely, if vomiting is noted prior to the onset of pain, a surgical abdomen is less likely (Miller, 2006).

In general, well-localized pain or tenderness, persisting for longer than 6 hours and unrelieved by analgesics, has an increased likelihood of acute peritoneal pathology.

Physical Examination

Examination begins with patient observation during initial questioning. Her general appearance, including facial expression, diaphoresis, pallor, and degree of agitation, often indicates the urgency of the clinical condition.

Elevated temperature, tachycardia, and hypotension will prompt an expedited evaluation, as the risk for intraabdominal pathology increases with their presence. Constant, low-grade fever is common in inflammatory conditions such as diverticulitis and appendicitis, and higher temperatures may be seen with pelvic inflammatory disease (PID), advanced peritonitis, or pyelonephritis.

Pulse and blood pressure evaluation ideally assess orthostatic changes if intravascular hypovolemia is suspected. A pulse increase of 30 beats per minute or a systolic blood pressure drop of 20 mm Hg or both, between lying and standing after 1 minute, is often reflective of hypovolemia. If noted, establishment of intravenous access and fluid resuscitation may be required prior to examination completion. Notably, certain neurologic disorders and medications, such as tricyclic antidepressants or antihypertensives, may also produce similar orthostatic blood pressure changes.

Abdominal examination is essential. Visual inspection of the abdomen focuses on prior surgical scars, which may increase the possibility of bowel obstruction from postoperative adhesions or incisional hernia. Additionally, abdominal distention may be seen with bowel obstruction, perforation, or ascites. After inspection, auscultation may identify hyperactive or high-pitched bowel sounds characteristic of bowel obstruction. Hypoactive sounds, however, are less informative.

Palpation of the abdomen systematically explores each abdominal quadrant and begins away from the area of indicated pain. Peritoneal irritation is suggested by rebound tenderness or by abdominal rigidity due to involuntary guarding or reflex spasm of the adjacent or involved abdominal muscles.

Pelvic examination in general is performed in reproductive-aged women, as gynecologic pathology and pregnancy complications are a common pain source in this age group. The decision to pursue this pelvic examination in geriatric and pediatric patients is based on clinical information.

Of findings, purulent vaginal discharge or cervicitis may reflect PID. Vaginal bleeding can stem from pregnancy complications, benign or malignant reproductive tract neoplasia, or acute vaginal trauma. Leiomyomas, pregnancy, and adenomyosis are common causes of uterine enlargement, and the latter two may also create uterine softening. Cervical motion tenderness reflects peritoneal irritation and can be seen with PID, appendicitis, diverticulitis, and intraabdominal bleeding. A tender adnexal mass may reflect ectopic pregnancy, tuboovarian abscess, or ovarian cyst with torsion, hemorrhage, or rupture. Alternatively, a tender mass may reflect an abscess of nongynecologic origin such as one involving the appendix or colon diverticulum.

Rectal examination can add information regarding the source and size of pelvic masses and the possibility of colorectal pathologies. Stool guaiac testing for occult blood, although less sensitive when not performed serially, is still warranted in many patients (Rockey, 2005). Those with complaints of rectal bleeding, painful defecation, or significant changes in bowel habits are examples.

In emergency departments, women with acute pain may experience waits between their initial assessment and subsequent testing. For these patients, literature supports early administration of analgesia. Fears that analgesia will mask patient symptoms and hinder accurate diagnosis have not been supported (McHale, 2001; Pace, 1996). Thus, barring significant hypotension or drug allergy, morphine sulfate may be administered judiciously in these situations.

Laboratory Testing

Despite benefits from a thorough history and physical examination, the sensitivity of these two in diagnosing abdominal pain is low (Gerhardt, 2005). Thus, laboratory and diagnostic testing are typically required. In women with acute abdominal pain, pregnancy complications are common. Thus, either urine or serum β-human chorionic gonadotropin (hCG) testing is recommended in those of reproductive age without prior hysterectomy. Complete blood count (CBC) can identify hemorrhage, both uterine and intraabdominal, and can assess the possibility of infection. Urinalysis can be used to evaluate possible urolithiasis or cystitis. In addition, microscopic evaluation and culture of vaginal discharge may add support to clinically suspected cases of PID.

Radiologic Imaging

Sonography

In women with acute pelvic pain, several imaging options are available. However, transvaginal and transabdominal pelvic sonography are preferred modalities if an obstetric or gynecologic cause is suspected (Andreotti, 2011). Sonography provides a high sensitivity for detection of structural pelvic pathology. It is widely available, can usually be obtained quickly, requires little patient preparation, is relatively noninvasive, and avoids ionizing radiation. Disadvantageously, examination quality is affected by the skill and experience of the sonographer.

In most cases, the transvaginal approach offers superior resolution of the reproductive organs. Transabdominal sonography may still be necessary if the uterus or adnexal structures are significantly large or if they lie beyond the transvaginal probe’s field of view. Color Doppler imaging during sonography permits evaluation of the vascular qualities of pelvic structures. In women with acute pain, the addition of Doppler studies is particularly useful if adnexal torsion or ectopic pregnancy is suspected (Twickler, 2010). Less common causes of acute pain amenable to sonographic diagnosis are perforation of the uterine wall by an intrauterine device (IUD) or hematometra caused by menstrual outflow obstruction from müllerian agenesis anomalies. For these, 3-dimensional (3-D) transvaginal sonography has become invaluable (Bermejo, 2010; Moschos, 2011).

Computed Tomography

Computed tomography (CT) and multidetector computed tomography (MDCT) are increasingly used to evaluate acute abdominal pain in adults. CT offers a global examination that can identify numerous abdominal and pelvic conditions, often with a high level of confidence (Hsu, 2005). Compared with other imaging tools, it has superior performance in identifying GI and urinary tract causes of acute pelvic and lower abdominal pain (Andreotti, 2011). For example, noncontrasted renal colic CT has largely replaced conventional intravenous pyelography to search for ureteral obstruction. For appendicitis, one study found that the false-positive diagnosis rate among adults decreased from 24 to 3 percent from 1996 to 2006. Investigators noted that this decrease correlated with the increased rate of CT use during the same interval (Raman, 2008). Appendiceal perforation also decreased from 18 to 5 percent. Considering that the false-positive diagnosis of appendicitis in women is as high as 42 percent, this certainly represents an improvement in clinical outcomes. For evaluation of GI abnormalities such as appendicitis, the combination of both oral and intravenous contrast is preferred.

In addition to its high sensitivity, CT has several advantages for most nongynecologic disorders. It is extremely fast; is not perturbed by gas, bone, or obesity; and is not operator dependent. Disadvantages include occasional unavailability, high cost, inability to use contrast media in patients who are allergic or have renal dysfunction, and exposure to low levels of ionizing radiation (Leschka, 2007).

The debate regarding CT safety and possible overuse is ongoing (Brenner, 2007). Of major concern is the potential increased cancer risk directly attributable to ionizing radiation, which is estimated to be even higher in younger patients and women (Einstein, 2007). Radiation doses from CT are generally considered to be 100 to 500 times those from conventional radiography (Smith-Bindman, 2010). Investigators in a large multicenter analysis found the median effective radiation dose from a multiphase abdomen and pelvic CT scan was 31 mSv, and this correlates with a lifetime attributable risk of four cancers per 1000 patients (Smith-Bindman, 2009). By way of comparison, health care workers are generally limited to 100 mSv over 5 years with a maximum of 50 mSv allowed in any given year (Fazel, 2009). But, in the acute clinical setting, CT imaging benefits frequently outweigh these risks.

Other Imaging

In some instances, plain film radiography is selected. Although its sensitivity is low for most gynecologic conditions, it still may be informative if bowel obstruction or perforation is suspected (Leschka, 2007). Dilated loops of small bowel, air-fluid levels, free air under the diaphragm, or the presence or absence of colonic gas are all significant findings when attempting to differentiate between a gynecologic and GI cause of acute pain.

Magnetic resonance (MR) imaging is becoming an important tool for women with acute pelvic pain if initial sonography is nondiagnostic. Common reasons for noninformative sonographic evaluations include patient obesity and pelvic anatomy distortion secondary to large leiomyomas, müllerian anomalies, or exophytic tumor growth. As a first-line tool, MR imaging is often selected for pregnant patients, for whom ionizing radiation exposure should be limited. However, for most acute disorders, it provides little advantage over 3-D sonography or CT (Bermejo, 2010; Brown, 2005). Lack of availability can be a disadvantage after hours, on weekends, or in smaller hospitals and emergency departments.

Laparoscopy

Operative laparoscopy is the primary treatment for suspected appendicitis, adnexal torsion, ectopic pregnancy, and ruptured ovarian cyst associated with ongoing symptomatic hemorrhage. Moreover, diagnostic laparoscopy may be useful if no pathology can be identified by conventional diagnostics. However, in stable patients with acute abdominal pain, noninvasive testing is typically exhausted before this approach is considered (Sauerland, 2006).

The decision to perform a surgical procedure for acute pelvic pain can be challenging. If the patient is clinically stable, the decision can be made in a timely manner, with appropriate evaluation and consultation completed preoperatively. In a less stable patient with signs of peritoneal irritation, possible hemoperitoneum, organ torsion, shock, and/or impending sepsis, the decision to operate is made decisively unless there are overwhelming clinical contraindications to immediate surgery.

