Management of Chronic Pelvic Pain

Table of Contents IntroductionPhysical Evaluation Laboratory and Imaging Evaluation RadiographyUrodynamic Testing and Intravesical Potassium SensitivityCauses of Chronic Pelvic PainUrologic Causes of Pelvic PainGastrointestinal Causes of Pelvic PainMusculoskeletal Causes of Pelvic Pain Psychological Causes of Pelvic PainChronic Pelvic Pain as a Diagnosis Introduction Chronic pelvic pain (CPP) is often accompanied by poorly defined symptoms and a sense of failure by both doctor and patient. 1 Although the pain is in the pelvis, it may not be gynecological in origin. Pain that is not gynecologic in origin requires a different approach and possible referral. Pain involves 4 phases: Nociception: The origination and detection of a neurologic signal based on a noxious event. Pain: The recognition of the signal or event. Suffering: The Affective responses to the event. Pain behavior: Adaptive changes (functional or dysfunctional) made based on the pain.1 The physiologic processes that evoke the perception of pain are few: Thermal (heat or cold) Mechanical (stretch, distention, or muscular contraction) Chemical irritation (liberation of histamines, bradykinin, prostaglandins, serotonin, acetyl choline, acids, proteolytic enzymes, and potassium ions released by ischemia, necrosis, or inflammation. The cause of chronic pain may be grouped into 3 categories: Structural (ongoing processes such as arthritis or cancer) Psychophysiologic (such as continuing muscle spasm causing pain after the original insult has passed) Somatic (as is found among those who internalize stresses and express them in the form of pain).1 Localization of the source of pain is often difficult and inaccurate. Visceral pain is transmitted by slow pain fibers and is characterized by burning or aching. This pain arises from conditions that affect a wide area such as inflammation or ischemia. Parietal pain is transmitted by fast pain fibers, which are well localized and are characterized by a sharp, moderately well localized sensation. Slow and fast pain fibers continue to generate pain signals for as long as the stimulus is present.They travel through different routes and therefore the perception of pain may be interpreted as arising from or referred to different areas of the body.1 CPP is non-menstrual pain lasting longer than 3 months that is localized to the anatomic pelvis and is severe enough to cause functional disability requiring medical or surgical treatment.2 Approximately 10% of all office visits to gynecologists are for symptoms of CPP.3 More than 40% of laparoscopies performed by gynecologists involve the diagnosis of CPP 4 Evaluation Strategies: Pain of any duration is assessed by history and physical examination. Laboratory and diagnostic studies may be helpful depending on the clinical findings.1 History: The history provides descriptions of the nature, intensity, and distribution of the pain. Pain charts and pain forms may be helpful in discerning the exact nature of the patient’s pain.5 Imprecise localization is typical with intra-abdominal processes. Radiation of the pain or coexisting pain in other locations should be assessed. The temporal patterns of the pain and any factors that modify the pain should be determined. Associated symptoms should be evaluated. Surgeries, infections, infertility, or obstetrical experiences may be significant. Characteristics of menstrual and non-menstrual bleeding and pain are important. Also the role of the pain in the patient’s life must be explored.1 The history should include a review of gastrointestinal, urologic, and musculoskeletal, myofascial, and psychological functions, including the relationship between these systems and the patient’s pain. Patients with pain are frequently depressed and depression increases the sensitivity to pain. This leads to a pain-depression cascade and should be addressed with each patient.6 Pain Questionnaire Pain Map for a Woman's Body Symptoms Check List Related History Form Monthly Pain Calendar Physical Evaluation: The physical examination of the patient with pain should be performed by observing the patient’s walk, by examining the patient in a standing position, a sitting position, and a supine position. Begin with a general physical and neurological assessment. Ask the patient to indicate the location of pain. A single finger locating the pain indicates a discreet source. A sweeping motion indicates a more generalized source. Standing Examination: Examine the patient for asymmetric gait, lordosis, kyphosis-lordosis, scoliosis, or one-leg standing. Evaluate for “typical pain posture” (TPPP) consisting of thoracic kyphosis and lumbar lordosis. Examine the patient standing on one leg to see if pain occurs at the pubic symphysis. Examine the iliac crest heights for inequality to determine if “short leg syndrome” is present. Examine in a standing position for incisional, femoral, ventral, and inguinal hernias. The standing position is also helpful for evaluation of pelvic floor relaxation defects, by placing the index finger of one hand in the vagina and the index finger of the other hand in the rectum while the patient bears down. Occult enterocele, rectocele, cystocele, and uterine prolapse may be diagnosed with this procedure more accurately than when the patient is in the lithotomy position.8 Sitting Examination: The patient is observed in the sitting position. Sitting with all of the weight on one buttock or consistently sitting forward may suggest levator ani spasm and pelvic floor pain syndrome.9 palpation of the upper and lower back and sacrum, including single digit palpation for trigger points can be performed at this time. If foci are noted that are consistent with trigger points it may be valuable to block them with 1% lidocaine to evaluate the contribution of the trigger points to the patient’s pain.8 Supine Examination: Inspect and palpate for lordosis or pelvic tilt. Active leg flexion, knee to chest, elicits low back dysfunction, low back pain, and abdominal weakness. Evaluate the obturator and psoas muscle for shortening, dysfunction, or spasm. Pain on straight leg raising may suggest possible herniated disc. Any of the following muscles or muscle groups may cause or contribute to CPP: rectus abdominus, external obliques, internal obliques, transversus abdominus, quadratus lumborum, pyramidalis, iliopsoas, coccygeus, levator ani, obturator internus, adductor magnus, and piriformis. Evaluate for hyperesthesias or hypersensitivity of the skin and check superficial abdominal reflexes. Perform single digit palpation for trigger points. The abdominal wall tenderness test (Carnett’s test) is useful. In this test while the area of the abdominal tenderness is palpated, the patient voluntarily tenses the abdominal muscles by raising her head. If the pain is increased it suggests that the pain is of myofascial origin. If the pain is decreased it suggests that the pain is intraabdominal.11 Examine carefully for myofascial or trigger point pain syndrome.12 Block any trigger points in the abdominal wall prior to performing the pelvic exam to help differentiate between abdominal and vaginal pain components.12 Surgical scars should be noted. Palpation for hernial defects should be repeated. Palpate for Spigelian hernias just lateral to the lateral margin of the rectus sheath, feeling for tenderness or weakness in the fascia. Palpate the pubic symphysis for tenderness. Then perform the usual components of the abdominal examination. Lithotomy Examination: Inspect the external genitalia for redness, discharge, abscess formation, excoriation, perineal fistula, ulceration, pigment changes, condylomata, atrophic changes, or signs of trauma. Basic sensory testing to sharpness, dullness and light touch, as well as bulbocavernosus and anal wink reflexes should be done. A cotton tipped swab is used to evaluate the vestibule for localized tenderness of vulvovestibulitis. The vestibule, vulva, hymen, and area of the minor vestibular glands are palpated gently with a cotton tipped swab. Patients with vulvovestibulitis demonstrate exquisite tenderness in localized areas of minor vestibular glands just external to the hymen with normal sensation in the adjacent vestibular and vulvar areas. Palpate the vulva and pubic arch for trigger points. Pain or tension in the pelvic floor muscles can be assessed by palpation of levator ani muscles for tension and tenderness. The traditional speculum exam is done for full visual inspection and to obtain requisite cytologic and bacteriologic specimens. However, this is best done after all other tests have been performed. The manual portion of the pelvic exam is initiated with a single index finger noting any introital tenderness or spasm. Vaginismus is dyspareunia or inability to have coitus owing to the involuntary spasm of primarily the bulbocavernosus muscles, but sometimes the levator ani muscles too. Next the levator ani muscles are directly palpated for tone and tenderness. They lie adjacent to the lateral vaginal walls just above the hymenal ring. Identification may be confirmed by having the patient contract her pelvic muscles. Normally this palpation causes only a pressure sensation, but in patient’s with pelvic floor pain syndrome (PFPS) it may cause pain consistent with at least part of the patient’s clinical pain symptoms. Several names have been used for pelvic floor pain syndrome, such as pelvic floor myalgia, piriformis syndrome, levator ani spasm syndrome, and coccydynia. PFPS may also result from trigger points in one or more of the muscles of the pelvis. The most common finding with PFPS is tenderness and spasm of one or more of the levator muscles of the pelvic floor. The piriformis, coccygeus, and obturator internus muscles should be gently palpated bilaterally seeking tenderness that reproduces the patient's pain. The anterior vaginal, urethral, and trigonal areas should be gently palpated to elicit any areas of tenderness, induration, or thickening. The urethra should be massaged to elicit any secretions. The bladder base should also be evaluated for tenderness. Its presence is consistent with trigonitis or interstitial cystitis. With deeper palpation the cervix, paracervical areas and vaginal fornices should be palpated with a single digit for tenderness or trigger points. Cervical tenderness may suggest problems such as cervicitis, repeated cervical trauma, or pelvic infection. Vaginal forniceal tenderness may suggest problems such as pelvic infection, endometriosis, ureteral tenderness or trigger points. The uterus should be compressed against the sacrum to evaluate uterine tenderness. Uterine tenderness may be consistent with diseases such as adenomyosis, pelvic congestion syndrome, pelvic infection or premenstrual syndrome. A uterus that is immobile and fixed in position, especially a retroflexed position, may suggest endometriosis or adhesions. The coccyx should be palpated with a single digit and an attempt be made to move it 30 degrees or less. Normally the coccyx moves 30 degrees without eliciting pain, but in patients with coccydynia this movement elicits pain. The adnexal areas should be palpated next, still using a single digit without the use of the abdominal hand. It is the degree of tenderness and the similarity to the chief pain complaint that are clinically useful in evaluation of the ovaries. The traditional bimanual exam is the last portion of the pelvic exam in the pelvic pain patient. It is the least sensitive portion of the evaluation because it involves stimulation of all layers of the abdominal wall, the parietal peritoneum and the palpated organ or organs. A retroverted uterus in a patient with deep dyspareunia may indicate a malposition of the uterus and this can be treated with uterine suspension.10, 13 Rectal and rectovaginal exam are performed last. With rectal examination as one starts in the posterior midline and sweeps laterally and anteriorly, the rectal finger passes over the piriformis, the coccygeus, and then the levator ani muscles. Rectal examination should also include evaluation for rectal masses. Tenderness in the anal canal may suggest abscesses or fissures in the canal. Testing for occult blood should be performed. Laboratory and Imaging Evaluation Laboratory: Laboratory studies should be dependent on the history and physical examination and should be tailored to the patient. The individual signs and symptoms may indicate the need for cultures, serum, chemistry and electrolyte evaluations or specific enzyme tests. Urinalysis and urine culture are usually performed. Persistent irritative bladder symptoms of frequency and urgency associated with chronic pelvic pain with negative urinalysis and culture and sensitivity may suggest interstitial cystitis. STD Testing: It is reasonable to test for sexually transmitted diseases in women with CPP. Cervical cultures or smears for gonorrhea, chlamydia, as well as syphilis serology, hepatitis B surface antigen screening and HIV testing are all appropriate. In patients with nodularity on the uterosacral ligaments antibody screening for chlamydia can be helpful in distinguishing between inflammation and endometriosis.15 With negative chlamydia titers endometriosis was seen in 83% of patients with focal tenderness of the uterosacral ligaments on pelvic exam. With positive chlamydia titers 66% were found to have endometriosis.15 In women with vulvovestibulitis urinary oxalate levels may be useful, although this testing has been seriously questioned by many investigators. A urine drug screen is indicated if there is a past history of substance abuse. Porphyria is a rare diagnosis, but can occur in patients with CPP. Porphobilinogen (PPG) in the urine is at twice normal levels in these patients. In patients with diarrhea and pelvic pain, possible infection with Giardia, amoebae and other parasites should be evaluated by testing stool specimens for ova and parasites. Microscopic examination, stool cultures, and tests for C. difficile may be indicated. Blood Testing: Complete blood count and sedimentation rate should be done. These allow a determination regarding infectious or inflammatory presence and the hemoglobin and hematocrit to detect the presence of anemia. B12 and folate levels are important, especially in patients in whom the dietary intake is inadequate. Other blood tests, such as evaluation for insulin resistance, lupus, and viral syndrome is dependent upon the history and physical examination. Hormonal Assays: Ovarian remnant syndrome can be evaluated by testing for premenopausal levels of follicle-stimulating hormone (less than 40 mIU/ml) or estradiol (30 pg/ml or more). Thyroid function should be evaluated with TSH and free T4, as well as thyroid antibodies, to detect the presence of thyroid dysfunction including thyroiditis. CA125: CA125 may be elevated in endometriosis or leiomyomata, but there are many other causes that are not related to pelvic pain. As a diagnostic test, CA125 has low sensitivity and specificity. 