Andrea J. Rapkin
Leena Nathan
• Acute pelvic pain is rapid in onset, often associated with unstable vital signs and obvious abnormalities on physical examination and laboratory assessment. Improper diagnosis can result in significant morbidity and even mortality.
• Timely and thorough assessment, guided by organ system (reproductive, gastrointestinal, urinary) and category of pathology will ensure effective diagnosis and management of infection, obstruction, ischemia (torsion), leakage of irritating substance (viscus or cyst rupture), neoplasia, or pregnancy-related pain.
• Chronic pelvic pain is a multifaceted disorder characterized by changes in the processing of afferent signaling in the pelvic organs, the surrounding somatic tissues, and the spinal cord and brain. The shared thoracolumbar and sacral innervations of the pelvic structures and the up-regulation processing of neural input in the central nervous system account for the multiplicity of somatic and psychological symptoms experienced by women with chronic pelvic pain.
• A thorough history and physical examination are important for successful management of both chronic and acute pain. The ancillary laboratory and diagnostic procedures performed to assess acute, life-threatening processes differ from those focused on chronic pain conditions. Chronic pelvic pain requires a multidisciplinary approach for both diagnosis and management.
Definitions
Acute pain is intense and characterized by sudden onset, sharp rise, and short course. Cyclic pain refers to pain that occurs with a definite association to the menstrual period. Dysmenorrhea, or painful menstruation, is the most common cyclic pain phenomenon and is classified as primary or secondary on the basis of associated anatomic pathology (1). Chronic pelvic pain is defined as pain of greater than 6 months in duration, localized to the anatomic pelvis, and severe enough to cause functional disability or necessitating medical care (2).
Whereas acute pain is generally associated with autonomic reflex responses, such as nausea, emesis, diaphoresis, and apprehension, such autonomic reflex responses are not present in women with chronic pelvic pain. Acute pain is affiliated with signs of inflammation or infection, such as fever and leukocytosis, which are absent in chronic pain states. The pathophysiology of acute pelvic pain involves mediators of inflammation present in high concentration as a result of infection, ischemia, or chemical irritation.
By contrast, the etiology of chronic pelvic pain often involves changes in modulation or “up-regulation” of normally nonpainful stimuli. Pain is out of proportion to the degree of tissue damage (3). Chronic pain is thus characterized by physiologic, affective, and behavioral responses that differ from those associated with acute pain (4). An inflammatory lesion, such as endometriosis, for example, can set up an environment of chronic neurogenic inflammation or stimulation, which can result in “plastic” changes in the peripheral and central nervous system and the persistence of chronic pain (5–7). Moreover, genetic predisposition, adverse environmental pressures, and hormonal milieu are thought to increase the vulnerability and predisposition for chronic pain disorders (8).
Acute Pain
The differential diagnosis of acute pelvic pain is outlined in Table 16.1. Assessing the character of the pain helps create a differential diagnosis. Rapid onset of pain is most consistent with perforation or rupture of a hollow viscus or ischemia following the torsion of a vascular pedicle. Colic or severe cramping pain is commonly associated with muscular contraction or obstruction of a hollow viscus, such as intestine, ureter, or uterus. Pain perceived over the entire abdomen suggests a generalized reaction to an irritating fluid within the peritoneal cavity such as blood, purulent fluid, or contents of an ovarian cyst.
Table 16.1 Differential Diagnosis of Acute Pelvic Pain
|
Gynecologic |
|
Acute Pain |
|
1. Complication of pregnancy a. Ectopic pregnancy b. Abortion, threatened or incomplete 2. Acute infections a. Endometritis b. Pelvic inflammatory disease (acute PID) or salpingo-oophoritis c. Tubo-ovarian abscess 3. Adnexal disorders a. Hemorrhagic functional ovarian cyst b. Torsion of adnexa c. Rupture of functional, neoplastic, or inflammatory ovarian cyst |
|
Recurrent Pelvic Pain |
|
1. Mittelschmerz (midcycle pain) 2. Primary dysmenorrhea 3. Secondary dysmenorrhea |
|
Gastrointestinal |
|
1. Gastroenteritis 2. Appendicitis 3. Bowel obstruction 4. Diverticulitis 5. Inflammatory bowel disease 6. Irritable bowel syndrome |
|
Genitourinary |
|
1. Cystitis 2. Pyelonephritis 3. Ureteral lithiasis |
|
Musculoskeletal |
|
1. Abdominal wall hematoma 2. Hernia |
|
Other |
|
1. Acute porphyria 2. Pelvic thrombophlebitis 3. Aortic aneurysm 4. Abdominal angina |
The first perception of visceral pain is a vague, deep, poorly localizable sensation associated with autonomic reflex responses. When the pain becomes localized to a region of the abdominal wall, the pain is called referred pain. Referred pain is well localized and more superficial and is appreciated within the nerve distribution or dermatome of the spinal cord segment innervating the involved viscus. The location of the referred pain provides insight into the location of the primary disease process (9). The innervations of the pelvic organs are outlined in Table 16.2. The upper vagina, cervix, uterus, and adnexa share the same visceral innervations with the large intestine, rectum, bladder, lower ureter, and lower small intestine. Pain from the reproductive organs, genitourinary (GU), and gastrointestinal (GI) tracts are therefore referred to the same dermatomes (10,11).