Persistent pain may be visceral, somatic, or mixed in origin. As a result, it may take several forms in women that include chronic pelvic pain (CPP), dysmenorrhea, dyspareunia, dysuria, musculoskeletal pain, intestinal cramping, or vulvodynia. Each of these forms is described here except for vulvodynia, discussed in Chapter 4. The list of pathologies that may underlie these symptoms is extensive and includes both psychological and organic disorders (Table 11-2). Moreover, pathology in one organ can commonly lead to dysfunction in adjacent systems. As a result, a woman with chronic pain may have more than one cause of pain and overlapping symptoms. A comprehensive evaluation of multiple organ systems and psychologic state is essential for complete treatment.

This common gynecologic problem has an estimated prevalence of 15 percent in reproductive-aged women (Mathias, 1996). No definition is universally accepted. However, many investigators define chronic pelvic pain as: (1) noncyclic pain that persists for 6 or more months; (2) pain that localizes to the anatomic pelvis, to the anterior abdominal wall at or below the umbilicus, or to the lumbosacral back or buttocks; and (3) pain sufficiently severe to cause functional disability or lead to medical intervention (American College of Obstetricians and Gynecologists, 2010).

Causes of CPP fall within a broad spectrum, but endometriosis, symptomatic leiomyomas, and IBS are often diagnosed. Of these, endometriosis is a frequent cause, but it typically is also associated with cyclic symptoms. It is discussed fully in Chapter 10. Chronic pain secondary to leiomyomas is described in Chapter 9.

The pathophysiology of CPP is unclear in many patients, but evidence supports a significant association with neuropathic pain, described earlier. CPP shows increased association with IBS, interstitial cystitis, and vulvodynia, which are considered by many to be chronic visceral pain syndromes stemming from neuropathic pain (Janicki, 2003).

History

More than with many other gynecologic complaints, a detailed history and physical examination are integral to diagnosis. A pelvic pain questionnaire can be used initially to obtain information. One example is available from the International Pelvic Pain Society and may be accessed at: http://www.pelvicpain.org/docs/resources/forms/History-and-Physical-Form-English.aspx. Additionally, a body silhouette diagram can be provided to patients for them to mark specific sites of pain. The McGill Pain Questionnaire and Short Form combines a list of pain descriptors with a body map for patients to mark pain sites (Melzack, 1987). Pain scales can also quantify discomfort and include visual analogue scales (VAS) and verbal descriptor scales (VDS) (Fig. 11-3). At minimum, the series of questions found in Table 11-3 may provide valuable information. As noted, many of these questions focus on gynecologic, surgical, and psychologic risk factors.

First, of gynecologic factors, CPP is more common in women than men and is often worsened by stress and menstruation. Also, pregnancy and delivery can be traumatic to neuromuscular structures and have been linked with pelvic organ prolapse, pelvic floor muscle myofascial pain syndromes, and symphyseal or sacroiliac joint pain. In addition, injury to the ilioinguinal or iliohypogastric nerves during Pfannenstiel incision for cesarean delivery may lead to lower abdominal wall pain even years after the initial injury (Whiteside, 2003). Following delivery, recurrent, cyclic pain and swelling in the vicinity of a cesarean incision or within an episiotomy suggests endometriosis within the scar itself (Fig. 10-3). In contrast, in a nulliparous woman with infertility, pain may stem more often from endometriosis, pelvic adhesions, or PID.

Second, prior abdominal surgery increases a woman’s risk for pelvic adhesions, especially if infection, bleeding, or large areas of denuded peritoneal surfaces were involved. Adhesions were found in 40 percent of patients who underwent laparoscopy for chronic pelvic pain suspected to be of gynecologic origin (Sharma, 2011). The incidence of adhesions increases with the number of prior surgeries (Dubuisson, 2010). Last, certain disorders persist or commonly recur, and thus information regarding prior surgeries for endometriosis, adhesive disease, or malignancy are sought.

Of psychologic risk factors, CPP and sexual abuse are significantly associated (Jamieson, 1997; Lampe, 2000). A metaanalysis by Paras and associates (2009) demonstrated that sexual abuse is linked with an increased lifetime diagnosis rate of functional bowel disorders, fibromyalgia, psychogenic seizure disorder, and CPP. Additionally, for some women, chronic pain is an acceptable means to cope with social stresses. Thus, patients are questioned regarding domestic violence and satisfaction with family relationships. Furthermore, an inventory of depressive symptoms is essential, as depression may cause or result from CPP (Tables 13-3 and 13-4). Other conditions bearing similarities to CPP include fibromyalgia, chronic fatigue syndrome, temporomandibular disorder, and migraine. These are referred to as functional somatic syndromes, and CPP can be comorbid with each of these (Warren, 2011).

Physical Examination

In a woman with chronic pain, even routine examination may be extremely painful. In those with neuropathic pain, mere light touch may elicit discomfort. Therefore, examination proceeds slowly to allow relaxation between each step. Moreover, a patient is reassured that she may ask for the examination to be halted at any time. Terms used to describe examination findings include allodynia and hyperesthesia, among others. Allodynia is a painful response to a normally innocuous stimulus, such as a cotton swab. Hyperalgesia is an extreme response to a painful stimulus.

Stance and Gait

Women with intraperitoneal pathology may compensate with changes in posture. Such adjustments can create secondary musculoskeletal sources of pain. Alternatively, musculoskeletal structures may be the site of referred pain from these organs (Table 11-4). Thus, careful observation of a woman’s posture and gait is integral.

Initially, a woman is examined while standing. Posture is evaluated anteriorly, posteriorly, and laterally. Anteriorly, symmetry of the anterior superior iliac spines (ASISs), umbilicus, and weight bearing is evaluated. If one leg bears most of the weight, the nonbearing leg is often externally rotated and slightly flexed at the knee. Next, the anterior abdominal wall and inguinal areas are inspected for abdominal wall or femoral hernias, described on page 267. Inspection of the perineum and vulva with the patient standing may identify varicosities. These are often asymptomatic or may cause superficial discomfort. Such varicosities may coexist with internal pelvic varicosities, the underlying cause of pelvic congestion syndrome.

Posteriorly, inspection for scoliosis and of horizontal stability of the shoulders, gluteal folds, and knee creases is completed. Asymmetry may reflect musculoskeletal disorders.

Lateral visual examination searches for lordosis and concomitant kyphosis. This combination has been noted in some women with CPP and termed typical pelvic pain posture (TPPP) (Fig. 11-4) (Baker, 1993). Also, abnormal tilt of the pelvic bones can be assessed by simultaneously placing an open palm on each side between the posterior superior iliac spine (PSIS) and the ASIS. Normally, the ASIS lies one-quarter inch below the level of the PSIS, and greater distances may suggest abnormal tilt. Pelvic tilt may be associated with hip osteoarthritis and other orthopedic problems (Labelle, 2005; Yoshimoto, 2005).

Any observed mobility limitation can be informative. Thus, a patient is asked to bend forward at the waist. Limitation in forward flexion may reflect primary orthopedic disease or adaptive shortening of back extensor muscles. This shortening is seen frequently in women with chronic pain and TPPP. In such cases, patients are unable to bend over at the waist to create the normal convex curve.

Muscle weakness may also indicate orthopedic disease. A Trendelenburg test, in which a patient is asked to balance on one foot, can indicate dysfunction of hip abductor muscles or hip joint. With a positive test, when a woman elevates a leg by flexing the hip, the ipsilateral iliac crest droops.

Gait is evaluated by having the patient walk across the room. An antalgic gait, known as a limp, refers to a gait that minimizes weight bearing on a lower limb or joint and indicates a higher probability of musculoskeletal pain.

Sitting and Supine

A patient is next invited to sit on the examining table. Myofascial pain syndrome may involve pelvic floor muscles and often leads to a patient shifting weight to one buttock or sitting toward a chair’s front edge.

With the patient supine, the anterior abdominal wall is evaluated for abdominal scars. These may be sites of hernia or nerve entrapment or may indicate a risk for intraabdominal adhesive disease. Auscultation for bowel sounds and bruits follows. Increased bowel activity may reflect irritable or inflammatory bowel diseases. Bruits prompt investigation for vascular pathology.

While supine, a woman is asked to demonstrate with one finger the point of maximal pain and then encircle the total surrounding area of involvement. Superficial palpation of the anterior abdominal wall by a clinician may reveal sites of tenderness or knotted muscle that may reflect nerve entrapment or myofascial pain syndrome. Moreover, pain with elevation of the head and shoulders while tensing the abdominal wall muscles, Carnett sign, is typical of anterior abdominal wall pathology. Conversely, if the source of pain originates from inside the abdominal cavity, discomfort usually decreases with such elevation (Thomson, 1991). Moreover, Valsalva maneuver during head and shoulder elevation may display diastasis of the rectus abdominis muscle or hernias. Diastasis recti can be differentiated in most cases from a ventral hernia. Specifically, with diastasis, the borders of the rectus abdominis muscle can be palpated bilaterally along the entire length of the protrusion. Last, deep palpation of the lower abdomen may identify pathology originating from pelvic viscera. Dullness to percussion or a shifting fluid wave may indicate ascites.

Mobility is also evaluated. In most cases, a woman can elevate her leg 80 degrees from the horizontal toward her head, termed a straight leg test. Pain with leg elevation may be seen with lumbar disc, hip joint, or myofascial pain syndromes. Additionally, symphyseal pain with this test may indicate laxity in the symphysis pubis or pelvic girdle. Both the obturator and iliopsoas tests may indicate myofascial pain syndromes involving these muscles or disorders of the hip joint. With the obturator test, a supine patient brings one knee into 90 degrees of flexion while the same foot remains planted. The ankle is held stationary, but the knee is gently pulled laterally and then medially to assess for tenderness. With the iliopsoas test, a supine woman with legs extended attempts to flex each hip separately against downward resistance from the examiner’s hand placed on the ipsilateral anterior thigh. If pain is described with hip flexion, the test result is positive.