14 Imaging Evaluation Abdominal and Pelvic Ultrasound: Ultrasonography can be valuable in women with leiomyomata. Transvaginal sonography may distinguish leiomyomas from adenomyomas. An adenomyoma usually appears as a disharmonious, circumscribed area in the myometrium with indistinct margins and echoic lacunae of various diameters. A leiomyoma is diagnosed with a nodular formation with well defined margins, heterogeneous structure, and variable echogenicity is detected in the myometrium. Ultrasonography may detect endometrial polyps or an unsuspected intrauterine device. Hysterosonography is usually effective in distinguishing endometrial thickening from endometrial polyps. Pelvic ultrasonography is also helpful if an adnexal cyst or mass is suspected. Abdominal wall ultrasound or CT scan may assist in the diagnosis of hernias of the linea alba and umbilical hernias. RADIOGRAPHY Plain Film: Plain films help with fractures, infection, ankylosing spondylitis, tumors, vertebral fractures, and osteophytes Barium Enema: Even in patients with intestinal endometriosis, evaluation of the intestinal tract is usually normal by barium enema. If inflammatory bowel disease is possible, barium enema and upper GI with small bowel follow through are often diagnostic. Barium enema is also helpful with diverticular disease. Hysterosalpingography: Although not commonly performed in women with CPP, it may detect uterine anomalies, endometrial polyps, or Asherman’s syndrome. It may also detect adenomyosis because the contrast medium may reveal short spicule-like structures extending 1 to 4 mm deep perpendicularly from the borders of the uterine cavity. Herniography: As inguinal and abdominal wall hernias may play a more important role in CPP than generally recognized, herniography can be a useful adjunct in diagnosis. However, it can be difficult to perform. Radiopaque contrast material is injected intraperitoneally and the patient is maneuvered through various positions in an attempt to introduce into and actual or potential hernia sac to demonstrate the sac radiographically. It can be helpful in evaluating the patient with unexplained groin pain. Herniography can also show obturator and perineal hernias. Culporectocystourethrography (CRCU) is a technique that uses radiopaque media in the urethra and bladder neck, vagina, rectum and anal canal to visualize dynamic changes of the pelvic organs caused by pelvic floor muscle activity. It is of use in women with CPP believed related to pelvic floor relaxation and possible pelvic floor pain syndromes. Pelvic Venography: Pelvic venography is performed in women with possible pelvic congestion syndrome and currently the only reliable way to diagnose this syndrome. Transuterine venography is performed by introducing water-soluble contrast medium into the uterine venous system via injection into the myometrium of the uterine fundus. Images are taken for 1 minute after injection. This method has a sensitivity of 91% and specificity of 89%. The images are scored based on the maximum diameter of the ovarian veins, time of disappearance of contrast, and the degree of congestion of the ovarian plexus. Selective ovarian venography has been used to diagnose pelvic congestion syndrome and can be performed via a jugular venous approach or a transfemoral approach. Computerized Tomography: Computerized Tomography (CT) may be diagnostically helpful in women with pelvic masses, but it is more expensive than sonography and not always necessary. In patients with suspected urinary tract involvement of endometriosis, ovarian remnant syndrome, ovarian retention syndrome, pelvic masses and so on, intravenous pyelography has been traditionally used, but CT with intravenous contrast is a more accurate and informational technique and is preferable in most cases. CT scans can also help identify urinary tract calculi, sciatic hernias, umbilical hernias and linea alba hernias, as well as Spigelian hernias. CT can also identify herniation into an incision site, as well as Spigelian hernias. It can be helpful in identifying abdominal tuberculosis. Musculoskeletal sources of pelvic pain are more readily identified with CT than with plain films. Magnetic Resonance Imaging: MRI using T2 weighted image with fat suppression shows diffuse adenomyosis as distorting the normal zonal anatomy of the uterus, causing enlargement of the junctional zone and shows this as a wide band with low signal intensity adjacent to the endometrium. MRI is also helpful in the evaluation for obstructive uterine anomalies in adolescents with endometriosis. It is also commonly used to evaluate possible spinal disc pathology, ligamentous tears, spinal cord tumors, as well as osteochondritis. URODYNAMIC TESTING & INTERAVESICAL POTASSIUM SENSITIVITY TEST Urodynamic testing is indicated in the woman with CPP if chronic urethral syndrome is suspected. Voiding and EMG studies reveal prolonged or intermittent voiding patterns and hyperactivity of the pelvic floor or external urethral sphincter. Urodynamics may also reveal uninhibited bladder contractions. Uroflowmetry also demonstrates the erratic, prolonged flow characteristic of vesical-sphincter dyssynergia. Pelvic floor EMG and pressure studies can also objectively document muscle spasms and inability to relax during voiding. The intravesical potassium sensitivity test can help identify the presence of the bladder origin pain of interstitial cystitis. A positive potassium sensitivity test is a valid indicator of abnormal epithelial permeability.16 Of 134 pelvic pain patients, 114 (85%) had positive potassium sensitivity. Positive sensitivity rates were similar across all clinical diagnosis including endometriosis, vulvodynia, and pelvic pain. A total of 75% of the subjects reported urologic symptoms, but only 2.9% received an initial diagnosis of interstitial cystitis.16 Gastrointestinal Function Testing: In patients with CPP and intractable constipation, anorectal manometry may be indicated. Patients with Hirschsprung disease or intestinal neuronal dysplasia may have loss of the recto-anal inhibitory reflex. Nerve Conduction and Electromyographic Studies: Electrophysiologic studies of nerve function may help in the localization and assessment of severity of compression or entrapment neuropathies. Anal electromyography (EMG) and measurement of pudendal nerve terminal latency (PNTML) are of value in assessing the electrical activity of the pelvic floor. EMG is particularly useful in diagnosing paradoxical puborectalis contraction and in revealing neuromuscular damage related to chronic straining. The technique of measuring PNTML is of use in assessing pudendal nerve injury and in discovering intrinsic neurologic injury to the striated and sphincter muscles of the pelvic floor. In patients with CPP, injury to pudendal nerve may be the cause of both their pain and the accompanying constipation. Endoscopy: Cystourethroscopy: Diseases associated with CPP that are best diagnosed by cystourethroscopy are interstitial cystitis, urethral diverticulum, urethral syndrome, radiation cystitis and bladder neoplasia. It is also helpful when chronic urinary tract infections; urolithiasis and uninhibited bladder contractions are considered in the differential diagnosis. Of the urologic diagnoses, interstitial cystitis (IC) appears to be the most common in women with CPP. In Howard’s study of 197 women with CPP as a presenting complaint, 4 (2%) were diagnosed with IC.17 This is at substantial variance with the 85% figure of Parsons.16 The role of interstitial cystitis in chronic pelvic pain still remains to be determined. Hysteroscopy: One-third of women with CPP have a uterine abnormality at the time of hysteroscopy. These findings, which include submucous leiomyomas, intrauterine polyps, cervical stenosis, intrauterine scarring, uterine septum and hyperplasia, are not necessarily contributing to the pain that the patients are experiencing. Hysteroscopy may also be of assistance in identifying adenomyosis. However, the role of hysteroscopy in the evaluation of a woman with CPP is not established. It is also not clear that treatment of hysterscopically found disease will affect the patient’s pain. However, since the procedure is quick and safe to do in the hands of an experienced surgeon, hysteroscopy should be done routinely at the time of laparoscopy for CPP.18 However, according to the ACOG 1996 technical bulletin on CPP, hysteroscopy is of little value in the evaluation of CPP.1 Laparoscopy: In selected cases, diagnostic laparoscopy may be helpful in evaluation and treatment of patients experiencing CPP. Laparoscopy is of greatest value when the pelvic examination is abnormal or when initial therapy fails.1 A survey of published laparoscopy series suggest that over 40% of gynecologic laparoscopies are done for CPP.4 Published series show that no visible pathology is detected in 35% of patients.19 Endometriosis is the most common pathologic diagnosis (approximately 33%), followed by adhesive disease (24%).19 Laparoscopy and Endometriosis: Sampson defined endometriosis as the presence of ectopic tissue which possesses the histologic structure and function of the uterine mucosa and this remains the currently accepted definition.20 The common sites in the pelvis and abdomen that must be closely inspected include the ovaries and ovarian fossae, pelvic peritoneum (particularly the cul-de-sac, periureteral and bladder peritoneum), uterine ligaments, sigmoid colon, appendix, fallopian tubes, and rectovaginal septum. Konickx, in a study of 716 women with endometriosis, found the following anatomic distributions: cul-de-sac and uterosacrals, 69%; ovaries, 45%; ovaricae, 33%; and vesical uterine fold 24%.21 One of the advantages of laparoscopic evaluation for endometriosis is the potential to treat it at the same time as the diagnostic evaluation. The technical objectives of surgery are: (A) to restore normal pelvic anatomy, and (B) to resect, coagulate and vaporize all endometriosis implants.22 However, good response to the surgical treatment of endometriosis depends on the skill of the surgeon, and the amount of time taken to destroy all of the endometriosis, including deep disease. Medication therapy, which gives similar response rates and pain control, does not depend on surgical skill and does not entail surgical risks.23 Therefore an alternative approach to the treatment of chronic pelvic pain is treatment with a GnRH agonist after NSAID’s and OC’s have failed to adequately treat the pain. In a high-quality, randomized, placebo controlled trial, Ling and colleagues demonstrated the efficacy of this treatment algorithm.24 In this study, the women treated with Depot leuprolide had significantly more improvement in pelvic tenderness and pelvic induration than the women treated with placebo. Laparoscopy and Adhesions: The physical appearance of adhesions is not specific to the underlying cause, so etiology is usually assigned based on the associated history or surgical diagnosis of PID, endometriosis, perforated appendix, prior surgery or inflammatory bowel disease.25 Preoperative history of at least one these etiologies is present in about 50% of women with pelvic adhesions.26 However one-half of women with adhesions have no historical reason for them, and more than one-fourth of women with adhesions have no preoperative findings by their history