Table 16.2 Nerves Carrying Painful Impulses from the Pelvic Organs
|
Organ |
Spinal Segments |
Nerves |
|
Abdominal wall |
T12–L1 |
Iliohypogastric, ilioinguinal, genitofemoral |
|
Lower abdominal wall, anterior vulva, urethra, clitoris |
L1–L2 |
Ilioinguinal, genitofemoral |
|
Lower back |
L1–L2 |
|
|
Pelvic floor, anus, perineum, and lower vagina |
S2–S4 |
Pudendal, inguinal, genitofemoral, posterofemoral cutaneous |
|
Upper vagina, cervix, uterine corpus, inner third of fallopian tubes, broad ligament, upperbladder, terminal ileum, and terminal large bowel |
T11–L2 S2–S4 |
Thoracolumbar autonomics (sympathetics) via hypogastric plexus; sacral autonomics (parasympathetics) via pelvic nerve |
|
Ovaries, outer two-thirds of fallopian tubes, and upper ureter |
T9–T10 |
Thoracic autonomics (sympathetics) via renal and aortic plexus and celiac and mesenteric ganglia, aortic and superior mesenteric plexuses |
Evaluation of Acute Pelvic Pain
In the evaluation of acute pelvic pain, early diagnosis is critical because significant delay increases morbidity and mortality. Central to correct diagnosis is an accurate history (Fig. 16.1). The date and character of the last and previous menstrual periods and the presence of abnormal bleeding or discharge should be ascertained. The menstrual, sexual, and contraceptive history and any history of sexually transmitted conditions and previous gynecologic disorders are relevant. Pain history should include how and when the pain started, pregnancy-related symptoms (amenorrhea, irregular bleeding, nausea, breast tenderness), GI symptoms (anorexia, nausea, vomiting, constipation, obstipation, absence of flatus, hematochezia), urinary symptoms (dysuria, urgency frequency, hesitancy, hematuria), signs of infection (fever, chills, purulent vaginal discharge), and symptoms attributable to a hemoperitoneum (orthostasis, abdominal distention, and right upper quadrant or shoulder pain). Document any past medical and surgical history, and current medications.
Figure 16.1 The biosynthesis and metabolism of prostaglandins and thromboxane derived from arachidonic acid. (From Chaudhuri G. Physiologic aspects of prostaglandins and leukotrienes. Semin Reprod Endocrinol 1985; 3:219, with permission.)
Baseline laboratory studies will include, at the least, a complete blood count with differential (CBC), clean catch mid-stream routine urine analysis (RUA), sensitive urine or serum pregnancy test, gonorrhea and chlamydia screening, and a transvaginal pelvic ultrasound. Other tests such as computerized tomography (CT) with and without contrast, chemistry panel, or blood type and screen (if transfusion is likely) may be indicated depending on the patient’s symptoms and the specific differential diagnosis.
Reproductive Tract Causes of Acute Pelvic Pain
Ectopic Pregnancy
All reproductive-aged women presenting with acute pain should be screened for pregnancy.
An ectopic pregnancy is defined as implantation of the fetus in a site other than the uterine cavity (see Chapter 20).
Symptoms of Ectopic Pregnancy
Implantation of the fetus in the fallopian tube produces pain with acute dilation of the tube. If tubal rupture occurs, localized abdominal pain tends to be temporarily relieved and is replaced by generalized pelvic and abdominal pain and dizziness with the development of a hemoperitoneum. A period of amenorrhea followed by irregular bleeding and acute onset of pain compose the classic triad of symptoms. A mass in the cul-de-sac may produce an urge to defecate. Referred pain to the right shoulder often develops if the intra-abdominal blood collection transverses the right colic gutter and irritates the diaphragm (C3 to C5 innervation).