Lithotomy

Pelvic examination begins with inspection of the vulva for generalized changes and localized lesions. Vulvar erythema often reflects infectious vulvitis, described in Chapter 3, or vulvitis stemming from dermatoses (Chap. 4). Vulvar skin thinning may reflect lichen sclerosus or atrophic changes. The vestibular area is also examined. Erythema of the vestibule, with or without punctate lesions, may indicate vestibulitis. Following this inspection, systematic pressure point palpation of the vestibule, as shown in Figure 4-1, is completed using a small cotton swab to assess for pain (allodynia). Last, the anocutaneous reflex, as described in Chapter 24, may also be performed to assess pudendal nerve integrity.

Prior to speculum examination, a single digit systematically evaluates the vagina. Pain elicited from pressure beneath the urethra may indicate urethral diverticulum. Pain with anterior vagina palpation under the trigone can reflect interstitial cystitis. Systematic sweeping pressure against the pelvic floor muscles along their length may identify isolated taut muscle knots from pelvic floor myofascial syndrome. Of these muscles, the pubococcygeus, iliococcygeus, and obturator internus muscles can usually be reached with a vaginal finger (Fig. 11-5). Next, insertion points of the uterosacral ligaments are palpated. Nodularity is highly suggestive of endometriosis, and palpation may reproduce dyspareunia symptoms. Cervical motion tenderness may be noted with acute and chronic PID. If pain follows gentle movement of the coccyx, then articular disease of the coccyx, termed coccydynia, is suspected. The importance of pelvic examination sequence cannot be overstated, as information from single-digit examination may be lost if preceded by bimanual examination.

Bimanual assessment of the uterus may reveal a large uterus, often with an irregular contour, due to leiomyomas. Globular enlargement with softening is more typical of adenomyosis. Immobility of the uterus may follow scarring from endometriosis, PID, malignancy, or adhesive disease from prior surgeries. Adnexal palpation may reveal tenderness or mass. Tenderness alone may reflect endometriosis, diverticular disease, or pelvic congestion syndrome. Adnexal mass evaluation is outlined in Chapter 9.

Rectal examination and rectovaginal palpation of the rectovaginal septum is included. Palpation of hard stool or hemorrhoids may indicate GI disorders, whereas nodularity of the rectovaginal septum may be found with endometriosis or neoplasia. Myofascial tenderness involving the puborectalis and coccygeus muscles can be noted by sweeping the index finger with pressure across these muscles. Last, stool testing for occult blood may be performed during digital rectal examination at the initial visit. Alternatively, home test kits for occult blood are available and discussed in Chapter 1.

Testing

For women with CPP, diagnostic testing may add valuable information. Results from urinalysis and urine culture can indicate stones, malignancy, or recurrent infection of the urinary tract as pain sources. Thyroid disease can affect physiologic functioning and may be found in those with bowel or bladder symptoms. Thus, serum thyroid-stimulating hormone (TSH) levels are commonly assayed. Diabetes can lead to neuropathy, and glucose levels can be assessed with urinalysis or serum testing.

Radiologic imaging and endoscopy may be informative, and of these, transvaginal sonography is widely used by gynecologists to evaluate CPP. Sonography of the pelvic organs may reveal endometriomas, leiomyomas, ovarian cysts, dilated pelvic veins, and other structural lesions. In those with suspected pelvic congestion syndrome, transvaginal color Doppler ultrasound is often a primary diagnostic tool (Phillips, 2014). With sonography, patients can be imaged standing, if necessary, and while performing a Valsalva maneuver to accentuate vasculature distention. However, despite its applicability for many gynecologic disorders, sonography has poor sensitivity in identifying endometriotic implants or most adhesions. Of other modalities, CT or MR imaging often adds little additional information to that obtained with sonography. These may be selected if sonography is uninformative or if anatomy is greatly distorted.

In those with bowel symptoms, barium enema may indicate intraluminal or external obstructive lesions, malignancy, and diverticular or inflammatory bowel disease. However, flexible sigmoidoscopy and colonoscopy may offer more information because colonic mucosa can be directly inspected and biopsied if necessary.

Cystoscopy, laparoscopy, flexible sigmoidoscopy, and colonoscopy may each be employed, and patient symptoms will dictate their use. In those with symptoms of chronic pain and urinary symptoms, cystoscopy is often advised. If GI complaints predominate, then flexible sigmoidoscopy or colonoscopy may be warranted. For many women with no obvious cause of their CPP, laparoscopy is performed. Importantly, intraoperative explanations for CPP are common despite normal preoperative examinations (Cunanan, 1983; Kang, 2007). Laparoscopy allows direct identification and, in many cases, treatment of intra­abdominal pathology. Therefore, laparoscopy is considered by many to be a “gold standard” for CPP evaluation (Sharma, 2011).

One laparoscopic approach to CPP is performed under local anesthesia with the patient conscious and available for questioning regarding sites of pain (Howard, 2000; Swanton, 2006). Termed conscious pain mapping, this technique has resulted in more targeted treatment and improved postoperative pain scores. However, its clinical use to date has been limited.

Treatment

Medical Options

In many women with CPP, an identifying source is found and treatment is dictated by the diagnosis. However, in other cases, pathology may not be identified, and treatment is directed toward dominant symptoms.

Treatment of pain typically begins with oral analgesics such as acetaminophen or nonsteroidal antiinflammatory drugs (NSAIDs) listed in Table 10-1. NSAIDs are particularly helpful if inflammatory states underlie the pain. Acetaminophen is a widely used and effective analgesic despite having no significant antiinflammatory properties. Of note, dosing recommendations from the Food and Drug Administration (2011) limit the maximum total daily dose of acetaminophen to 4 g.

If satisfactory relief is not achieved, then opioid analgesics such as codeine or hydrocodone may be added (Table 42-2). Importantly, opioid maintenance therapy for CPP is considered only if all other reasonable pain control attempts have failed and if benefits outweigh harms (Chou, 2009; Howard, 2003). Opioids are most effective and least addictive if given on a scheduled basis and at doses that adequately relieve pain. If pain persists, stronger opioids such as morphine, methadone, fentanyl, oxycodone, and hydromorphone can replace milder ones. However, this is balanced against side effects. Close and regular surveillance is essential, and consultation with pain management experts may be beneficial (Baranowski, 2014; Chou, 2009). Unlike classic opioids, tramadol hydrochloride has a mild central opioid effect but also inhibits serotonin and norepinephrine reuptake.

Estrogen support is integral to endometriosis. Thus, an empiric trial of sex-steroid hormone suppression may be considered, especially in those with coexistent dysmenorrhea or dyspareunia and who lack dominant bladder or bowel symptoms. As discussed in Chapter 10, combination oral contraceptives, progestins, gonadotropin-releasing hormone (GnRH) agonists, and certain androgens are effective options.

For many, CPP represents neuropathic pain, and therapy with antidepressants or anticonvulsants has been extrapolated from treatment of such pain in other disorders. Tricyclic antidepressants reduce neuropathic pain independent of their antidepressant effects (Saarto, 2010). Moreover, antidepressants are a logical choice, as clinically significant depression is commonly comorbid with pain. Amitriptyline (Elavil) and its metabolite nortriptyline (Pamelor) have the best documented efficacy for neuropathic and nonneuropathic pain syndromes (Table 11-5) (Bryson, 1996). Selective serotonin-reuptake inhibitors do not have strong evidence to support their efficacy for CPP (Lunn, 2014). Of anticonvulsants, gabapentin and carbamazepine are most commonly used to reduce neuropathic pain (Moore, 2014; Wiffen, 2014).

Combining drugs with different sites or mechanisms of action may often improve pain. For example, an NSAID and an opioid may be partnered, especially in conditions in which inflammation is dominant. If muscle spasm underlies pain, then pairing a tranquilizer or a muscle relaxant with an opioid or with an NSAID may improve results (Howard, 2003).

Surgery

Nerve destruction, termed neurolysis, involves nerve transection or injection of a neurotoxic chemical. Nerve transection cuts a specific peripheral nerve or may be performed on an entire nerve plexus.

Presacral neurectomy (PSN) describes interruption of somatic pain fibers from the uterus that course within the superior hypogastric plexus (Fig. 38-13). This procedure is performed by incising the pelvic peritoneum over the sacrum and then identifying and transecting the sacral nerve plexus. In women so treated, approximately 75 percent note a greater than 50 percent decline in pain (American College of Obstetricians and Gynecologists, 2010).

However, PSN is technically challenging and requires familiarity with operating in the presacral space. Surgery has been associated with long-term constipation and urinary retention postoperatively. Infrequently, life-threatening hemorrhage may be encountered from the middle sacral vessels, which run in the presacral space.

Alternatively, laparoscopic uterosacral nerve ablation (LUNA) involves the destruction of nerve fibers that pass to the uterus through the uterosacral ligament. During LUNA, approximately 2 cm of uterosacral ligament near its attachment to the uterus is excised or obliterated using electrosurgery or carbon dioxide (CO₂) laser (Lifford, 2002). Based on pelvic innervation, PSN or LUNA is indicated only for treatment of centrally located pelvic pain, and both have been performed to treat refractory endometriosis-related CPP and dysmenorrhea.