and physical examination that suggest the presence of adhesions. The only definitive way to diagnose adhesions is by surgical visualization. This is usually done by laparoscopy. The presence of pelvic adhesions in not a reliable predictor of pelvic pain. Laparoscopic studies reveal adhesions in 24% of CPP patients and 17% of non-CPP patients.26 Chronic PID, in which adhesive disease has a significant role, has not been a common laparoscopic diagnosis in CPP patients. It represents 5% of all diagnoses.27 It has been difficult to definitively demonstrate that adhesions cause CPP and it has been difficult to show that adhesiolysis relieves CPP.27 Laparoscopy and Ovarian Cyst: Laparoscopic evaluations of patients with CPP reveal ovarian cysts in only 3% of all cases.27 The issue of when or if ovarian cysts are cause of CPP is clinically important because the ovaries tend to form significant adhesions when surgically manipulated and such adhesions may cause CPP or infertillity. Clearly surgery on the ovary is best avoid unless benefits are likely, a judgment that is not always easy.28 Laparoscopy and Pelvic Varicosities: It is possible to visualize pelvic varicosities at laparoscopy by decreasing the intraabdominal pressure and gradually placing the patient in reverse Trendelenburg position. However, transuterine pelvic venography and retrograde ovarian venography that demonstrate increased uterine or ovarian venous diameters, venous stasis, and venous congestion are the recognized techniques of diagnosis.28 CAUSES OF CHRONIC PELVIC PAIN Endometriosis Adhesions Pelvic Varicosities There are no symptoms that uniquely identify genitourinary structures as the source of a patient’s pain. For this reason all patients require a thorough and wide ranging evaluation that includes assessments of other organ systems and structures, in addition to genitourinary structures.1 (Table 1.1) Adhesions Adnexal cysts Chronic ectopic pregnancy Chlamydial endometritis or salpingitis Endometriosis Endosalpingiosis Ovarian retention syndrome (residual ovary syndrome) Ovarian remnant syndrome Ovarian dystrophy or ovulatory pain Pelvic congestion syndrome Postoperative peritoneal cysts Residual accessory ovary Subacute salpingooophoritis Tuberculous salpingitis Gynecologic-Uterine Adenomyosis Atypical dysmenorrhea or ovulatory pain Cervical stenosis Chronic endometritis Endometrial or cervical polyps Intrauterine contraceptive device Leiomyomata Symptomatic pelvic relaxation (genital prolapse) Urologic Bladder neoplasm Chronic urinary tract infection Interstitial cystitis Radiation cystitis Recurrent, acute cystitis Recurrent, acute urethritis Stone/urolithiasis Uninhibited bladder contractions (detrusor-sphincter dyssynergia) Urethral diverticulum Urethral caruncle Gastrointestinal Neurologic dysfunction Carcinoma of the colon Chronic intermittent bowel obstruction Colitis Constipation Diverticular disease Inflammatory bowel disease Irritable bowel syndrome Musculoskeletal Abdominal wall myofascial pain (trigger points) Chronic coccygeal pain Compression of lumbar vertebrae Degenerative joint disease Disk Faulty or poor posture Fibromyositis Hernias: ventral, inguinal, femoral, Spigelian Low back pain Muscular strains and sprains Neoplasia of spinal cord or sacral nerve Neuralgia of iliohypogastric ilioinguinal, and/or genitofemoral nerves Pelvic floor myalgia (levator ani spasm Piriformis syndrome Rectus tendon strain Spondylosis Other Abdominal cutaneous nerve entrapment in surgical scar Abdominal epilepsy Abdominal migraine Bipolar personality disorder Depression Familial Mediterranean fever Porphyria Shingles Sleep disturbances Somatic referral 29 In this section the characteristics of two or three of the primary causes or contributors to CPP from each section will be discussed. ENDOMETRIOSIS: Introduction Endometriosis is the presence of ectopic endometrial glands and stroma – that is endometrium located outside of the uterine cavity. In women who undergo a laparoscopy to evaluate chronic pelvic pain the prevalence of endometriosis ranges from 2% to 80%. In patients who have been evaluated carefully for other sources of chronic pelvic pain and in whom a laparoscopy is deemed essential for evaluation of gynecologic causes of pelvic pain, the range has been 74% 30 to 80% 31. Additionally, it appears that about 70% of women with endometriosis have some type of pelvic pain symptoms.32 It is accepted that endometriosis can cause dysmenorrhea, dyspareunia, and other pelvic pain. however, it has been observed that the severity of pain frequently does not correlate with the severity of the endometriosis. 33 Etiology None of the theories proposed alone explains the protean manifestations of endometriosis or the predilection of some women to symptomatic endometriosis. 33 Sampson’s theory is that endometriosis is due to retrograde flow of menstrual effluent through the fallopian tube into the peritoneal cavity.20 Metaplasia of coelomic epithelium, the epithelium from which the Mullerian duct is derived, can result in endometrium. The theory of lymphatic and vascular metastasis is invoked to explain the occurrence of endometriosis in remote locations. A defect of the immunologic system is supported by a good deal of research and helps to explain why not all women develop endometriosis secondary to retrograde menstruation. It also ties into the theory of genetic predisposition because any immunological disorder may well be inherited.33. Endometriosis cells have been found to have an abnormal production of aromatase cytochrome P450, an enzyme that is not present in normal endometrium and is integral to the conversion of androstenedione and testosterone to estrogen. This ability to produce estrogen locally may directly stimulate the growth of endometrial cells of endometriotic lesions. Also, there are several clinical observations that suggest that the development and persistence of endometriosis is estrogen dependent. 33 Estradiol levels of 10 to 20 pg/ml usually result in atrophy of endometriotic lesions and levels greater than 60 pg/ml usually are associated with growth of endometriotic lesions. 34 Pathology based on the gross appearance of lesions are often categorized into atypical and typical lesions. Atypical lesions are often non-pigmented and difficult to see. They tend to be superficial with 2 mm of infiltration or less. In contrast, typical lesions tend to be deeply infiltrating. The atypical lesions can be symptomatic and may actually be the most metabolically active endometriosis. The presence of pelvic pain does not correlate specifically with either typical or atypical lesions. 33 The gross appearance of endometriosis is frequently insufficient to make a diagnosis because endometriosis is a pathologic diagnosis. To definitively diagnose endometriosis one must see histologically both the endometrial glands and stroma. Symptoms or History Endometriosis is a disease of women of reproductive age, so most women with endometriosis associated pain are 20 to 45 years of age. Seventy percent of women with endometriosis and CPP are nulligravid. Women with endometriosis present with one or more of the following triad: an adnexal mass (endometrioma), infertility, or pelvic pain. 33 Seventy-five percent of women with endometriosis associated pelvic pain have dysmenorrhea as a component of their pain symptoms. Dyspareunia with deep penetration is also a frequent component of endometriosis associated pain, occurring in 8% to 33% of cases. It may also continue postcoitally for several hours. When dyspareunia is referred to the rectum or lower sacrococcygeal area it may suggest rectovaginal septum or uterosacral ligament involvement. Abnormal uterine bleeding, particularly intermenstrual bleeding, may occur in women with endometriosis. Intestinal involvement occurs in 12% to 37% of women with endometriosis. Severity of symptoms does not correlate with the extent of involvement. Urinary tract involvement occurs in 10% to 20% of women with endometriosis. Endometriosis may rarely cause significant pulmonary symptoms with lung involvement. 33 Signs or Examination In many women with endometriosis – associated pelvic pain – the physical examination is completely normal. In other there is tenderness only during menses. For this reason it is sometimes helpful to do the examination during the first day or two of menstrual flow in women with suspected endometriosis. 33 Focal tenderness may be noted in women with endometriosis. Ripps and Martin found that 76% of women with endometriosis had focal tenderness at the site of one or more of their endometriosis lesions. 15 A fixed retroverted uterus with tenderness posterior to it is suggestive of endometriosis. Tender nodularity of the uterosacral ligaments and cul-de-sac on rectovaginal exam may be present. Narrowing of the posterior vaginal fornex or asymmetry of the position of the cervix, as well as cervical stenosis may be present. 33 Diagnostic Studies Martin et. al. found that with increased awareness of atypical lesions and liberal use of biopsies, the frequency of diagnosis of endometriosis at laparoscopy markedly increased (from 42% in 1982 to 72% in 1988). 35 With laparoscopy small lesions of 180 to 400 micrometers may be seen with “near contact” laparoscopy. Chronic pelvic pain is the reason for 40% of laparoscopies and a cause is diagnosed in only about 40% of these procedures. 4 If laparoscopy is performed it is important to realize that endometriosis presents with a variety of appearance. Laparoscopic visual diagnosis may be inaccurate in some cases. Atypical lesions generally mean red, yellow, white or clear lesions, whereas typical refer to the black – brown, black, or puckered black stellate scar lesions. In a study of 716 women with endometriosis, Koninckx et. al. found the following anatomic distributions: cul-de-sac and uterosacrals 69%; ovaries 45%, fossa overica 30, 33%; and vesicouterine fold 24%. Endometriosis can also occur in other sites such as the appendix. 21 Misdiagnoses are likely if the traditional pattern of seeking only black lesions is followed, but solely visual diagnosis can lead to over-diagnosis, because by appearance the following lesions have been confused with both typical and atypical endometriosis: hemangiomas, old suture, ovarian carcinoma, residual carbon deposits from prior surgery, ectopic pregnancy, adrenal cortical rest, Walthard rest, epithelial inclusions, reaction or oil-based hysterosalpingogram medium, inflammatory cystic inclusions, inflammation with or without Psammoma bodies, endosalpingiosis, submesothelial microbleeding, and normal peritoneum. Ling and The Pelvic Pain Study Group concluded that Depot leuprolide confirms the clinical diagnosis of endometriosis as well as laparoscopy. 24 Therefore the ACOG practice bulletin concluded that therapy with GnRH agonist is an appropriate approach to the management of chronic pelvic pain even in the absence of surgical confirmation of endometriosis. However, the initial evaluation must fail to demonstrate some other cause of pelvic pain. 36 Based on this information it is appropriate for the physician to either proceed with laparoscopy for diagnostic study to confirm endometriosis or proceed with a therapeutic trial of GnRH agonist if the initial evaluation failed to demonstrate some other cause of the pelvic pain. A preoperative ultrasound is prudent before a laparoscopic evaluation for CPP so that the surgeon is prepared for the treatment of an endometrioma at the time of surgical evaluation. About 15% to 20% of women with endometriosis have endometriomas, generally ranging in size from 3 to 8 cm and they are not always palpable on examination. 33. Management and Treatment There are many different medical and surgical treatments for endometriosis associated pelvic pain. The general treatment options are observation with palliative treatment, conservative surgery, hormonal suppression, combined medical and surgical treatments and definitive extirpative surgery. None of these can be considered ideal for all patients. The medical treatments for endometriosis include oral contraceptives, medroxyprogesterone acetate, Danazol, and gonadotropin-releasing hormone analogues (GnRH analogues). The technical objectives of surgery are to restore normal pelvic anatomy and to resect, coagulate, or vaporize all endometriotic implants. 37 The technical objectives can be accomplished with a number of different surgical techniques, but pain relief does not always follow. There is only one placebo controlled double-blind, randomized clinical trial of surgical treatment published by Sutton 38 in 1994 which used laser energy to destroy the endometriotic lesions. An average decrease in pain of about 50% was found 6 months after laser laparoscopy due solely to the effect of the treatment. Medical therapy with gonadotropin-releasing hormones in patients with laparoscopically diagnosed endometriosis resulted in a 47% 5-year treatment success in a separate study. 39 When patients have a recurrence of pain within 1 year of treatment, re-treatment with GnRH analogues appears to be fairly effective with about two-thirds of patients showing a significant reduction of pain levels during re-treatment. 