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).
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.
Rating scales for pain. The visual analogue, numeric, and verbal rating scales are shown.
TABLE 11-3Questions Relevant to Chronic Pelvic Pain ||Download (.pdf) TABLE 11-3 Questions Relevant to Chronic Pelvic Pain
Describe the location, quality, severity, and timing of your pain.
When and how did your pain start and how has it changed?
What makes your pain better or worse?
What other symptoms or health problems do you have?
Do you have frequency, urgency, or bloody urine?
Do you have nausea or vomiting, diarrhea, constipation, or rectal bleeding?
Do you have pain with your periods?
Did your pain start initially as menstrual cramps?
Have you had surgery? What was the reason?
How many pregnancies have you had?
How did you deliver? Was there an episiotomy?
What form of birth control do you use and have you used in the past?
Have you ever been treated for a sexually transmitted disease or pelvic infection?
Do you have pain with deep penetration during intercourse?
Are you depressed or anxious?
Have you been treated for mental illness in the past?
Have you been or are you now being abused physically or sexually?
What prior evaluations or treatments have you had for your pain?
Have any of the previous treatments helped?
What medications are you taking now?
How has the pain affected your quality of life?
What do you believe or fear is causing your pain?
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).
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.
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.
TABLE 11-4Musculoskeletal Origins of Chronic Pelvic Pain ||Download (.pdf) TABLE 11-4 Musculoskeletal Origins of Chronic Pelvic Pain
|Structure ||Innervation ||Referred Pain Site(s) |
|Hip ||T12–S1 ||Lower abdomen; anterior medial thigh; knee |
|Lumbar ligaments, facets/disks ||T12–S1 ||Low back; posterior thigh and calf; lower abdomen; lateral trunk; buttock |
|Sacroiliac joints ||L4–S3 ||Posterior thigh; buttock; pelvic floor |
|Abdominal muscles ||T5–L1 ||Abdomen; anteromedial thigh; sternum |
|Pelvic and back muscles || || |
| Iliopsoas ||L1–L4 ||Lateral trunk; lower abdomen; low back; anterior thigh |
| Piriformis ||L5–S3 ||Low back, buttock; pelvic floor |
| Pubococcygeus ||S1–L4 ||Pelvic floor; vagina; rectum; buttock |
| Obturator internal/external ||L3–S2 ||Pelvic floor; buttock; anterior thigh |
| Quadratus lumborum ||T12–L3 ||Anterior lateral trunk; anterior thigh; lower abdomen |
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).
Concurrent lordosis and kyphosis are common postural changes associated with chronic pelvic pain. TPPP = typical pelvic pain posture.
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.
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.
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.
Pelvic floor muscle examination. (Used with permission from Ms. Marie Sena.)
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.
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.
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).
TABLE 11-5Antidepressants and Antiepileptic Drugs Used in Chronic Pain Syndromes ||Download (.pdf) TABLE 11-5 Antidepressants and Antiepileptic Drugs Used in Chronic Pain Syndromes
|Drug (Brand name) ||Dosage ||Side Effects |
|ANTIDEPRESSANTS || || |
| Tricyclic antidepressants || ||Dry mouth, constipation, urinary retention, sedation, weight gain |
|Amitriptyline (Elavil) a |
Imipramine (Tofranil) a
|For both, 10–25 mg at bedtime; increase by 10–25 mg per week up to 75–150 mg at bedtime or a therapeutic drug level ||Tertiary amines have greater anticholinergic side effects |
|Desipramine (Norpramin) a |
Nortriptyline (Pamelor) a
|For both, 25 mg in the morning or at bedtime; increase by 25 mg per week up to 150 mg per day or a therapeutic drug level ||Secondary amines have fewer anticholinergic side effects |
| Selective serotonin reuptake inhibitors || |
|Fluoxetine (Prozac) a |
Paroxetine (Paxil) a
|For both, 10–20 mg per day; up to 80 mg per day for fibromyalgia ||Nausea, sedation, decreased libido, sexual dysfunction, headache, weight gain |
| Novel antidepressants || || |
|Bupropion (Wellbutrin) a ||100 mg per day; increase by 100 mg per week up to 200 mg twice daily (400 mg per day) ||Anxiety, insomnia or sedation, weight loss, seizures (at dosages above 450 mg per day) |
|Venlafaxine (Effexor) a ||37.5 mg per day; increase by 37.5 mg per week up to 300 mg per day ||Headache, nausea, sweating, sedation, hypertension, seizures |
Serotoninergic properties in dosages below 150 mg per day; mixed serotoninergic and noradrenergic properties in dosages above 150 mg per day
| ANTIEPILEPTIC DRUGS || || |
| First-generation agents || || |
|Carbamazepine (Tegretol) ||200 mg per day; increase by 200 mg per week up to 400 mg three times daily (1200 mg per day) ||Dizziness, diplopia, nausea, aplastic anemia |
|Phenytoin (Dilantin) a ||100 mg at bedtime; increase weekly up to 500 mg at bedtime ||Blood dyscrasias, hepatotoxicity |
| Second-generation agents || |
|Gabapentin (Neurontin) ||100–300 mg at bedtime; increase by 100 mg every 3 days up to 1800 to 3600 mg per day taken in divided doses three times daily ||Drowsiness, dizziness, fatigue, nausea, sedation, weight gain |
|Pregabalin (Lyrica) ||150 mg at bedtime for diabetic neuropathy; 300 mg twice daily for postherpetic neuralgia ||Drowsiness, dizziness, fatigue, nausea, sedation, weight gain |
|Lamotrigine (Lamictal) a ||50 mg per day; increase by 50 mg every 2 weeks up to 400 mg per day ||Dizziness, constipation, nausea; rarely, life-threatening rashes |
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).
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
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.
Color Doppler transvaginal image of tortuous and dilated pelvic vessels in the right adnexa in a patient with chronic pelvic pain. (Used with permission from Dr. Elysia Moschos.)
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.