Regarding efficacy, in one randomized trial, investigators performed laparoscopy with and without LUNA for 487 patients with CPP but found no difference in pain, dysmenorrhea, dyspareunia, or quality-of-life measures (Daniels, 2009). Similarly, a metaanalysis found no pain improvement difference between those who did and those who did not undergo LUNA (Daniels, 2010). Moreover, comparisons of LUNA and PSN show significantly greater long-term pain relief with PSN (Proctor, 2005). In sum, available evidence does not support frequent use of LUNA.

Hysterectomy and bilateral salpingo-oophorectomy (BSO) at times may serve as definitive management if thorough evaluation is complete and conservative therapies have failed. For many women with CPP, hysterectomy is effective in resolving pain and improving quality of life (Hartmann, 2004; Stovall, 1990). However, pain may not be resolved in a significant number of women. For example, authors of one prospective study monitored 308 women for 1 year after hysterectomy for CPP and found that 75 percent had complete discomfort resolution, 21 percent had persistent but improved pain, and 5 had unchanged or worsening pain. Pain may persist despite hysterectomy more commonly in those who are younger than 30 years, those who have mental illness, or those with no identifiable pelvic pathology (Gunter, 2003). Almost 40 percent of women with no identified pelvic pathology will have persistent pain after hysterectomy (Hillis, 1995).

Failure of hysterectomy to relieve pain may be multifactorial. First, visceral reflexes may produce multiple pain syndromes within the same patient. Second, hysterectomy does not address nongynecologic etiologies for pelvic pain. Last, pain from interstitial cystitis, pelvic floor myofascial syndrome, or musculoskeletal disorders may worsen following surgery due to its potentially negative effects on innervation, musculature, or vasculature.

Accordingly, before hysterectomy is considered, efforts to accurately diagnose CPP causes and to conservatively manage the pain are first exhausted. Women are given reasonable expectations for symptom relief from hysterectomy and informed of the potential for persistent or worsening pain. As with any operation, the anticipated benefits should outweigh potential risks.

If hysterectomy is planned for endometriosis, concurrent BSO is reasonable. This is more fully discussed in Chapter 10). In one analysis of 138 women monitored for 58 months after hysterectomy with ovarian conservation for endometriosis, the relative risk for pain recurrence was 6 and relative risk for reoperation approximated 8 (Namnoum, 1995). In contrast, data regarding bilateral oophorectomy efficacy at time of hysterectomy for idiopathic CPP are lacking and are individualized.

Specific Causes of Chronic Pelvic Pain

Pelvic Adhesions

Adhesions are fibrous connections between opposing organ surfaces or between an organ and abdominal wall, at sites where there should be no connection. They vary in vascularity and thickness. These fibrous connections are common, and in laparoscopies performed for CPP, adhesions are found in approximately one quarter of cases (Howard, 1993). However, not all adhesive disease creates pain. For example, Thornton and associates (1997) found no relationship between pelvic pain and intraabdominal adhesions.

In those with pain, adhesions are believed to stretch the peritoneum or organ serosa as it moves. This theory is supported by studies using conscious pain mapping, in which filmy adhesions that allowed significant movement between two structures had the highest association with pain, whereas adhesions that prohibited movement had the lowest pain scores. Moreover, adhesions that had a relationship to the peritoneum had a high association with pain (Demco, 2004). Sensory nerve fibers have been identified histologically, ultrastructurally, and immunohistochemically in human peritoneal adhesions obtained at laparotomy, lending additional support to the above theories (Suleiman, 2001).

Risks for adhesions include prior surgery, prior intraabdominal infection, and endometriosis. Less commonly, inflammation from radiation, chemical irritation, or foreign-body reaction may be causes. Pain is typically aggravated by sudden movement, intercourse, or other specific activities.

Laparoscopy is the primary tool used to diagnose adhesions. In general, sonography lacks sensitivity. However, Guerriero and coworkers (1997) noted a positive correlation with ovarian adhesions if the ovarian surface borders appeared blurred or if the ovary appeared immediately adjacent to the uterus and this intimate position persisted despite transducer manipulation of both.

Surgical lysis is often used to treat pain symptoms, and several observational studies have shown pain improvement (Fayez, 1994; Steege, 1991; Sutton, 1990). However, two randomized studies comparing adhesion lysis with expectant management found no difference in pain scores after 1 year (Peters, 1992; Swank, 2003). Others who support the continued judicious use of adhesiolysis in the treatment of pelvic pain question the statistical methods used in these studies (Roman, 2009). When performed, adhesiolysis is associated with a significant risk of adhesiogenesis, especially in cases involving endometriosis (Parker, 2005). Thus, the decision to lyse adhesions is individualized.

If adhesiolysis is performed, steps are taken to minimize reformation (Hammoud, 2004). Gentle tissue handling, adequate hemostasis, and minimally invasive techniques are essential. Many studies have evaluated the efficacy of various instillates and barriers placed over organs following surgery to minimize adhesion formation. Bioresorbable sheets that are Food and Drug Administration (FDA)-approved and often used in gynecology include brands Seprafilm and Interceed. One peritoneal instillate is icodextrin solution (Adept Adhesion Reduction Solution). Of these options, the American Society for Reproductive Medicine (2013) notes that barrier sheets reduce postoperative adhesions but also state that no substantial evidence shows their use decreases pain. They also report “insufficient evidence to recommend peritoneal instillates.” Similarly, two Cochrane reviews reported insufficient evidence regarding the efficacy of any of these agents (Ahmad, 2014; Hindocha, 2015).

Ovarian Remnant Syndrome and Ovarian Retention Syndrome

After oophorectomy, remnants of an excised ovary may create symptoms that are termed ovarian remnant syndrome. Distinction is made between this syndrome and ovarian retention syndrome, also known as residual ovary syndrome. Ovarian retention syndrome involves symptoms stemming from an ovary intentionally left at the time of previous gynecologic surgery (El Minawi, 1999). Although differentiated by the amount of ovarian tissue involved, both syndromes have nearly identical symptoms and are diagnosed and treated similarly.

Although an uncommon cause of CPP, women with symptomatic ovarian remnants most typically complain of chronic or cyclic pain or dyspareunia. Those with BSO performed for endometriosis may be at particular risk (Kho, 2012). The onset of symptoms is variable and may begin years following surgery (Nezhat, 2005). Women with these syndromes may have a pelvic mass palpable on bimanual examination. Sonography is often informative. In those with ovarian remnants, ovaries may be identified in some cases by a thin rim of ovarian cortex surrounding a coexistent ovarian cyst (Fleischer, 1998). Indeterminate cases may require CT or MR imaging. In cases where ureteral compression is suspected, radiographic or CT pyelography or MR imaging may be warranted. Laboratory testing, specifically follicle-stimulating hormone (FSH) levels, can aid diagnosis in reproductive-aged women with prior BSO. If these levels lie in the premenopausal range, then retained ovarian tissue is likely (Magtibay, 2005).

Although medical treatment has included hormonal manipulation to suppress functioning tissue, surgical excision is required in most symptomatic cases (Lafferty, 1996). Because the ureter is commonly intimately involved with adhesions encasing a remnant, laparotomy is prudent in some cases. However, surgeons with advanced skills in minimally invasive surgery can achieve successful outcomes (Nezhat, 2005; Zapardiel, 2012).

Pelvic Congestion Syndrome

Retrograde blood flow through incompetent valves can often create tortuous, congested ovarian or pelvic veins. Chronic pelvic ache, pressure, and heaviness may result and is termed pelvic congestion syndrome (Beard, 1988). Currently, it is not clear whether congestion results from mechanical dilatation, ovarian hormonal dysfunction, or both. Higher rates of ovarian varicosities and pelvic congestion syndrome are noted in parous women. A mechanical theory describes a dramatic increase in pelvic vein diameter during late pregnancy that leads to ovarian vein valve incompetence and pelvic varicosities. Estrogen is implicated in pelvic congestion syndrome in that it acts as a venous dilator. Moreover, pelvic congestion syndrome resolves following menopause, and antiestrogenic medical therapy has been shown to be effective (Farquhar, 1989; Gangar, 1993). Most likely, both factors play roles. The cause of pain with pelvic congestion remains unclear, but increased dilatation, concomitant stasis, and release of local nociceptive mediators have been suggested.

Affected women may describe pelvic ache or heaviness that may worsen premenstrually, after prolonged sitting or standing, or following intercourse. On physical examination, tenderness at the junction of the middle and lateral thirds of a line drawn between the symphysis and anterior superior iliac spine or direct ovarian tenderness may be found. In addition, varicosities in the thigh, buttocks, perineum, or vagina may be associated (Venbrux, 1999).

The left ovarian venous plexus drains into the left ovarian vein, which empties into the left renal vein. The right ovarian vein generally drains directly into the inferior vena cava. Both ovarian veins have numerous trunks, any of which may be involved. Clinical practice guidelines recommend noninvasive sonography or CT or MR venography for suspected cases. Sonographic findings with applied Doppler include a dilated tortuous ovarian vein with a diameter ≥6 mm, slow blood flow ≤3 cm/sec, and a dilated arcuate vein in the myometrium that communicates to the pelvic varicosities (Fig. 11-6) (Park, 2004). With positive findings, then retrograde ovarian and internal iliac venography is preferred if intervention is planned (Gloviczki, 2011). Diagnostic laparoscopy can also identify varicosities. However, because all these modalities are performed while a woman is supine or in Trendelenburg position, varicosities often decompress and may be missed. CO₂ insufflation pressure also contributes to the high false-negative rate of laparoscopy to diagnose pelvic varicosities.