40 When re-treatment with GnRH analogues is used or when treatment with GnRH analogues is given to a patient with low bone density, add-back therapy with very low dose estrogen or with oral norethindrone acetate can be used. Bisphosphonate therapy can also be given. Surgical therapy for laparoscopically diagnosed endometriosis or medical therapy for either laparoscopically or clinically diagnosed endometriosis has similar long-term results. If surgical therapy is applied first, medical treatment may be initiated if patients have persistent or recurrent pain, or if the physician suspects untreated disease remains. The physician must recognize that the finding of endometriosis in women with CPP does not ensure that medical or surgical treatment of endometriosis will result in effective relief of pain. Although treatment of endometriosis in women with pelvic pain is clearly indicated based on randomized, placebo-controlled, double-blind clinical trials, pain relief of 6 or more months duration due to treatment can be expected in only about 40% to 70% of women with endometriosis associated CPP. 33 ADHESIONS Introduction: Adhesions are fibrous tissue by which anatomic structures abnormally adhere to one another. Their role as a cause of chronic pelvic pain (CPP) is controversial. Intraabdominal and pelvic adhesions are found at laparoscopy in about 25% of women with CPP. This is a higher incidence than generally reported in women without CPP (25% versus 17%) suggesting an association between adhesions and CPP. 4 If adhesions cause CPP, then adhesiolysis might be expected to relieve pain. However, the only randomized trial of adhesiolysis failed to show any significant improvement in pain symptoms after lysis of adhesions by laparotomy, compared to a surgical control group that did not undergo adhesiolysis. 41 However, a number of observational studies have shown significant improvement in pain in women with CPP after adhesiolysis, suggesting that adhesions may contribute to CPP. 42, 43 Symptoms and Signs: Adhesions contain nerve fibers suggesting that pain originates in the adhesions themselves 44, 45 The adhesions, therefore, that are most likely to be symptomatic are those under tension or those restricting normal organ mobility, presumably resulting in stretching that stimulates the nociceptors in the adhesions or peritoneum. 46 Therefore adhesions are believed to cause pelvic pain that is made worse by sudden movements, intercourse, or certain physical activities. Often the pain is consistent in location. A history of one of the classic causes of adhesions-pelvic inflammatory disease, endometriosis, perforated appendix, prior abdominopelvic surgery, or inflammatory bowel disease- makes this a more likely diagnosis. 46 Diagnosis: The only definitive way to diagnose adhesions is by surgical visualization. Laparoscopy is the gold standard for diagnosing pelvic adhesive disease. Conscious pain mapping may help in determining whether adhesions that are present are likely to be responsible for the pain that the patient is experiencing. Treatment: The preferred method of treatment of adhesions is by laparoscopic adhesiolysis. Because many patients undergoing laparoscopy for treatment of adhesions have histories of prior abdominopelvic surgery, the risk of periumbilical, omental, or bowel adhesions is significant. A left upper quadrant Veress needle and 5 mm trocar placement insertion allows visualization in an area that is very rarely affected by adhesions. 46 After surgical adhesiolysis strategies for preventing recurrence should be considered such as placing barriers in localized areas of tissue injury. PELVIC VARICOSITIES AND PELVIC CONGESTION SYNDROME Introduction: Pelvic congestion syndrome (PCS) is a syndrome associated with pelvic varicosities and congestion (slow drainage of dilated pelvic veins and resultant stasis) characterized by pelvic pain and dyspareunia. 47 Pelvic congestion syndrome may result from anatomic dysfunction (venous overload and/or valvular incompetence); orgasmic dysfunction (vasocongestion occurs during the plateau phase); psychosomatic dysfunction; hormonal dysfunction (varicosities seen with PCS could be “a result of relaxation of the smooth muscle in the walls of the pelvic veins caused by some vasoactive substance as yet unidentified) 48 or iatrogenically induced dysfunction (post tubal ligation syndrome after destructive mid segment tubal sterilization procedures) 49 Symptoms: Dull aching pain in the pelvic area with occasional acute exacerbations of sharp pain. Low back ache, apparently a result of generalized congestion and increased uterine size has also be frequently reported. Sexually related pain is very common. Deep dyspareunia is one of the most consistent symptoms of PCS with an incidence ranging from 71% to 78% 50 Dysfunctional uterine bleeding occurs in 54% of women with PCS. Vaginal discharges are also a common symptom, most often being clear and mucoid in nature.50 Signs: Superficial vulvar and paravulvar varicies have often been described. Abdominal palpation reveals tenderness at the ovarian point, which lies at the junction of the upper and middle thirds of a line drawn from the anterior superior iliac crest to the pubic symphysis. Deep abdominal pressure at this point reproduces the pelvic pain complained of by the patient. Ovarian point tenderness on abdominal palpation with post coital ache has been found to be 94% sensitive and 77% specific for pelvic congestion as confirmed by pelvic venography 50 The cervix is often blue because of engorgement and there is frequently an excessive, clear mucoid discharge. Bimanual examination of the cervix elicits pain and tenderness on movement. The uterosacral ligaments and parametrium are also tender. 47 Diagnostic Studies: It is possible to visualize varicosities at laparoscopy by decreasing the intraabdominal pressure and gradually placing the patient in a reverse Trendelenburg position. Pelvic venography has an advantage in its ability to provide a detailed picture of the pelvic venous anatomy, the exact location of any varicosities, and grading of their severity. Both transuterine and selective retrograde ovarian venography have been described. 47 Ultrasound can be used in all patients suspected of having pelvic congestion. The presence of linear or circular anechogenic structures of a diameter greater than 5mm and lateral to the uterus and cervix, that increase by Valsalva or by standing suggest pelvic varicies. 51 Treatment: Surgical treatment includes hysterectomy and ovarian vein ligation. Twenty-two percent of patients had persistent pelvic pain after hysterectomy in the Stovall group. 52 When oophorectomy was added to the hysterectomy a dramatic improvement in pain scores was observed in all patients. 53 If hysterectomy is performed, bilateral salpingo-oophorectomy is recommended since failure to remove the ovaries has lead to recurrent pain. 54, 52 Ovarian vein ligation has been used for pelvic congestion, but a review of a number of studies dealing with this procedure showed that only 52% of patients were cured, 17% showed improvement and the remainder had no change in symptoms. 47 Ovarian hormones are important in the etiology of pelvic congestion syndrome and medical therapy can be applied to reduce the impact of hormones. Suppression of ovarian function using 30 mg of medroxyprogesterone acetate daily for 6 months in 22 women with lower abdominal pain caused by pelvic congestion resulted in 17 of these women (77%) having a venographically demonstrable reduction in pelvic congestion and a statistically significant reduction in pain scores. 55 However, oral contraceptives did not relieve pelvic congestion and ovarian suppression alone is not enough as it is not generally a feasible long-term treatment. It may be beneficial for short-term treatment until a more permanent solution to the patient’s symptoms is found. Radiological: Radiologic transcatheter embolization of the ovarian veins has been used with various degrees of pain relief. More prospective studies are needed to determine its eventual role in the management of PCS. 47 GYNECOLOGIC-UTERINE CAUSES OF PELVIC PAIN Adenomyosis Dysmenorrhea Dyspareunia ADENOMYOSIS Introduction: Adenomyosis is an ingrowth of endometrial glands and stroma into the myometrium at least 1 or 2 higher power fields from the endometrium. Ectopic glands and stroma of adenomyosis should be located at least 2 to 3mm below the endometrial surface. 56 Adenomyosis was first described by Rokitansky in 1860. 57 Women less than 30 years of age account for about 17% of cases. Eighty percent of cases are found in the fourth and fifth decades of life. Adenomyosis occurs when the normal boundary between the basal layer of the endometrium and the myometrium is breached. Since 80% to 90% of cases are found in parous patients, it has been suggested that uterine trauma of childbirth or postpartum endometritis might cause initial break in the normal boundary. 58 Adenomyosis is characterized by the presence of a diffusely enlarged uterus caused by the benign invasion of the myometrium by endometrial glands and stroma. This ectopic tissue is associated with hypertrophy and hyperplasia in the myometrium. The adenomyotic foci may be diffusely distributed throughout the endometrium or can be well localized leading to the formation of adenomyomas. Symptoms and History: The classic description is abnormal uterine bleeding associated with dysmenorrhea in a parous woman who has a regularly enlarged, slightly tender uterus. However, the diagnosis is confirmed histologically in only 20% of cases. In addition not all women with adenomyosis are symptomatic. It has been reported as an incidental finding in 19% to 35% of women undergoing hysterectomy. 59 The mechanism for the development of menorrhagia in patients with adenomyosis is unclear. Dysmenorrhea probably occurs when the volume of adenomyotic lesions exceeds a certain threshold percentage of total uterine volume. It has been noted that when the glandular invasion of adenomyosis exceeds 80% or more of the myometrium. 60 Signs and Examination: Physical examination usually shows a symmetrically enlarged, tender uterus less than 14 weeks size when an exam is performed just prior to or during menses. The uterus is diffusely boggy to palpation or it may have a nodular consistency. Only 2% to 26% of cases are diagnosed preoperatively. 56 Diagnostic Studies: With hystosalpingography (HSG) some contrast material may fill short spicule-like structures extending perpendicularly from the borders of the uterine cavity 1 to 4mm deep. 61 On transvaginal sonography adenomyoma is diagnosed as a disharmonious, circumscribed area in the myometrium with indistinct margins and anechoic lacunae of various diameters. The most suggestive sonographic finding of adenomyosis was generalized uterine enlargement with conservation of normal myometrium architecture. Magnetic resonance imaging provides excellent soft tissue contrast, is minimally invasive and avoids ionizing radiation. On T2 weighted images diffuse adenomyosis distorts normal zonal anatomy of the uterus, causing enlargement of the junctional zone seen as a wide band with low signal intensity adjacent to the endometrium. Adenomyosis appears as a diffuse, ill-defined lesion extending adjacent to the endometrium. In a prospective study conducted on 93 women, an accurate diagnosis was obtained in 92 of these. In one case of nodular adenomyosis, MRI could not distinguish this from a degenerating myoma. 62 D&C rarely establishes a diagnosis of adenomyosis. Diagnostic hysteroscopy alone is not sufficient for a diagnosis of adenomyosis. Hysteroscopic myometrial biopsy is required to confirm the diagnosis at hysteroscopy. The sensitivity of a single myometrial sample for diagnosing adenomyosis ranges from 8% to 19%. The specificity is 100%. 63 Management and Treatment: The principle method of diagnosis and therapy of adenomyosis is still hysterectomy. Conservative surgical interventions combined with medical treatment can be applied in specific instances to improve chances for fertility. GnRH agonists may provide temporary relief of symptoms. Because estrogen synthesis is higher in adenomatous tissue than in normal myometrium and endometrium, Danocrine can be used to suppress symptoms of adenomyosis. Danocrine blocks aromatase activity in adenomyosis in cell cultures64 DYSMENORRHEA: Introduction: Dysmenorrhea is the term applied to severe cramping pain in the lower abdomen, lower back, and upper thighs that occurs during menses. Severe dysmenorrhea should not be tolerated as a normal part of femininity. 65 Seventy-two percent suffer from primary dysmenorrhea among a cohort of 586 nineteen year old women. Mild symptoms were reported by 34%, moderate by 23%, and severe by 15% of the women surveyed. 66 Dysmenorrhea is classified as primary dysmenorrhea when no pelvic pathology is found that accounts for the painful menstruation. Secondary dysmenorrhea is diagnosed when there is pelvic pathology that is believed to cause pain with menstruation. Etiology: Primary dysmenorrhea is due to principally prostaglandins released from the endometrium at menses, in particular F2α and E2. PGF2α produces uterine cramps and pain, diarrhea, vomiting, headache, and syncope when injected intravenously. In women with primary dysmenorrhea there is an abnormal increase in prostaglandin levels that leads to excessive, abnormal uterine contractions. Increase intrauterine pressure leads to uterine ischemia and accumulation of anaerobic metabolites. The most intense pain occurs during the phase of decreased flow when contraction amplitude exceeds 200 mm Hg. 67 Also intermediate products in prostaglandin synthesis have direct pain producing properties. Circulating vasopressin levels also increase fourfold in patients with primary dysmenorrhea. Purely psychological factors are rarely, if ever, the cause of dysmenorrhea. Psychological factors may significantly affect dysmenorrhea by either intensifying or diminishing the severity of the pain. 65 Secondary dysmenorrhea is due to a pathological condition within the pelvis. Cervical stenosis may be congenital, secondary to infection, or iatrogenic due to conization or cryocautery. The resultant narrowing impedes menstrual flow and increased intrauterine pressure at menses. Other causes include adenomyosis, leiomyomata, endometrial polyps, congenital malformation, as well as extrauterine causes including endometriosis, pelvic inflammatory disease, pelvic tuberculosis, pelvic congestion syndrome, Allen-Master’s syndrome, imperforate hymen, and iatrogenic causes such as an intrauterine conception device. Symptoms: Primary dysmenorrhea begins 6 to 12 months after menarche and coincides with the onset of ovulatory cycles. Patients complain of spasmodic or cramping lower abdominal pain that may radiate suprapubically, to the low back, and to the anterior medial aspects of the thighs. Other symptoms such as headache, nausea, vomiting, diarrhea, and fatigue often accompany menstrual pain. Symptoms typically last 48 hours or less. Secondary dysmenorrhea tends to start at a later age than primary dysmenorrhea. Pain starting before menstruation is often due to pelvic inflammatory disease, pelvic congestion syndrome, endometriosis, or premenstrual syndrome. 68 Signs: Abnormal physical exam findings suggest dysmenorrhea is secondary. Primary dysmenorrhea is a diagnosis of exclusion. The general physical exam and pelvic exam reveal no abnormalities. Diagnostic Studies: No laboratory tests are diagnostic or specific in primary or secondary dysmenorrhea. Treatment: Medical: Oral contraceptives provide significant relief of primary dysmenorrhea. They suppress ovulation, resulting in lower levels of prostaglandins and also reduce spontaneous uterine activity. Non-steroidal anti-inflammatories (NSAIDs) that inhibit prostaglandin synthetase have a pivotal role in treating primary dysmenorrhea. Seventy-two percent of patients had significant relief with NSAIDs compared to placebo 69 With secondary dysmenorrhea therapy is directed at the underlying condition. Treatment: Surgical: Surgical interruption of neuropathways from the uterus may be done to decrease the pain of primary or secondary dysmenorrhea. Presacral neurectomy consists of transection of the sympathetic nerves of the superior hypogastric plexus at the sacral promontory. It has an efficacy of about 75% in relieving midline dysmenorrhea. 65 , 70 Secondary causes of dysmenorrhea are treated by their appropriate therapies. DYSPAREUNIA Introduction: Dyspareunia is recurrent or persistent pain that occurs with intercourse and is often a component of the symptoms complex of women with chronic pelvic pain. 71 Etiology: Entry dyspareunia, also termed introital dyspareunia refers to pain with initial penetration of the vaginal introitus. Causes of entry dyspareunia include anal fissure, Bartholin gland infection, Bartholin duct obstruction, chronic vulvitis, contact vulvovaginitis, episiotomy scar, hemorrhoids, inadequate sexual arousal, Mullerian abnormality, post-traumatic pubic symphysis pain, rigid hymeneal ring, urethral carbuncle, urethral diverticulum, urethritis, vaginal atrophy, vaginismus, vaginal dystrophy, vulvar vestibulitis, vulvodynia, and vulvovaginitis. Deep dyspareunia is painful intercourse with deep vaginal penetration. Causes of deep dyspareunia include adenomyosis, endometriosis, fixed uterine retroversion, inflammatory bowel disease, interstitial cystitis, irritable bowel syndrome, leiomyomas, ovarian pathology, pelvic adhesions, pelvic floor relaxation, pelvic inflammatory disease, radiation induced vaginal scarring, shortened vagina, and urethral syndrome. Symptoms and History: It is important to ask all women, including those with chronic pelvic pain, about their sexual activity. 71 A minimum of three questions should be a routine part of the history: Are you sexually active?; Are you having pain with intercourse?; and Do you have any problems of questions regarding your sexual activity?. Entry pain that involves the entire vulvar and introital area suggests vulvitis, vulvar dystrophy, or vulvodynia. Entry pain that is concentrated only at the vaginal opening may suggest vulvar vestibulitis, vaginismus, inadequate lubrication, or vulvovaginitis. Dyspareunia associated with endometriosis, adhesive disease, pelvic congestion syndrome, or retroverted uterus is usually deep dyspareunia and not infrequently characterized by continued aching for hours or days after coitus. Postcoital aching pain is a particular characteristic of pelvic congestion syndrome. 50 Signs and Physical Examination: Physical examination should be done so as to educate the patient and also allow her to direct the evaluation. Palpation with a moist cotton-tipped swab can identify exquisitely tender sites at the vestibule in patients with vulvar vestibulitis. This simple Q-tip test should be performed on all patients with dyspareunia. Palpation of the muscles of the pelvic floor can identify trigger points and tender points of the muscles that can contribute to dyspareunia. Reproduction of the patient’s pain with deep palpation of a retroverted uterus can indicate this is a source of the deep dyspareunia. Management and Treatment: Medical: Medical treatment can be applied for patients with inadequate lubrication. This may involve specific re-education regarding the couple’s sexual attitudes and practices. 71 Vaginismus is in many cases a condition response. Behavioral treatment through the use of biofeedback with electromyographic sensors, such as used for treatment of stress urinary incontinence, can be helpful. The treatment of pelvic floor myalgia is twofold. First, find and treat any persistent tissue injury that may be triggering the spasm (endometriosis or interstitial cystitis). Second, begin muscle retraining with physical therapy. This includes pubococcygeus and piriformis stretching, as well as biofeedback. Heat, exercise, and trigger point injections are also helpful adjuncts to full recovery. Management and Treatment: Surgical: Surgical treatment specific to diseases that may be the cause of deep dyspareunia such as endometriosis, adhesions, symptomatic uterine retroversion, or pelvic congestion syndrome is sometimes appropriate and therapeutic. The deep retroverted uterus can be repositioned using a laparoscopic approach as a primary procedure for the treatment of deep dyspareunia or as an adjunct to laparoscopic treatment of endometriosis. 72 The most common surgical treatment of vulvar vestibulitis is vestibulectomy, in which the vestibule is excised and the vaginal tissue is advanced to cover the defect. Success rates as high as 70% to 90% have been reported. 73 UROLOGIC CAUSES OF PELVIC PAIN INTERSTITIAL CYSTITIS Introduction: Interstitial cystitis (IC) is a chronic inflammatory condition of the bladder. The definition and diagnostic criteria are controversial, but most commonly it is defined clinically by the following triad: A) irritative voiding symptoms, B) absence of objective evidence of another disease that could cause the symptoms, and C) a characteristic cystoscopic appearance of the bladder. 74 IC occurs predominantly in women of 30 to 59 years of age. The incidence is not known, but has been estimated at 36 cases per 100,000 women in the United States. Pelvic pain is reported by up to 70% of women with IC and occasionally it is the presenting symptoms or chief complaint. 75, 76 Parsons recently reported that of 134 patients with chronic pelvic pain 85% had a positive potassium sensitivity indicating that their pain may have a bladder component (interstitial cystitis). 16 Etiology: The etiology of interstitial cystitis is unknown. Current thinking suggests that patients with IC have defects in the glycosaminoglycans layer of the bladder wall. This micellar layer acts as a barrier between transitional epithelial cells and urine. A defect in this layer allows “leaking” of the epithelium resulting in a dysfunctional epithelium with excessive permeability and exposure of the transitional epithelium and muscularis to noxious substances in the urine. 77 The mechanism by which the permeability or leakiness of the glycosaminoglycans layer occurs may be autoimmune. The physiological causes of pain with interstitial cystitis are also not clear. The inflammatory reaction of the bladder may cause nociceptor stimulation of visceral neural pathways. Such chronic visceral pain may result in spasm of the pelvic floor muscles (levator ani syndrome) with resultant pelvic pain. Symptoms and History: Unremitting frequency and urgency of urination are characteristic symptoms of IC. Patients give history of recurrent treatment for urinary tract infections. Nocturia with voiding three or more times per night is also a characteristic. Pelvic pain occurs in 50% to 70% of women with IC. The pain is suprapubic and it may radiate to the low back or groin. Patients also complain of dyspareunia. They also experience pelvic floor muscle spasm. Pain increases with bladder filling and decreases after voiding. Signs and Examination: Patients may have anterior vaginal wall tenderness under the trigone and suprapubic pelvic tenderness. Levator ani or piriformis muscle tenderness may be present. Diagnostic Studies: Urinalysis is generally normal. Twenty percent of patients have 5 to 10 white blood cells per high power microscopic field. The potassium challenge test is a useful diagnostic test. The patient rates her baseline pain level and the bladder is infused with 40 mL of sterile water and again she is asked to rate her pain level. The water is retained for 3 to 5 minutes. The water is then drained and 40 ml of a 400 mEq/L solution of potassium chloride is infused into the bladder. The patient again rates her symptoms. When a patient has a change of 2 or more on the pain or urgency scale with the potassium chloride solution, this is a positive test. The potassium challenge test is positive in 70% of patients with IC and is negative in 96% of patients who are normal. 74 Cystoscopy in patients with IC shows glomerulations on a second filling of the bladder together with linear cracking and Hunners ulcer. Management and Treatment: The therapy of interstitial cystitis can be a frustrating experience. Methods of therapy include hydrodistention of the bladder; autodilation; dimethylsulfoxide, 50%, intravesical; heparin either intravesical or subcutaneous; pentosan polysulfate oral; non-steroidal anti-inflammatory drugs; chromaline sodium; transcutaneous electrical stimulation unit; and cystectomy. The success rate of sodium pentosan polysulfate may be as high as 50%. Further studies are being done to determine if increases in dosage may result in improvement and symptomatic relief. GASTROINTESTINAL CAUSES OF PELVIC PAIN IRRITABLE BOWEL SYNDROME Introduction: Irritable bowel syndrome is a common functional bowel disorder of uncertain etiology characterized by chronic, relapsing pattern of abdominal-pelvic pain and bowel dysfunction with constipation and/or diarrhea. Symptoms suggestive of IBS are present in 50% to 80% of women with CPP. 78 IBS affects 15% of the population. It accounts for 3 million visits per year to primary care providers. The diagnostic criteria (“Rome” criteria of the International Congress of Gastroenterology) include: At least 3 months of continuous or recurrent symptoms of: 1) abdominal pain or discomfort that is: a) related with defecation b) and/or associated with a change in frequency of stools c) and/or associated with a change in consistency of stool and 2) two or more of the following, at least one-quarter of occasions or days: a) altered stool frequency b) altered stool form c) altered stool passage d) passage of mucus e) bloating or feeling of abdominal distention.79 Etiology: IBS is a functional disorder so no structural or biochemical abnormalities have been found that explain the symptoms. Patients with IBS who do not seek medical treatment do not have psychological profiles that are different from those of a control population without IBS. One potential explanation of IBS relates to the basal myoelectrical cyclic rhythm of the colon. Patients with IBS have a slow wave frequency one-half of that of normal, healthy individuals. Symptoms and History: The characteristic symptoms of IBS are