Common treatments for pelvic congestion syndrome are hormonal suppression, ovarian vein embolization, or hysterectomy with BSO. First, medical treatment with medroxyprogesterone acetate, 30 mg orally daily, or with a GnRH agonist is effective for some women with pelvic congestion syndrome, although symptoms typically recur after medication is discontinued (Reginald, 1989; Soysal, 2001). Second, embolization appears to afford effective treatment, and pain improves in 70 to 80 percent of women (Hansrani, 2015). Third, Beard and coworkers (1991) studied 36 patients who underwent hysterectomy and BSO for pelvic congestion syndrome and intractable pelvic pain. Although 12 of 36 had residual pain at 1 year, only one patient had pain affecting daily life. They concluded that pain and quality-of-life scores were improved. Importantly, none of these options are definitive, and evidence-based studies supporting their efficacy are limited.

Cyclic pain with menstruation is common and accompanies most menses (Weissman, 2004). This pain is classically described as cramping and is often accompanied by low backache, nausea and vomiting, headache, or diarrhea. The term primary dysmenorrhea describes cyclic menstrual pain without an identifiable associated pathology, whereas secondary dysmenorrhea frequently complicates endometriosis, leiomyomas, PID, adenomyosis, endometrial polyps, and menstrual outlet obstruction. For this reason, secondary dysmenorrhea may be associated with other gynecologic symptoms, such as dyspareunia, dysuria, abnormal bleeding, or infertility.

Compared with secondary dysmenorrhea, primary dysmenorrhea more commonly begins shortly after menarche. Pain characteristics, however, typically fail to permit differentiation between the two types, and primary dysmenorrhea is usually diagnosed following exclusion of known associated causes.

When other factors are removed, primary dysmenorrhea equally affects women regardless of race and socioeconomic status. However, increased pain duration or severity is positively associated with earlier age at menarche, long menstrual periods, smoking, and increased body mass index (BMI). In contrast, parity appears to improve symptoms (Harlow, 1996; Sundell, 1990).

Pathophysiologically, prostaglandins are implicated in dysmenorrhea. During endometrial sloughing, endometrial cells release prostaglandins as menstruation begins. Prostaglandins stimulate myometrial contractions and ischemia. Women with more severe dysmenorrhea have higher levels of prostaglandins in menstrual fluid, and these levels are highest during the first 2 days of menstruation. Prostaglandins are also implicated in secondary dysmenorrhea. However, anatomic mechanisms are also suspected, depending on the type of accompanying pelvic disease.

Diagnosis

In women with menstrual cramps and no other associated findings or symptoms, no additional evaluation may be initially required, and empiric therapy can be prescribed (Proctor, 2006). In women at risk for PID, cultures for Chlamydia trachomatis and Neisseria gonorrhoeae are prudent. Moreover, if pelvic evaluation is incomplete due to body habitus, then transvaginal sonography may be informative to exclude structural pelvic pathology.

Treatment

Of options, NSAIDs are often preferred. Because prostaglandins are suspected in the genesis of dysmenorrhea, NSAID administration is logical, and studies support their use (Marjoribanks, 2010). These drugs and their dosages are found in Table 10-1.

Steroid hormone contraception leads to endometrial atrophy and in turn lower endometrial prostaglandin levels. Of choices, combination hormone birth control methods are believed to improve dysmenorrhea by lowering prostaglandin production. Studies of combination oral contraceptives (COCs) note improved dysmenorrhea in many users (Brill, 1991; Wong, 2009). In addition, extended or continuous administration of COCs, described in Chapter 5, may be helpful for women with pain not controlled by the traditional cyclic pill schedule (Sulak, 1997). Progestin-only contraceptives are also used for dysmenorrhea. Namely, the levonorgestrel-releasing intrauterine system (LNG-IUS), depot medroxyprogesterone acetate injection, and progestin-releasing implanted rods all are reasonable choices (Lindh, 2013).

GnRH agonists and androgens are other options. The estrogen-lowering effects of these lead to endometrial atrophy and diminished prostaglandin production. Although GnRH agonists and androgens such as danazol lessen dysmenorrhea, their substantial side effects preclude their routine and long-term use. A fuller discussion and dosages for these agents and their side effects are found in Chapter 10.

Complementary and alternative medicine has been evaluated for dysmenorrhea. Oral vitamins E, fish oil, low-fat diet, and Chinese herbal medicine have all been shown to improve dysmenorrhea. However, evidence derives from small and typically nonrandomized trials (Barnard, 2000; Harel, 1996; Zhu, 2008; Ziaei, 2001). Additionally, data are limited but positive toward the use of exercise, topical heat, acupuncture, and transcutaneous electrical nerve stimulation (TENS) (Akin, 2001; Brown, 2010; Proctor, 2002; Smith, 2011).

Cases of dysmenorrhea refractory to conservative management are unusual, and in such instances, surgery may be indicated. Hysterectomy is effective in treating dysmenorrhea, but those desiring future fertility may decline it. For these women, presacral neurectomy can be considered.

This is a frequent gynecologic complaint, and in reproductive-aged women in the United States, the 12-month prevalence is 15 to 20 percent (Glatt, 1990; Laumann, 1999). Painful intercourse may be associated with vulvar, visceral, musculoskeletal, neurogenic, or psychosomatic disorders. Coexistent etiologies may also lead to similar symptoms. For example, women with vulvodynia have been shown in many cases to have coexistent pelvic floor muscle spasm, both of which may cause dyspareunia (Reissing, 2005). Because of the frequent association between dyspareunia and CPP and frequent overlap of etiologies, physical examination and diagnostic testing often follow that for women with CPP.

Dyspareunia may be subclassified as insertional, that is, pain with vaginal entry, or deep, which is associated with deep penetration. Of insertional dyspareunia cases, vulvodynia, vulvitis, and poor lubrication form the majority. Of deep dyspareunia cases, endometriosis, pelvic adhesions, and bulky leiomyomas are frequent causes. In many women, both insertional and deep dyspareunia may be present.

Additional terms include primary dyspareunia, which describes the onset of painful intercourse coincident with coitarche, and secondary dyspareunia, which is painful intercourse that follows an earlier period of pain-free sexual activity. Sexual abuse, female genital mutilation, and congenital anomalies most frequently lead to primary dyspareunia, whereas sources of secondary dyspareunia are more varied. Last, dyspareunia is clarified as generalized, occurring in all episodes of intercourse, or as situational, associated with only specific partners or sexual positions. Recent changes in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) have merged dyspareunia and vaginismus into the term genito-pelvic pain/penetration disorder (American Psychiatric Association, 2013).

Diagnosis

During history taking, patients are questioned regarding associated symptoms such as vaginal discharge, vulvar pain, dysmenorrhea, CPP, dysuria, or scant lubrication. Onset of symptoms and their temporal association with obstetric delivery, pelvic surgery, or sexual abuse is often informative. In addition, dyspareunia may be found in those who breast feed, presumably because of hypoestrogenism-derived vaginal atrophy seen with lactation (Buhling, 2006; Signorello, 2001). Psychosocial topics such as relationship satisfaction or depression are also covered.

Inspection of the vulva mirrors that for chronic pain. In particular, generalized erythema, episiotomy scars, or atrophy is sought. Erythema may indicate contact or allergic dermatitis or infection, particularly fungal infection. Accordingly, a historical inventory of potential skin irritants, a saline slide preparation, vaginal pH testing, and vaginal cultures are performed. Specifically, a vaginal fungal culture may be required in some cases as several noncandidal species may be poorly detected if microscopic analysis is solely used (Haefner, 2005).

Some studies, but not all, have found a positive correlation between degree of pelvic organ prolapse and dyspareunia (Burrows, 2004; Ellerkmann, 2001). If noted, its degree is assessed as described in Chapter 24.

Physical examination evaluates the distal, mid-, and proximal vagina. Evaluation may first begin with palpation of the Bartholin and paraurethral glands. Additionally, cotton-swab testing is used to map painful areas (Fig. 4-1). Next, insertion of a single digit into the distal vagina may elicit vaginismus, that is, reflex contraction of the muscles associated with distal vaginal penetration (Basson, 2010). This contraction response is normal, but prolonged spasm of the bulbospongiosus, pubococcygeus, piriformis, and obturator internus muscles may cause pain. Spasm is thought to be a conditioned response to current or former physical pain.

With deeper digital examination, midvaginal pain may be triggered. This may be seen with interstitial cystitis, in congenital anomalies, or following radiation therapy or pelvic reconstructive surgeries.

Deep dyspareunia is more commonly caused by disorders that also cause CPP. Focal points of this vaginal examination are discussed on page 257. Similarly, diagnostic testing for deep dyspareunia in large part mirrors that for CPP. Urine and vaginal cultures may indicate infection, and radiologic imaging may reveal structural visceral disease.

Treatment

Resolution of dyspareunia is highly dependent on the underlying cause. For those with vaginismus, structured desensitization is effective. Patients gradually gain control in comfortably inserting dilators of increasing size into the introitus. Concurrent psychological counseling in such cases is often warranted. Poor lubrication may be countered with education directed toward adequate arousal techniques and use of external lubricants. As discussed in Chapter 22, estrogen cream or the selective estrogen-receptor modulator ospemifene (Osphena) will usually resolve genitourinary syndrome of menopause, which is the new preferred term for vulvovaginal atrophy.

Surgery may be indicated for structural pathologies and may include ablation of endometriosis, lysis of adhesions, and restoration of normal anatomy. For those with dyspareunia confidently attributed to a retroverted uterine position, uterine suspension has been shown, albeit in small studies, to be effective (Perry, 2005).