abdominal pain, bloating, belching, excessive flatus, diarrhea, constipation, painful defecation, and the sense of incomplete evacuation. Abdominal pain is most often in the left lower quadrant. Either diarrhea or constipation, or alternating episodes of both may be present. Both pain and diarrhea resolve during sleep. IBS symptoms often exacerbate during menses. Signs and Physical Examination: Patients with IBS often seem anxious and tense. Otherwise the general physical exam is usually normal. Abdominal inspection may reveal mild to moderate distention. Tenderness may be elicited in the left lower quadrant or may be generalized. Diagnostic Studies: Irritable bowel syndrome is a diagnosis of exclusion. There is no one simple physical finding, blood test or x-ray that unquestionably confirms the diagnosis. Appropriate testing such as white blood cell differential, electrolyte studies, stool for ova and parasites, culture and sensitivity, and occult blood should be performed to rule out other causes of the patients symptoms. Management and Treatment: Treatment is directed to relief of symptoms. For gas and bloating a trial of an anti-spasmodic is suggested. For constipation symptoms a trial of increased roughage and psyllium is prescribed. In IBS patients with diarrhea – predominant symptomatology - loperamide (Imodium) is commonly used. MUSCULOSKELETAL CAUSES OF PELVIC PAIN ABDOMINAL WALL AND PELVIC MYOFASCIAL TRIGGER POINTS Introduction: A myofascial trigger point is a hyperirritable spot of skeletal muscle that is associated with a hypersensitive palpable nodule and a taut band. This spot is painful on compression and can give rise to characteristic referred pain, referred tenderness, motor dysfunction and autonomic phenomena. Myofascial trigger points are always tender, prevent full lengthening of the muscle, weakens the muscle and refers a patient recognized pain on direct compression, mediates a local twitch response of muscle fibers when stimulated, and when compressed within the patient’s pain tolerance, produces referred motor phenomena. 80 The prevalence of myofascial trigger points among patients complaining of pain anywhere in the body ranges from 30% to 93%. 80 In one study of 177 chronic pelvic pain patients 131 (74%) had abdominal wall trigger points which were found with needle localization uniformly identifying the source as fat and fascial planes above the aponeurosis. 12 In 71% of these patients’ focal pain areas were found in the vaginal wall. In 500 patients treated consecutively 15% were found to have primarily myofascial trigger points at sites including the abdominus rectus, obliques, levator ani, obturator internus, piriformis, iliopsoas, and adductors muscle as well as their musculoskeletal attachments. 81 The critical abnormality in the trigger point is a neuromuscular dysfunction at the motor end point of an extrafusal skeletal muscle fiber, implying that myofascial pain caused by trigger points (TrPs) is a neuromuscular disease. 80 Perpetuating factors act clinically like a missing link that converts acute muscle syndrome into a chronic pain syndrome. 82 These factors may be systemic or mechanical. Systemic factors increase irritability of the skeletal muscles throughout the body. Mechanical factors overload and aggravate TrPs in specific muscles. A patient with chronic pain due to myofascial TrPs usually has one or more perpetuating factors. The presence of significant perpetuating factors is confirmed by poor response to a trial of specific myofascial therapy applied to the muscle or muscles causing the myofascial pain. Systemic perpetuating factors include enzyme dysfunctions because of nutritional inadequacy, metabolic and endocrine dysfunction, chronic infection, and psychological stress. One time traumatic occurrences can activate TrPs, but are not responsible for perpetuating them. Situations that cause repeated or chronic muscular overload can activate TrPs and then perpetuate them. Mechanical stresses that tend to activate myofascial trigger points acutely include wrenching movement, automobile accidents, falls, fractures, joint sprains, dislocations, or direct blow to the muscle. Structural inadequacies, postural stresses, constriction of muscle and vocational stress and repetitive movements are all mechanical perpetuating factors for TrPs. Two common and closely related structural inadequacies are a short leg and a small hemipelvis. Symptoms and History: Myofascial TrPs may cause constant pain, intermittent pain or no pain. patients in constant pain caused by TrPs are usually unaware of activities that aggravate the pain. They already have such intense pain that they do not perceive an increase and thus cannot distinguish what makes it worse. Most patients with active TrPs experience intermittent pain that is characteristically aggravated by specific movements and may be alleviated, at least temporarily, by a certain position. These patients may have some relatively pain-free days. Latent TrPs give no primary pain clues and must be identified by postural changes, muscle dysfunction and physical examination. The onset of pain following activation of a TrP due to muscle overload can be delayed as long as 12 to 20 hours. Myofascial pain may start abruptly or gradually. Sometimes the pain was felt at the moment of stress. Acute onset events associated with TrPs in women include: adductor attachment TrPs resulting from force positioning in ballet; adductor attachment resulting from strenuous soccer movement; abdominal rectus, abdominal obliques, transversus abdominus and pyramidalis attachment TrP resulting from intense abdominal contraction exercise; levator ani TrPs resulting from split-level falls; obturator internus and adductor TrPs sustained after vigorous “frog-leg” kicks in swimming competition; multiple pelvic muscle TrPs sustained from “picket fence” type injuries; and multiple TrPs sustained from falls and repetitive activities involved in horseback riding and cheerleading activities. Myofascial TrP pain is characteristically aggravated by: 1) strenuous use of the muscles, especially in the shortened position, 2) passively fully stretching the muscle 3) pressure on the TrP, 4) placing the involved muscle in the shortened position for a prolonged period, 5) sustained or repeated contraction of the involved muscle, 6) cold, damp weather, viral infections and periods of marked nervous tension, 7) exposure to a cold draft, especially when the muscle is fatigued. Myofascial TrP pain is decreased by: 1) a short period of rest, 2) slow, steady passive stretching of the involved muscles, 3) moist heat applied over the TrP, 4) short periods of light activity with movement, 5) specific myofascial therapy. Signs and Physical Examination: The common clinical characteristics of an active myofascial TrP include the following components: 1) compression of the myofascial TrP elicits local and referred pain that is similar to the patient’s usual clinical complaint, 2) snapping palpation compression across the muscle fibers at the TrP elicits a local twitch response, 3) rapid repeated insertion of a needle into the myofascial TrP elicits a local twitch response, 4) painfully restricted stretch of motion of the involved muscle is present, 5) the muscle with the myofascial TrP may be weak due to inhibition caused by pain, 6) patients may also have localized autonomic reflex phenomena. An active TrP is one that produces a pain complaint such as spontaneous pain or pain in response to movement. A latent myofascial TrP is a localized spot that produces discomfort only response to compression. Spot tenderness, pain recognition and taut bands are the most reliable signs and the minimal criteria needed to identify a myofascial TrP. Diagnostic Studies: Laboratory studies are generally normal. Surface electromyography can be helpful because TrPs cause distortion of normal muscle function. The muscle with TrP shows evidence of threefold problem: it exhibits increased responsiveness, delayed relaxation, and increased fatigability. Intravaginal EMG readings of patients with levator ani TrPs consistently show hypertonus in the resting state and decreased excursion compared to normal with attempted maximal contraction. In addition, the fast twitch fibers activate more slowly and the slow twitch fibers show rapid degradation of activity. 83 Pressure algometry can quantify the sensitivity of myofascial TrPs and identify abnormal tenderness. Needle electromyography is helpful when spontaneous low-voltage motor endplate noise activity, as well as high voltage spike activity, is present. Blood testing for vitamin B12, folate, sedimentation rate, and C-reactive protein, TSH, free T4, thyroid peroxidase antibodies and thyroglobulin antibodies can be helpful. 83 Management and Treatment: Acute myofascial pain due to TrPs caused by a clearly identifiable strain of one muscle can usually be fully relieved and normal function restored. Usually, the longer the period between the acute onset of pain and the beginning of TrP treatment, the greater the number of treatments that will be required over a longer period of time. 80 Treatment is successful if after treatment the patient returns pain free with complete restoration of full range of motion and the prior TrP sites are no longer abnormally tender. If the pain relief was complete for some hours or days, one can assure the patient that a muscular cause of the pain is present and that it can be relieved. However, repeated treatment without first resolving the perpetuating factors that make the TrPs so hyperirritable may not be successful. A major effort should then focus on identifying and eliminating the perpetuating factors. Techniques of treatment of TrPs include: TrP release which include spray and stretch, voluntary contraction and release methods, TrP pressure release, deep stroking massage, and TrP injections. All of these techniques can be very beneficial when properly applied. 83 Biofeedback has also been demonstrated to be effective, especially for patients who experience severe chronic introital dyspareunia and tenderness of the vulvar vestibule resulting from hypertonus of the pelvic floor muscles. 84 HERNIAS Incisional Hernias Groin Hernias Femoral Hernias Sciatic Hernias Introduction: Hernia has been defined as a protrusion of organs or parts thereof from their natural place in a cavity through an abnormal opening. However, it is the hernial defect, the opening through which a protrusion may occur, that characterizes hernias, not the protrusion of a viscus. Consistent with this, the designation of various hernias uses not the protruded viscus but the location or region in which a hernia can take place. 85 Hernias can occur in the following locations: 1) Hernias of the pelvic wall, perineum, and pelvic floor (sciatic hernia, obturator hernia, perineal hernia); 2) Groin hernias (direct inguinal hernia, indirect inguinal hernia, femoral hernia); 3) Hernias of the abdominal wall (epigastric hernia, umbilical hernia, Spigelian hernia, incisional hernia); 4) Internal abdominal hernia (internal supravesical hernia and hernia through broad ligaments) 5) Sports hernias; 6) Pelvic floor support defects. Each of these hernias has characteristic symptoms and signs. 86 Of these three will be discussed: incisional hernias, groin hernias, and sciatic hernias. INCISIONAL HERNIAS: An incisional hernia is the abnormal protrusion of peritoneum through a separation of the edges of a musculoaponeurotic wound. They are common after open abdominal procedures and occur in 0.5% to 14% of abdominal operative procedures. Seventy percent occur within the first year and 97% within 5 years of surgery. 87 Incisional hernias occur after laparoscopy with risk of herniation through a 12mm trocar site (3.1%) approximately 13-fold greater than that for a 10mm trocar site (0.23%) 88 Laparoscopic incisional hernias can be prevented, however, by mass closure of the fascia an peritoneal layers under direct laparoscopic vision 89 Etiology: Infection, obesity, postoperative strain, inadequate suture material, and nerve injury are some of the etiological factors of incisional hernias. Symptoms and History: Patients may complain of intermittent pain or dragging sensation. They may also complain of distention and severe abdominal pain if they have herniated small bowel. Physical Examination: Palpation of the wound site may identify separation and tenderness in the area of the separation without a small bulge being present. When the patient is asked to cough a small bulge may be seen or a pulsation felt by the examining finger. Diagnostic Studies: The diagnosis of herniation into an incision site can be made by CT scan or ultrasonography. If only the separation is present without the protrusion of tissue, the diagnosis may be difficult without exploration. However, the defect can frequently be palpated and is a source of pain. Treatment: The treatment of the incisional hernia is surgical placement of graft material of an appropriate size for the hernia present. GROIN HERNIAS: Groin hernias include direct inguinal, indirect inguinal, and external supravesical which emerge through the abdominal wall by way of the external inguinal ring above the inguinal ligament and femoral hernia which emerges beneath the inguinal ligament by way of the femoral canal. The incidence of inguinal hernias is 10% to 15%. Indirect inguinal hernias are congenital, and direct inguinal and femoral hernias are considered acquired. 87 Etiology: The processus vaginalis is a diverticulum of the peritoneal cavity which is patent in 80% of 90% of newborns, but which closes until at adulthood 15% to 30% have a patent processus vaginalis. Many women with patent processus vaginalis remain asymptomatic. However, this is held to be a prime cause of indirect inguinal hernia. Three factors are involved in generating inguinal hernias: the presence of a performed sac, repeated elevation in the intraabdominal pressure, and weakening of the body muscles and tissues with time. Raised intraabdominal pressure, such as that which occurs during pregnancy, can make a hernia appear for the first time. The cause of hernia is multifactorial. In the case of indirect hernia, a performed sac (patent processus vaginalis), is present, but bowel is prevented from entering by efficient muscular action. A sudden and unusually high increase in intraabdominal pressure may be sufficient to overcome this protective mechanism and a hernia may quite suddenly appear. In direct hernia there is no performed sac; in fact there is no real peritoneal sac at all. The protective mechanisms fail. The weakened transversalis fascia, on its own, cannot withstand the repeatedly raised intraabdominal pressure and stretches or simply tears. Symptoms and History: The primary symptoms are pain, and in the case of an acute event, ecchymosis of the inguinal region. The patient may feel some discomfort in the groin and notice a small bulge when coughing or straining that immediately subsides. Physical Examination: Physical examination reveals tenderness along the edges of separation, or a bulge that increases in size with coughing that can usually be reduced. When the patient stands, a cough impulse can be felt at the tip of the finger after introducing it into the inguinal canal through the external ring by invagination. Diagnostic Studies: Herniography can be performed for the diagnosis of inguinal hernia. Laparoscopically an indirect inguinal hernia is evident as an opening adjacent to the round ligament. A direct or femoral hernia may not be clearly seen until the peritoneum is open. 90 Surgical Treatment: A sheet of prosthetic mesh is used to reconstruct the inguinal floor. These procedures can be performed laparoscopically and the prosthesis used to cover and overlap all potential defects in the myopectineal orifice. 90 FEMORAL HERNIA: Femoral hernia is a protrusion of preperitoneal fat or intraperitoneal viscus through a weak transversalis fascia into the femoral ring and the femoral canal. It is not unusual for individuals to develop a femoral hernia who have had a previous repair of an inguinal hernia. Etiology: Natural weakness of the tissues and loss of elasticity is the basic cause. They are more common in multiparous women. Symptoms or History: The patient may notice a small reducible lump in the medial aspect of the groin. Physical Examination: The diagnosis can usually be made on finding a soft tumor at the femoral fossa. Diagnostic Studies: If suspected by symptoms, a gentle push with a blunt instrument at the time of laparoscopy will reveal weakness in the peritoneum. Surgical Treatment: Non-absorbable mesh is placed appropriately to occlude the orifice. SCIATIC HERNIA: A sciatic hernia is a protrusion of a peritoneal sac and its contents through the greater or lesser sciatic foramen. In one study of women with CPP diagnosed and treated during laparoscopy, sciatic hernia was diagnosed in 20 of 1100. This gives an incidence of 1.8% in women with CPP requiring laparoscopic intervention.91 Symptoms or History: Sciatic hernias present with pain originating in the pelvis. Patients may report ipsilateral posterior thigh or buttocks pain or both. Compression of the sciatic nerve may occur, causing pain to radiate down the posterior thigh that is aggravated by dorsiflexion. Physical Examination: Sciatic hernias pass downward and may present under the lower border of the gluteus maximus muscle in the posterior medial aspect of the thigh. Sciatic hernias, however, are only rarely evident on physical examination. If the ureter herniates into the sciatic foramen it may give rise to a urographic appearance of a redundant, horizontally oriented ureter within a hernia sac that has been called a “curlicue” ureter. Laparoscopically a sciatic hernia may be found to be filled with the ipsilateral ovary or fallopian tube. A prior history of laparoscopic evaluation may not preclude the need for re-evaluation. Surgical Treatment: When the sciatic hernia is approached laparoscopically, its contents are reduced and the peritoneum overlying the sciatic hernia is elevated and transected transversely with scissors. Mesh is then placed in the space created by the atrophic piriformis muscle. A second piece of mesh is trimmed to the size of the peritoneal defect and placed over the folding mesh. This overlying mesh is secured to the obturator internus fascia laterally and the coccygeus medially. The peritoneum is then closed over the mesh.86 MUSCULOSKELETAL Fibromyalgia Pelvic Floor Pain Syndrome FIBROMYALIGIA: Fibromyalgia syndrome (FMS) is chronic, diffuse painful muscles with chronic fatigue and dysautonomia. The criteria for diagnosis of fibromyalgia includes a history of widespread pain along with a finding of at least 8 out of a possible 18 specific tender points on physical examination. Symptoms: CPP is very common. Pain is the hallmark of FMS. It is common for one specific area to dominate. Painful areas involve the muscles, but it may localize to sites of tendinous attachment to the bone. Fatigue is often the most debilitating symptom of FMS. Sleep disturbance is common. Physical Examination: The eliciting of pain slight pressure over at least 11 of the 18 designated sites confirms the diagnosis of FMS. There are no laboratory or imaging studies diagnostic for FMS. Treatment: Treatment includes analgesics and anti-inflammatories, anti-depressants and hypnotics. Physical therapy techniques are an integral part of relief for FMS symptoms. PELVIC FLOOR PAIN SYNDROME: Pelvic floor pain syndrome refers to pelvic pain caused by or associated with pain or tenderness of one or more of the muscles of the pelvic floor, levator ani, coccygeus, or piriformis or their associated fascia or insertions. 93 Symptoms and History: Symptoms are usually vague and poorly localized. In a significant number of patients the pain is unilateral. The pain may be quite severe. Low back pain and radiation of pain to the sacrum at the area of insertion of the levator ani is not uncommon. The pain may mimic that due to diseases of the reproductive organs, with alterations and cycle variations. Physical Examination: The most common finding with PFPS is tenderness and spasm of one or more muscles of the pelvic floor. Digital pressure on the involved muscle characteristically reproduces or intensifies the patient’s pain symptoms. It is not unusual for the tenderness to be unilateral. Treatment: The classic treatment for PFPS is Thiel’s massage. This is done with the rectal finger massaging the involved tender muscles with a firm sweeping motion, 15 to 20 strokes, taking about 5 minutes, are done at each treatment. Treatments are repeated daily or for 4 to 5 days, then every other day until improvement. The technique may be modified to transvaginal massage rather than transanal. PSYCHOLOGICAL CAUSES OF CHRONIC PELVIC PAIN DEPRESSION Introduction: Depression is a state of significantly decreased emotional, psychological, and social functioning, with neurovegetative symptoms lasting at least 2 weeks. Anger, fear, and hopelessness become turned in upon the self, eventually producing or worsening biochemical changes. Symptoms and History: The symptoms of depression vary and occur as a spectrum that leads to a range of diagnostic categories. There are nine symptoms of a major depressive episode. Sad or down mood, most of every day Significant loss of interest or pleasure in all activities Significant weight change Insomnia or hypersomnia daily Psychomotor agitation or retardation Lack of energy or daily fatigue Feeling worthless Problems with decision making, thinking or concentration Recurrent thoughts of death or suicide These symptoms must last at least two weeks and must include either A) Sad or blue mood, or B) the loss of interest or pleasure in nearly all activities. Signs and physical examination to diagnose depression in patients with CPP is mostly clinical and can be made upon the list of symptoms presented above. Two useful objective signs are depressed affect and psychomotor retardation. There are no diagnostic laboratory findings. However, psychomotor testing using psychological tests such as the Beck Depression Inventory or Hamilton Depression Test are helpful.94 Management or Treatment: The treatment of depression in CPP is pharmacologic. Antidepressant medications have long been used and are very helpful. CHRONIC PELVIC PAIN AS A DIAGNOSIS CONCLUSION CPP AS A DIAGNOSIS Although the etiology is not known after 4 to 6 months duration, the pain itself can become an illness itself. 95 Therapy directed at the treatment of chronic pain as a diagnosis may be classified generally as: Pharmacologic Psychological Physical Neuroablative Reasonable goals when treating chronic pain as a disease include: To relieve suffering: Treatment of identifiable symptoms and concurrent psychological morbidity. To restore normal function To improve quality of life my managing symptoms To prevent recurrence of chronic symptoms and disability. Pharmacologic Treatments: Pharmacological treatments include analgesics, including both non-steroidal anti-inflammatories and opiod analgesics. Anti-depressants may also be required. Empiric treatment with antibiotics is often given, although there is no published evidence for efficacy of such empiric treatments. Psychological Treatment: The goals of psychological pain therapies are to: Treat excess pain and disability Teach patients to live and cope better Teach patients to live well despite their pain. Cognitive-behavioral psychological pain management techniques include the following: Goal control pain a. Relaxation techniques b. Stress management c. Pain coping strategies d. Distraction technique Reduce disability interventions a. Progressive activities b. Pain behavior modification c. Re-employment 3. Promote wellness and improve lifestyle interventions a. Eating behavior and nutrition b. Sleep hygiene c. Physical exercise d. Treat substance abuse 4. Treat psychological morbidity. Interventions include: a. Treat depression and anxiety b. Sex therapy c. Couples and family counseling Neurolytic Therapies: Neurolytic therapies may be done by surgical transection or excision of nerves, injection of neurotoxic chemicals or use of energy sufficient to destroy neural tissue. The surgical procedures that are used to treat CPP are superior hypogastric plexus excision (presacral neurectomy), paracervical denervation (uterosacral neurectomy, uterine nerve ablation, or uterosacral ligament resection), and uterovaginal ganglion excision. Neurolytic treatment can be done with cryoablation, thermal coagulation, or injection of chemical agents. Multi-Disciplinary Pain Centers: The goals of the specialized pain center are to give the patient responsibility for and control of her healthcare and to restore her normal functioning. These goals reflect the fact patients referred to a multi-disciplinary pain center can have: Severe disease Limited psychological or environmental resources or limited social supports to provide the motivation needed to meet the challenges associated with functional living in the presence of chronic pain.95 Although treating patients with CPP may pose a challenge, such patients can often be treated successfully. Effective modalities are available to lessen the impact of pain and offer the reasonable expectation of return to normal function.1 A partial list of surgical interventions for pain include the following: Partial vulvectomy and vestibulectomy for chronic vulvodynia and vestibulitis.Trigger point injections and physical therapy for myofascial pain syndromes.Hernia repairs for herniasVaginal vault hernia repairs for vaginal vault relaxation.Uterine suspension procedures for deep dyspareunia and dysmenorrhea.Cervical dilation for cervical stenosis and associated severe dysmenorrhea.Resection of intracavitary and submucous myomas and intracavitary polyps for dysmenorrhea and pelvic pain.Laparoscopic uterosacral nerve ablation for dysmenorrhea.Presacral neurectomy for severe central dysmenorrhea.Adhesiolysis for pain from adhesions.Appendectomy for chronic right-sided abdominal pain associated with chronic appendicitis.Ovarian and tubal surgery for pain associated with the ovary or tube.Myomectomy for pain associated with leiomyoma.Hysterectomy with bilateral salpingo-oophorectomy for patients who fail to obtain long-term relief of their gynecologic pain with medical therapy.Excision, vaporization, and ablation of endometriosis for pain associated with endometriosis. Through the proper use of diagnostic tools, including comprehensive history and physical, and the application of appropriate therapeutic modalities it is possible to provide patients with some relief from their pain. As Albert Schweitzer once wrote: “We must all die. But that I can save him from days of torture, that is what I feel is my great and ever new privilege. Pain is a more terrible lord of mankind than even death itself.” References: References: 1. ACOG pelvic pain technical bulletin #223, May 1996: pge 371-379 2. Ling FW. Contemporary management of chronic pelvic pain (Preface). Obstet Gynecol Clin North Am. 1993; 20: XI 3. Reiter RC. A profile of women with chronic pelvic pain. Clin Obstet Gynecol. 