Evaluation of dysuria begins with a careful pelvic inspection to exclude vaginitis, vulvar lesions, and urethral diverticulum. A voiding diary can be informative, and for those with associated dyspareunia, a sexual history is obtained. The most common cause of dysuria is infection, and urinalysis and urine culture are therefore initial tests. Similarly, C trachomatis and herpes simplex virus infections are excluded. For those with chronic dysuria, urodynamic studies may help to identify those with detrusor overactivity, significantly decreased compliance, or bladder outlet obstruction (Chap. 23). Cystoscopy is used to identify the hallmark mucosal findings of interstitial cystitis and exclude neoplastic growths or stones (Irwin, 2005). Adjunctively, sonography or laparoscopy may be indicated to exclude structural pelvic pathology or endometriosis.

Interstitial Cystitis/Painful Bladder Syndrome

This chronic inflammatory disorder of the bladder is typified by frequency, urgency, and pelvic pain. With interstitial cystitis (IC), this triad is found in combination with characteristic mucosal changes and reduced bladder capacity. In contrast to cases with classic IC findings, painful bladder syndrome describes chronic IC symptoms in those who lack cystoscopic findings of IC or other bladder pathology (Abrams, 2002).

The prevalence of IC in the United States is variable and cited at 0.5 to 3 percent (Berry, 2011; Jones, 1997). It is diagnosed more commonly in women, in whites, in smokers, and in those in their 40s (Kennedy, 2006; Propert, 2000). There is a strong association between IC and endometriosis. The two conditions share similar symptoms, and many patients evaluated for chronic pelvic pain have been found to have either one or both conditions (Butrick, 2007; Paulson, 2007). In addition, IC is association with IBS, generalized pain disorders, fibromyalgia, pelvic floor dysfunction, and depression (Aaron, 2000; Clauw, 1997; Novi, 2005; Peters, 2007).

The exact cause of IC is unknown, and current theories include increased mucosal permeability or mast cell activation (Sant, 2007; Warren, 2002). Glycosaminoglycans are an important component of the mucin layer that covers and protects the bladder urothelium. One theory explains that IC symptoms originate from a defect in the protective bladder glycosaminoglycan component. This leads to increased permeability of the bladder mucosa (Parsons, 2003).

Diagnosis

IC is considered in women with unexplained chronic pelvic pain and voiding symptoms. Warren and colleagues (2006) found that the key descriptor “pelvic pain” fit 100 percent of an affected population. Other relevant descriptors are “pressure” and “discomfort” (Sirinian, 2005). Of voiding complaints, frequency, urgency, nocturia, and pain with bladder filling or emptying are often reported. Dyspareunia and postcoital ache are common. As with most chronic pain syndromes, symptoms may worsen premenstrually. Given the broad spectrum of triggers (alcohol, caffeine, smoking, spicy foods, citrus fruits and juices, carbonated drinks, and potassium), patients may not relate exacerbation of their symptoms to these. Cranberry juice, frequently advised for urinary tract infection, can acutely exacerbate pain from IC.

Single-digit vaginal examination in the patient with IC may demonstrate urethral or anterior vaginal/bladder base tenderness as well as pelvic floor hypertonus, tenderness, or trigger points. The basic laboratory examination includes urinalysis and culture, and unevaluated microhematuria typically prompts cytology, especially in smokers, to exclude neoplasia. Cystoscopy and urodynamic studies may add clarity to complex presentations or exclude of other entities that mimic IC. However, consensus on cystoscopic or urodynamic criteria for IC is lacking (Hanno, 2011). Cystoscopically, Hunner ulcers are reddish-brown mucosal lesions with small vessels radiating toward a central scar (Fig. 11-7). These ulcers are rare but considered diagnostic for IC. The more common finding is glomerulations, which are small petechiae or submucosal hemorrhages. However, these may be present in patients without IC symptoms and undergoing cystoscopy for other indications (Waxman, 1998). Urodynamic testing may reveal sensory urgency at low bladder volumes, decreased compliance, and decreased capacity. The potassium sensitivity test (PST) indicates increased urothelial permeability but is painful and may trigger a severe symptom flare. Moreover, a negative result does not eliminate suspicion for IC. In one study, 25 percent of patients meeting strict IC criteria had a negative PST result (Parsons, 1998).

Given the broad symptom spectrum, its frequent association with other pelvic pain syndromes, and symptoms that overlap with other pain disorders, diagnosing IC can be challenging. Moreover, uniform consensus on diagnostic criteria is lacking. Thus, the diagnosis of interstitial cystitis remains clinical and is mostly one of exclusion. Not surprisingly, misdiagnosis, underdiagnosis, or delayed diagnosis of IC is common.

Treatment

The American Urological Association has provided evidence-based guidelines for IC management (Hanno, 2011, 2015). First-line treatment provides patient education and behavioral modification, especially avoidance of bladder irritants. Second-tier options are pelvic floor physical therapy to resolve trigger points or pelvic floor hypertonus or to implement pharmacological management. Suitable agents include amitriptyline, cimetidine, hydroxyzine, or pentosan polysulfate sodium (Elmiron), which is a weak anticoagulant. Also, intravesical therapy may consist of direct bladder instillation of heparin, lidocaine, or dimethyl sulfoxide (DMSO). For patients who do not respond, cystoscopy coupled with short-duration, low-pressure bladder distention and fulguration of Hunner ulcers may afford relief. FDA approval is lacking for treatment with cyclosporin A, intradetrusor botulinum toxin A, or sacral neuromodulation, which is described in Section 45-12. However, their use may be considered in patients who fail to respond to other therapies. Major surgery such as cystoplasty or urinary diversion is performed rarely for carefully selected patients in whom all other therapies have failed to provide adequate symptom control.

In numerous cases, GI disease is found as an underlying cause of chronic pelvic pain. GI causes may be organic or functional (see Table 11-1). Thus, initial screening may follow that for CPP. However, symptoms such as fever, GI bleeding, weight loss, anemia, and abdominal mass will prompt a stronger search for organic pathology. Investigations may include sigmoidoscopy or colonoscopy to exclude inflammation, diverticula, or tumors. For those with diarrhea, stool examination for leukocytes or for ova and parasites may be indicated. Moreover, serologic testing for celiac disease can be valuable. When indicated, sonography may aid in distinguishing GI from gynecologic pathology.

Colonic Diverticular Disease

Colon diverticula are small defects in the muscular layer of the colon through which colonic mucosa and submucosa herniate. Diverticular disease is common and typically affects the sigmoid or descending colon. Chronic symptoms include abdominal pain that localizes to the left lower quadrant, obstipation, and rectal fullness. More seriously, diverticula may cause acute or chronic GI bleeding or may become infected. Clinically, infection can be difficult to distinguish from PID or tuboovarian abscess. In these cases, CT is the preferred imaging technique and has a sensitivity for diagnosis exceeding 90 percent and a specificity approaching 100 percent (Ambrosetti, 1997).

Chronic diverticular disease is usually treated with a high-fiber diet and long-term suppressive therapy with antibiotics. With acute severe infection, hospitalization, parenteral antibiotics, surgical or percutaneous abscess drainage, or partial colectomy may be required. Suspected rupture of a diverticular abscess with peritonitis is an indication for immediate surgical exploration (Jacobs, 2007).

Celiac Disease

This is an inherited autoimmune intolerance to gluten, which is a component of wheat, barley, or rye. In affected individuals, gluten ingestion creates an immune-mediated reaction that damages the small intestine mucosa and leads to varying degrees of malabsorption. Thus, treatment dictates a gluten-free diet for life (Rubio-Tapia, 2013). Celiac disease is common, and its incidence in the general population approaches 1 percent (Green, 2007). Its incidence is suspected to be even higher if those with GI symptoms are screened. There is a gender bias to the disease, and two to three times as many women as men are affected (Green, 2005).

The most common presenting symptoms are abdominal pain and diarrhea. Other findings include weight loss, osteopenia, and fatigue from anemia, all of which stem from malabsorption. In addition, celiac disease has been associated with infertility, although the mechanism is not understood (Tersigni, 2014).

Celiac disease is suspected in those with characteristic findings and in those with a family history of the disorder. Diagnosis requires both duodenal biopsy and a positive response to a gluten-free diet. However, numerous patients presenting with abdominal pain and diarrhea do not have celiac disease. Thus, to avoid unnecessary biopsy, many physicians will screen with noninvasive serologic tests. Of these, serologic screening for IgA antitissue transglutaminase antibodies is preferred and is performed while patients maintain a gluten-containing diet during testing (Rubio-Tapia, 2013).

Functional Bowel Disorders

Also known as functional gastrointestinal disorders (FGIDs), this group of functional disorders has symptoms attributable to the lower GI tract and includes those listed in Table 11-6. In defining these chronic conditions, symptoms must have begun more than 6 months previously and have occurred more than 3 days a month during the last 3 months (Longstreth, 2006). The diagnosis always presumes the absence of a structural or biochemical explanation for symptoms (Thompson, 1999).

Irritable Bowel Syndrome

This functional bowel disorder is defined as abdominal pain that improves with defecation and is associated with a change in bowel habits. Subtypes are divided by the predominant stool pattern and include constipative, diarrheal, and mixed categories. Although defining criteria are listed in Table 11-6, other symptoms that support the diagnosis include abnormal stool frequency or stool form, straining, urgency, passing mucus, and bloating (Longstreth, 2006).