1990; 33: 130-136. 4. Howard FM. The role of laparoscopy in chronic pelvic pain: promise and pitfalls. Obstet Gynecol Surv. 1993; 48: 357-387. 5. Carter JE. A systematic history for the patient with chronic pelvic pain. JSLS (1999) 3: 245-252. 6. Kramlinger KG, Swanson DW, Maruta T. Are patients with chronic pain depressed? Am J Psych 1983; 140: 747-750. 7. Carter JE. Chronic Pelvic Pain: Diagnosis and Management. Medical Education Collaborative. Golden, CO. pp 35. 8. Howard FM. Physical examination In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 30. 9. Steege JF. Office assessment of chronic pelvic pain. Clin Obstet Gynecol 1997; 40: 554-563. 10. Howard FM. Physical examination In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 31. 11. Carter JE. Rectus abdominus pain In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 434 12. Slocumb JC. Neurologic factors in chronic pelvic pain: trigger points and the abdominal pelvic pain syndrome. Am J Obstet Gynecol 1984; 149: 536-543. 13. Carter JE. Laparoscopic uterine suspension. Operative Techniques in Gynecologic Surgery. 2000; 5: 34-40. 14. Howard FM. Laboratory and Imaging Evaluation In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pp 43-52. 15. Ripps BA, Martin DC. Focal pelvic tenderness, pelvic pain, dysmenorrhea and endometriosis. J Reprod Med, 1991; 36: 470-472. 16. Parsons CL, Bullen M, Kahn BS, Stanford EJ. Gynecologic presentation of interstitial cystitis as detected by intravesical potassium sensitivity. Obstet Gynecol 2001; 98: 127-32. 17. Howard FM. Endoscopy In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 53. 18. Howard FM. Endoscopy In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 55. 19. Howard FM. The role of laparoscopy in the evaluation of chronic pelvic pain: pitfalls with a negative laparoscopy. J AM Assoc Gynecol Laparoscop 1996; 4: 85-94. 20. Sampson JA. Peritoneal endometriosis due to dissemination of endometrial tissue into the peritoneal cavity. Am J Obstet Gynecol 1927; 14: 422 21. Koninckx PR, D’Hooghe TD, Oosterlynck D. Response to letter to editor. Fertil Steril 1991; 56:590. 22. Howard FM. Endoscopy In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 57. 23. APGO Educational Series on Women’s Health Issue. Chronic Pelvic Pain: An Integrated Approach. Medical Education Collaborative. 1800 Jackson Street, Golden, CO 80401. Jan 2000: pge 27. 24. Ling FW. For the pelvic pain study group. Randomized controlled trial of Depot leuprolide in patients with chronic pelvic pain and clinically suspected endometriosis. Obstet Gynecol. 1999; 93: 51-58. 25. Reich H. Laparoscopic adhesiolysis techniques. Female Patient 1990; 15: 85. 26. Stovall TG, Elder RF, Ling FW. Predictors of pelvic adhesions. J Reprod Med 1989; 34: 345. 27. Howard FM. Endoscopy In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 59. 28. Howard FM. Endoscopy In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 60 29. Howard FM. Introduction In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 5 30. Koninckx PR, Lesaffre E, Meuleman C, et al. Suggestive evidence of pelvic endometriosis as a progressive disease, whereas deeply infiltrating endometriosis is associated with pelvic pain. Fertil Steril 1991; 55: 759-765 31. Carter JE. Combined hysteroscopic and laparoscopic findings in patients with chronic pelvic pain. J Am Assoc Gynecol Laparoscop 1994; 2: 43-47 32. Kistner RW. Gynecology: Principle and Practice. Chicago: Yearbook Medical Publishers, 1979: 447-448. 33. Howard FM. Endometriosis and Endosalpingiosis In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 125-150. 34. Barbieri RL. Hormone treatment of endometriosis: the estrogen threshold hypothesis. Am J Obstet Gynecol 1992; 166: 740-745. 35. Martin DC, Hubert GD, Bander Zwaag R, et. al. Laparoscopic appearance of peritoneal endometriosis. Fertil Steril 1989; 51: 63. 36. ACOG practice bulletin Clinical Management Guidelines for the Obstetrician-Gynecologist #11 December 1999. pp14. 37. Cook AS, Rock JA. The role of laparoscopy in the treatment of endometriosis. Fertil Steril 1991; 55: 663-680. 38. Sutton CJG, Ewen SP, Whitelaw N et. al. Prospective, randomized, double blind trial of laser laparoscopy in the treatment of pelvic pain associated with minimal, mild and moderate endometriosis. Fertil Steril 1994; 62: 696-700. 39. Waller KG, Shaw RW. Gonadotropin-releasing hormone analogs for the treatment of endometriosis: long-term follow up. Fertil Steril 1993; 59: 511-515. 40. Hornstein MD, Yuzpe AA, Burry K, et. al. Re-treatment with nafarelin for recurrent endometriosis symptoms: efficacy, safety and bone mineral density. Fertil Steril 1997; 67: 1013-1018. 41. Peters AAW, Trimbos-Kemper GCM, Admiraal C, et. al. A randomized clinical trial on the benefit of adhesiolysis in patients with intraperitoneal adhesions and chronic pelvic pain. Br J Obstet Gynecol 1992; 99: 59-62. 42. Steege JF, Stout A. Resolution of chronic pelvic pain after laparoscopic lysis of adhesions. Am J Obstet Gynecol 1991; 165: 278-283. 43. Nezhat FR, Crystal RA, Nezhat CH, Nezhat CP. Laparoscopic adhesiolysis and relief of chronic pelvic pain. JSLS. 2000 Oct-Dec; (4): 281-285. 44. Kligman I, Drachenberg C, Papadimitriou J, et. al. Immunohistochemical demonstration on nerve fibers in pelvic adhesions. Obstet Gynecol 1993; 82: 566-568. 45. Tulandi T, Chen MF, Al-Took S, Watkin K. A study of nerve fibers and histopathology of post-surgical, post-infectious in endometriosis-related adhesions. Obstet Gynecol 1998 Nov; 92 (5): 766-768. 46. Perry CP, Howard FM. Adhesions In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 93-97. 47. El-Minawi AM. Pelvic Varicosities and Pelvic Congestions Syndrome In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 171-183 48. Beard RW, Highman JH, Pearce S, et. al. Diagnosis of pelvic varicosities in women with chronic pelvic pain. Lancet 1984; 2: 946-949. 49. El-Minawi MF, Derbala S, Ahmad MM, et. al. Transvaginal doppler sonographic study in patients with post tubal ligation syndrome. Med J Cairo Univ 1991: 59 (4): 1003-1010. 50. Beard RW, Reginald PW, Wadsworth J. Clinical features of women with chronic lower abdominal pain and pelvic congestion. Br J Obstet Gynecol 1988; 95: 153-161. 51. Giacchetto C, Cotroneo GB, Marincolo F, et. al. Ovarian varicocele: ultrasonic and phlebographic evaluations. J Clin Ultrasound 1990; 18: 551-555. 52. Stovall TG, Ling FW, Crawford DA. Hysterectomy for chronic pelvic pain and presumed uterine etiology. Obstet Gynecol 1990; 75: 676-679. 53. Beard RW, Kennedy RG, Gangar KF, et. al. Bilateral oophorectomy and hysterectomy in the treatment of intractable pelvic pain associated with pelvic congestion. Br J Obstet Gynecol 1991; 98: 988-992. 54. Smith KM , Reginald PW. Treatment Options in Women with Unexplained Chronic Pelvic Pain In: Stud D J Ed. The Yearbook of the Royal Obstetricians and Gynecologists. London: RCOG Press, 1996: 193-204. 55. Reginald PW, Adams J, Franks S, et. al. Medroxyprogesterone acetate in the treatment of pelvic pain due to venous congestion. Br J Obstet Gynecol 1989; 96: 1148-1152. 56. Carter JE. Adenomyosis. In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 86-92. 57. Rokitansky K, Ueber. uterus neubildung. Z Gesellshaft Wien 1860; 16: 577. 58. Siegler AM, Camilien L. Adenomyosis. J Reprod Med 1994; 39: 841-853. 59. Lee NC, Dicker RC, Reuben GL. Confirmation of the preoperative diagnosis for hysterectomy. Am J Obstet Gynecol 1984; 150: 283 60. Nishida M. Relationship between onset of dysmenorrhea and histological findings in adenomyosis. Am J Obstet Gynecol 1991; 165: 229-232. 61. Hunt RB, Siegler AM. Hystosalpinography: Techniques and Interpretation. Chicago: Yearbook Medical Publishers, 1990: 75. 62. Mark AS, Hricak H, Heinrich LW. Adenomyosis and leiomyoma: differential diagnosis with MR imaging. Radiology 1987; 168: 527-529. 63. McCausland AM. Hysteroscopic myometrial biopsy: it’s use in diagnosing adenomyosis and its clinical applications. Am J Obstet Gynecol 1992; 166: 1619-1628. 64. Ota H, Maki M, Shidara Y. Effects of danazol at the immunological level in patients with adenomyosis with special reference to auto-antibodies: A multi-center cooperative study. Am J Obstet Gynecol 1971; 110: 275-284. 65. El-Minawi AM, Howard FM. Dysmenorrhea In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 108-107. 66. Andersch B, Milsom I. An epidemiological of young women with dysmenorrhea. Am J Obstet Gynecol 1982; 144: 655-657. 67. Akerlund M, Andersson K-E, Ingemarsson I. Effects of terbutaline on myometrial activity, uterine blood flow and lower abdominal pain in women with primary dysmenorrhea. Br J Obstet Gynecol 1976; 83: 673. 68. Wood C, Larsen L, Williams R. Menstrual characteristics of 2.343 women attending the Shepherd Foundation. Aust N Z J Obstet Gynaecol 1979; 19: 107-110. 69. Owen PR. Prostaglandin synthetase inhibitors in the treatment of primary dysmenorrhea: outcome trials reviewed. Am J Obstet Gynecol 1984; 148: 96-99. 70. Carter JE. Laparoscopic presacral neurectomy utilizing contact-tip Nd YAG laser. Keio J Med 1996; 45(4): 332-335 71. Howard FM. Dyspareunia In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 112-121. 72. Carter, JE. Carter-Thomason Uterine Suspension and Positioning by Ligament Investment, Fixation and Truncation. Journal of The Society of Reproductive Medicine 1999; 44: 417-422. 73. Bornstein J, Goldik, Z, Stolar Z, et. al. Predicting the outcome of surgical treatment of vulvar vestibulitis. Obstet Gynecol 1997; 89: 695-698. 74. Howard FM. Interstitial Cystitis In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 260-270 75. Summit RL. Jr. Urogynecologic causes of chronic pelvic pain. Obstet Gynecol Clin North AM 1993; 20: 685-698. 76. Ramahi AJ, Richardson DA. A practical approach to the painful bladder syndrome. J Reprod Med 1990; 35: 805-809. 77. Parsens CL. Sodium pentosan polysulfate treatment of interstitial cystitis: an update. Urology (Suppl) 1987; 29: 14-16. 78. Walker EA, Katon WJ, Jemelka R, et al. The prevalence of chronic pelvic pain and irritable bowel syndrome in two university clinics. J Psychosom Obstet Gynecol 1991; 12 (Suppl): 65. 79. Howard FM. Irritable Bowel Disease In: Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 238-245. 80. Simons DG, Travell JG, Simons LS: Travell and Simons, Myofascial pain and dysfunction: The trigger point manual Vol. I, Second Ed. Baltimore: Williams and Wilkins, 1999 1,038 pp. 81. Carter JE. Surgical treatment for chronic pelvic pain. J Soc Laparoendosc Sur, 2: 129-139, 1998. 82. Simons DG, Simons LS. Chronic myofascial pain syndrome. In: Tollison CD ed. Handbook of pain management second ed. Baltimore. Williams and Wilkins, 1994; 556-577. 83. Carter JE. Abdominal Wall and Pelvic Myofascial Trigger Points. In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 314-358 84. Glazer HI, Rodke G, Swencionis C, Hertz R, Young AW. Treatment of vulvar vestibulitis syndrome with electromyographic biofeedback of pelvic floor musculature. J Reprod Med; 40: 283-290, 1995. 85. Netter FH, Iason AH, Pansky B. Hernias section 16. In: Oppenheimer E, ed The CIBA Collection of Medical Illustrations. CIBA New Jersey 1962:204-230. 86. Carter JE. Hernias In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 385-413. 87. Abrahamson J,. Hernias In: Zinner MJ, Schwartz SI, Ellis H, eds, Maingot’s abdominal operation. Stanford, CT: Appleton & Lange, 1997: 479-580. 88. Kadar N, Reich H, Liu CY, et al. Incisional hernias after major laparoscopic gynecologic procedures. Am J Obstet Gynecol 1993; 168:1493-5. 89. Carter JE. A new technique of fascial closure for laparoscopic incisions. J Laparoscop Endoscop Surg 1994;4:143-148. 90. Kavic MS. Laparoscopic hernia repair. The Netherlands: Harwood Academic Publishers, 1997: 117. 91. Miklos JR, O’Riley MJ, Saye WB. Sciatic hernias as a cause of chronic pelvic pain in women. Obstet Gynecol 1998; 91: 998-1001. 92. Perry CP. Fibromyalgia In Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 381-384. -458 93. Howard FM. Pelvic Floor Pain Syndrome In: Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 pge 238-245. 94. Carter JE, Kinback K. Depression In: Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000 95. Howard FM. Chronic Pelvic Pain as a Diagnosis In: Howard FM, Perry CP, Carter JE, El-Minawi AM. Pelvic Pain: Diagnosis and Management. Lippincott New York 2000