IBS is common, and its general population prevalence is estimated to approximate 10 percent (Canavan, 2014; Lovell, 2012). The prevalences of diarrhea-predominant and constipation-predominant IBS are equivalent (Saito, 2002).

The pathophysiology of IBS is complex, and neural, hormonal, genetic, environmental, and psychosocial factors are variably involved (Drossman, 2002). The primary mechanism of IBS, however, is thought to stem from poorly regulated interactions between the CNS and the enteric nervous system (ENS). Such brain-gut dysfunction may eventually cause alterations of GI mucosal immune response, intestinal motility and permeability, and visceral sensitivity. In turn, these produce abdominal pain and altered bowel function (Mayer, 2008). Specifically, serotonin (5-hydroxytryptamine, 5-HT) is involved with regulating intestinal motility, visceral sensitivity, and gut secretion and is thought to play an important role in IBS (Atkinson, 2006; Gershon, 2005).

Prior to assigning a diagnosis of IBS, clinicians ideally exclude organic disease. However, for young patients who have typical IBS symptoms and no organic disease symptoms, few tests are required. Testing is individualized, and factors that typically prompt greater evaluation include older patient age, longer duration and greater severity of symptoms, absent psychosocial factors, organic disease symptoms, and family history of GI disease.

Treatment

Nonpharmacologic approaches may improve symptoms. First, no specific diet suffices for all patients, but foods known to trigger symptoms are logically avoided. Combination probiotics in general improve global IBS symptoms, bloating, and flatulence, although current data limit recommendation of preferred species (Ford, 2014a,c).

Drug therapy is directed toward dominant symptoms. For those with constipation-dominant IBS, commercial soluble fiber analogues or psyllium husk may help if increased dietary fiber is unsuccessful (Bijkerk, 2009). Of these, psyllium husk is gradually titrated to improve tolerability to a dosage of 3 to 5 g orally twice daily. Of note, dietary fiber is effective in treating constipation but is not effective for diarrhea-dominant IBS or for IBS-associated pain (Ruepert, 2011). Another agent, linaclotide (Linzess), a guanylate cyclase agonist, stimulates increased fluid secretion and transit time (Chey, 2012b; Rao, 2012). It is taken orally as a 290-μg capsule once daily. Alternatively, lubiprostone (Amitiza) is a GI chloride-channel activator that is taken orally twice daily as an 8-μg capsule. It also enhances intestinal fluid secretion to improve intestinal motility (Chey, 2012a; Drossman, 2009). No longer available due to cardiovascular adverse events, tegaserod (Zelnorm) was a partial serotonin-receptor agonist (Food and Drug Administration, 2012b).

For those with diarrhea-dominant symptoms, treatments often strive to slow bowel motility because as substances stay longer in the gut, more water is absorbed from fecal matter to bulk stool. Indirect evidence supports loperamide (Imodium), 2 mg orally once or twice daily (Trinkley, 2014; Weinberg, 2014). For those with severe diarrhea, alosetron (Lotronex), a selective serotonin 5-HT₃-receptor antagonist, interacts with ENS neuron receptors to slow bowel motility. This drug decreases pain, urgency, and stool frequency (Camilleri, 2000; Chey, 2004). However, due to cases of ischemic colitis associated with its use, alosetron is now available only through a strictly regulated FDA prescribing program (Chang, 2006; Food and Drug Administration, 2012a).

For patients with pain secondary to bowel spasm, antispasmodic agents decrease intestinal smooth muscle activity and are thought to decrease abdominal discomfort. Agents available in the United States include dicyclomine (Bentyl) and hyoscyamine sulfate (Levsin). Dicyclomine is begun at 20 mg orally four times daily and increased after 1 week to 40 mg. Hyoscyamine sulfate is dosed at 0.25 to 0.5 mg orally daily and can be increased as needed up to four times daily. Although having benefits for IBS, the anticholinergic side effects of these agents often limit their long-term use (Ruepert, 2011; Schoenfeld, 2005). Peppermint oil, another effective antispasmodic, can be taken orally as over-the-counter capsules at dosages of 550 mg once daily or 187 mg three times daily (Khanna, 2014).

Tricyclic antidepressants may help patients with IBS both by an anticholinergic effect on the gut and by mood-modifying action. Tricyclic antidepressants may slow intestinal transit time and have been shown to be effective in treatment of diarrhea-dominant IBS (Hadley, 2005). Last, psychological or behavioral treatments may help some patients (Ford, 2014b).

Clinical syndromes involving the muscles, nerves, and skeletal system of the lower abdomen and pelvis are frequently encountered but often overlooked by gynecologists. Importantly, unrecognized musculoskeletal pain may lead to unnecessary surgery or promote development of pelvic pain syndromes.

Hernia

Defects in anterior abdominal wall or femoral fascia can lead to herniation of bowel or other intraabdominal contents through these rents. Such herniation can create pain locally at the defect site or cause referred pain along the distribution of a compressed sensory nerve. Moreover, if blood supply to the contents is acutely compromised, then bowel obstruction or ischemia will require surgical intervention. Hernias that involve the anterior abdominal wall and pelvic floor are most commonly associated with CPP. Much less frequently, sciatic hernia, which is herniation of peritoneum and peritoneal contents through the greater sciatic foramen, and obturator hernia, which is that through the obturator canal, are also described sources of acute or chronic pain.

Hernias may develop at sites of inherent anatomic weakness, and common types in women include ventral, umbilical, and incisional hernias. Indirect inguinal, direct inguinal, and femoral hernias are types less often found in females. Spigelian hernias are rare. As shown in Figure 11-8, ventral hernias are caused by fascial defects typically occurring in the midline. Umbilical hernias are those involving defects of the umbilical ring. Indirect inguinal hernias are those in which abdominal contents herniate through the internal inguinal ring and into the inguinal canal. As shown in Figure 11-9, contents may then exit the external inguinal ring. In contrast, contents of a direct inguinal hernia bulge through a fascial defect within Hesselbach triangle. Spigelian hernias can occur anywhere along the lateral border of the rectus abdominis muscle. However, the most frequent location is this border’s intersection point with the arcuate line.

Conditions that increase intraabdominal pressure such as pregnancy, ascites, peritoneal dialysis, and chronic cough are known hernia risk factors. Congenital or acquired anatomic weakness or connective tissue disorders are also associated.

For diagnosis, patients with CPP or abdominal pain ideally are examined while standing and also during Valsalva maneuver. Because of the potential risks associated with content herniation and strangulation, hernias are typically repaired once identified. Small ventral, umbilical, or incisional hernias may be repaired by gynecologic surgeons. In these cases, the hernia sac is excised and fascia reapproximated. Patients with larger hernias, which usually require mesh placement, or hernias in the inguinal area are typically referred to a general surgeon.

Myofascial Pain Syndrome

Primary musculoskeletal (MS) conditions may lead to CPP (see Table 11-2). In other cases, secondary myofascial pain syndromes can originate from endometriosis, interstitial cystitis, or IBS. Such chronic visceral inflammatory conditions can create pathologic changes in nearby muscles and/or nerves to cause abdominal wall or pelvic floor pain. Thus, awareness of these complex associations allows a physician to more effectively address all components leading to pain, rather than narrowly focusing on an isolated visceral disorder.

With myofascial pain, a hyperirritable area within a muscle promotes persistent fiber contraction (Simons, 1999). The primary reactive area within the muscle is termed a trigger point (TrP) and is identified as a palpable taut, ropy band. Trigger points are thought to form as the end of a metabolic crisis within a muscle. Dysfunction of a neuromuscular endplate can lead to sustained acetylcholine release, persistent depolarization, sarcomere shortening, and creation of a taut muscle band. Affected fibers compress capillaries and decrease local blood flow. The resulting ischemia leads to release of substances that activate peripheral nerve nociceptors and in turn cause pain (McPartland, 2004). A persistent barrage of nociceptive signals from TrPs may eventually lead to central sensitization and the potential for neuropathic pain. Signals may spread segmentally within the spinal cord to cause localized or referred pain (Gerwin, 2005). TrPs can also initiate viscerosomatic convergence that can generate autonomic responses such as vomiting, diarrhea, and bladder spasm.

TrPs can affect any muscle, and those involving muscles of the anterior abdominal wall, pelvic floor, and pelvic girdle can be sources of CPP. The incidence of myofascial disease is unknown. However, in an evaluation of 500 patients with CPP, Carter (1998) found that 7 percent of patients primarily had TrPs as a source of their pain. Moreover, of nearly 1000 women evaluated for CPP, 22 percent were found to have significant tenderness of the levator ani muscles and 14 percent had piriformis muscle tenderness (Gomel, 2007). Prevalence appears to be greatest at ages between 30 and 50 years. Risk factors are varied, although many trigger points can be traced to a prior specific trauma such as a sports injury or to chronic biomechanical overload of a muscle (Sharp, 2003). Accordingly, a detailed inventory of sports injuries, traumatic injuries, obstetric deliveries, surgeries, and work activities is essential.

Diagnosis

Having the patient mark painful sites on a body silhouette diagram can be an informative first step. Involvement of specific muscles will often give characteristic patterns. Patients typically describe the pain as aggravated by specific movement or activity and relieved by certain positions. Cold, damp exposure generally worsens pain. Pressure on a trigger point causes pain and produces effects on a target area or referral zone. This specific and reproducible area of referral rarely coincides with dermatologic or neuronal distribution and is the feature that differentiates myofascial pain syndromes from fibromyalgia (Lavelle, 2007).

Muscle examination may be completed by flat palpation, pincer palpation, or deep palpation depending on muscle location. Flat palpation uses fingertips to roll over superficial muscles, which are accessible only at the surface (Fig. 11-10). This technique is commonly used to assess the anterior abdominal wall. In muscles with greater accessibility, pincer palpation grasps the muscle belly between the thumb and fingers. With any of the palpation techniques, spot tenderness and taut muscle bands are sought. Classically, the involved muscle displays weakness and restricted stretch. TrP pressure may also elicit a local muscle twitch response, reproduce a patient’s referred pain, or both.

Specific Muscle Groups

Anterior abdominal wall muscles—that is, the rectus abdominis, the obliques, and transversus abdominis muscles—may all develop TrPs, and somatovisceral pelvic symptoms from these muscles may include diarrhea or urinary frequency, urgency, or retention. Rectus abdominis muscle TrPs are frequently found along the linea semilunaris, which is the term for this muscle’s lateral margin (Suleiman, 2001). Additional rectus abdominis TrPs may develop at the muscle’s insertion into the pubic bone and also below the umbilicus. Within the external oblique muscle, trigger points frequently involve its lateral attachment to the anterior iliac crest. Pain usually refers to the pubic bone.

After examination of the anterior abdominal wall, muscles of the pelvis are evaluated. Following careful inspection of the external genitalia, vaginal examination proceeds slowly with the index finger only and initially without a palpating abdominal hand. Muscles within the pelvis include the levator ani, coccygeus, obturator internus, and deep transverse perineal and piriformis muscles, and these are assessed for painful TrPs (see Fig. 11-5) (Vercellini, 2009). TrPs involving these muscles and anal sphincter muscles are frequently associated with poorly localized pain that may be described as involving the coccyx, hip, or back (Fig. 11-11). Dyspareunia is common.

Levator Ani Syndrome

Pain stemming from TrPs involving the levator ani muscles has had various names including levator ani spasm syndrome and coccydynia (see Fig. 11-11). Currently, levator ani syndrome is preferred. Coccydynia is reserved for coccygeal pain originating from skeletal trauma to the coccyx.

The levator ani muscles, including their supporting fascia, overlying parietal peritoneum, and intimately associated visceral peritoneum, are connected by common sensory nerves to the spinal cord. These provide the basis for viscerosomatic convergence (Spitznagle, 2014). Spasm of these muscles can result in lower abdominal pain, low back pain, dyspareunia, and chronic constipation.

Treatment

Regardless of TrP location, the treatment goal is TrP inactivation, which then allows stretching and release of taut muscle bands. Of methods, TrP point massage or more aggressive ischemic compression massage are effective (Hull, 2009). Biofeedback, relaxation techniques, or psychotherapy may be helpful therapy adjuncts. Analgesics, antiinflammatory drugs, muscle relaxants, or neuroleptics may also be prescribed. Finally, electrical stimulation, TrP dry needling, or TrP injection may be required. In those who are unresponsive to injection of local anesthetic agents, botulinum toxin A injection may be considered (Gyang, 2013). At our institution, as in many other tertiary referral centers, we often consult pelvic floor physical therapy experts for many of these treatments.

Peripartum Pelvic Pain Syndrome

Also known as pelvic girdle pain, this condition is characterized by persistent pain that begins during pregnancy or immediately postpartum. Pain is prominent around the sacroiliac joints and symphysis and is thought to originate from injury or inflammation of the pelvic and/or lower spine ligaments. Muscle weakness, postural adjustments of pregnancy, hormonal changes, and weight of the fetus and gravid uterus are all potential contributing factors (Mens, 1996). Pelvic girdle pain is common. Significant pain is estimated to afflict approximately 20 percent of pregnant women and 7 percent of those during the 3 months following delivery (Albert, 2002; Wu, 2004). Diagnosis is usually clinical and based on findings during specific orthopedic joint manipulation tests. These are used to recreate or provoke the pain. Treatment includes physical therapy, exercise, and analgesics typically used for CPP (Vermani, 2010; Vleeming, 2008).

Anterior Abdominal Wall Nerve Entrapment Syndromes

Nerve compression can lead to chronic pelvic pain and may involve nerves of the anterior abdominal wall or those within the pelvis. Anterior abdominal wall pain is frequently mistaken for visceral pain. Common causes include entrapment of the anterior cutaneous branches of the intercostal nerves or compression of branches of the ilioinguinal, iliohypogastric, genitofemoral nerves, and lateral femoral cutaneous nerves (Greenbaum, 1994). These peripheral nerves can be compressed either within narrow anatomic canals or rings or beneath tight ligaments, fibrous bands, or sutures. For example, each anterior cutaneous branch of an intercostal nerve traverses anteriorly through the rectus abdominis muscle. Each branch and its corresponding vessels travels through a fibrous ring found within the lateral aspect of rectus abdominis muscle (Fig. 11-12). Clinically, these nerve branches are those often seen during Pfannenstiel incision creation as the anterior rectus sheath is dissected off each rectus belly (Fig. 43-2.3). On crossing the anterior rectus sheath, each nerve branch divides and then courses within the subcutaneous layer. Within the fibrous ring, fat surrounding the neurovascular bundle appears to pad the enclosed structures (Srinivasan, 2002). However, if this bundle receives excessive intra- or extraabdominal pressure, compression of the bundle against the fibrous ring causes nerve ischemia and pain (Applegate, 1997).

Nerve entrapment, injury, or neuroma formation may also involve branches of the ilioinguinal, iliohypogastric, lateral femoral cutaneous, or genitofemoral nerves, as described in Chapter 40. Involvement may follow inguinal hernia repair, low transverse abdominal incisions, and lower abdominal laparoscopic trocar placement. Hypoesthesia is the more common finding with these injuries, but pain may variably develop within months of surgery or after several years.

Criteria for diagnosing nerve entrapment are clinical and include: (1) pain aggravated by patient movement or light skin pinching over the affected area and (2) pain improvement following local anesthetic injection. In general, electromyography is uninformative because it lacks adequate sensitivity (Knockaert, 1996). For local injection, 1- or 2-percent lidocaine and a 40-mg/mL concentration of triamcinolone can be combined in a 1:1 ratio. However, the corticosteroid may be omitted. Less than half a milliliter is injected at each pain site. Injections of the mixture may be repeated if initially successful. Additional treatments can include oral analgesics, biofeedback, and gabapentin. If conservative options fail to bring sufficient relief, neurolysis with injection of 5- to 6-percent absolute alcohol or phenol, or surgical neurectomy may be required (Madura, 2005; Suleiman, 2001).

Pudendal Neuralgia

Neuralgia is sharp, severe, shooting pain that follows the distribution of the involved nerve. Pudendal nerve entrapment may create this type of pain on the perineum. The three branches of this nerve are the perineal nerve, the inferior rectal nerve, and the dorsal nerve to the clitoris (Fig. 38-28). Thus, pain may involve, alone or in combination, the clitoris, vulva, or rectum. Pudendal neuralgia is rare, is usually unilateral, and typically develops after age 30. In affected individuals, allodynia and hyperesthesia may be extreme to the point of disability. The pain is aggravated by sitting, is relieved by sitting on a toilet seat or standing, and may progress during the day.

The diagnosis of pudendal neuralgia is clinical, and Nantes criteria are used by many. As inclusion criteria: pain follows the pudendal nerve innervation path, is worse with sitting, has no associated sensory loss, does not awaken patients, and is relieved by nerve blockade (Labat, 2008). Clinical suspicion may be supported by objective testing. This may include neurophysiologic testing such as pudendal nerve motor latency and electromyography (EMG), both described in Chapter 25. However, abnormal findings with these are not specific for pudendal neuralgia. Rarely, CT or MR imaging may be informative, although these may be performed to exclude other pathology (Khoder, 2014).

Treatment can involve physical therapy; behavioral modification; gabapentin or tricyclic antidepressants; pudendal nerve blockade, with or without corticosteroids; botulinum toxin A injection; and pudendal nerve stimulation. If these are unsuccessful, surgical nerve decompression may be elected.

Piriformis Syndrome

Compression of the sciatic nerve by the piriformis muscle may lead to buttock or low back pain in the distribution of the sciatic nerve (Broadhurst, 2004). This is termed the piriformis syndrome. Proposed mechanisms for compression include: contracture or spasm of the piriformis muscle from trauma, overuse and muscle hypertrophy, and congenital variations, in which the sciatic nerve or its divisions pass directly through this muscle (Hopayian, 2010).

Fishman and associates (2002) estimate the piriformis syndrome to be responsible for 6 to 8 percent of cases of low back pain and sciatica in the United States each year. Symptoms include pain and tenderness involving the buttocks, with or without radiation into the posterior thigh. Pain is worse with activity, prolonged sitting, walking, and internal rotation of the hip (Kirschner, 2009). Dyspareunia has a common but variable association and has been demonstrated in 13 to 100 percent of cases (Hopayian, 2010).

Diagnosis of the syndrome is clinical and based on findings during specific orthopedic joint manipulation tests (Michel, 2013). Nerve conduction and EMG are typically nondiagnostic. Uncommonly, MR imaging may be helpful by identifying a swollen or enlarged piriformis muscle or anatomic muscle variants (Petchprapa, 2010). Treatment is conservative and includes physical therapy, NSAIDs, muscle relaxants, or neuropathic pain agents such as gabapentin, nortriptyline, or carbamazepine. Therapeutic injections of local anesthetics, with or without corticosteroids, or of botulinum toxin A may be used. Surgery is reserved for refractory cases.