Signs
Vital signs often reveal orthostatic changes in the case of a ruptured ectopic. Orthostasis is diagnosed by obtaining a patient’s pulse and blood pressure while they are supine, then after sitting for 3 minutes, and finally after standing for 3 minutes. If the systolic blood pressure decreases by 20 mm Hg or the diastolic blood pressure decreases by 10 mm Hg when standing from a supine position, orthostasis is confirmed. Although pulse rate is not specifically included in the definition of orthostasis, it is easy to obtain and an increase in pulse rate can be suggestive of orthostasis. Elevated temperature is generally absent with an ectopic.
Abdominal examination is notable for tenderness and guarding in one or both lower quadrants. With the development of hemoperitoneum, generalized abdominal distention and rebound tenderness are prominent and bowel sounds are decreased. Pelvic examination generally reveals mild tenderness on motion of the cervix. Adnexal tenderness is present, usually more pronounced on the side of the ectopic pregnancy, and a mass may be palpated. The diagnostic approach and the medical and surgical management of ectopic pregnancy are discussed in Chapter 20 (12,13).
Leaking or Rupture of an Ovarian Cyst
Functional cysts (e.g., follicle or corpus luteum) are the most common ovarian cysts and are more likely to rupture than benign or malignant neoplasms. The pain associated with rupture of the ovarian follicle at the time of ovulation is called mittelschmerz. The small amount of blood leaking into the peritoneal cavity and high concentration of follicular fluid prostaglandins contribute to this midcycle pelvic pain. The pain is usually mild to moderate and self-limited, and with an intact coagulation system, hemoperitoneum is unlikely.
A hemorrhagic corpus luteum cyst develops during the luteal phase of the menstrual cycle. The rapidly expanding ovarian capsule or, with rupture, the blood in the peritoneal cavity is responsible for the acute pain. Rupture of this cyst can produce either a small amount of intraperitoneal bleeding or frank hemorrhage, resulting in significant blood loss and hemoperitoneum.
Cystic ovarian neoplasms or inflammatory ovarian masses, such as endometriomas or abscesses, can leak or rupture. A history of a dermoid cyst or endometrioma that has not yet undergone surgical extirpation is not uncommon. Surgical exploration is indicated if the rupture leads to significant hemoperitoneum (corpus luteum) or chemical peritonitis (endometrioma or dermoid), which could impair future fertility, or an acute abdomen (abscess), which is life threatening.
Symptoms
An ovarian cyst that is not undergoing torsion, rapidly enlarging, infected, or leaking does not usually cause acute pain. A corpus luteum cyst is the most common cyst to rupture and leads to hemoperitoneum. Symptoms of a ruptured corpus luteum cyst are similar to those of a ruptured ectopic pregnancy. The patient is in the luteal phase or can have delayed menses due to the persistently functioning corpus luteum. The onset of pain is usually sudden and is associated with increasing pelvic then generalized abdominal pain and dizziness or syncope with development of significant hemoperitoneum.
A ruptured endometrioma or benign cystic teratoma (dermoid cyst) produces similar symptoms; however, dizziness and signs of hypovolemia are not present because blood loss is minimal.
Signs
Orthostasis resulting from hypovolemia is present only when there is intravascular volume depletion, such as with a hemoperitoneum. Fever is rare. The most important sign is the presence of significant abdominal tenderness, often associated with localized or generalized lower quadrant rebound tenderness because of peritoneal irritation. The abdomen can be moderately distended with decreased bowel sounds. On pelvic examination, a mass is often palpable if the cyst is leaking and has not completely ruptured.
Diagnosis
The diagnosis and the type of ruptured cyst are ascertained by blood tests and transvaginal ultrasound. Pregnancy test, complete blood count, and, if orthostasis is present, type and screening should be ordered.Leukocytosis is uncommon. The hematocrit is decreased if active bleeding is present. If ultrasound is not available, a culdocentesis will reveal the nature of the intraperitoneal fluid. If orthostasis is absent and the peripheral hematocrit is relatively normal, clinically significant hemoperitoneum is unlikely. This conclusion is supported by culdocentesis findings of clear or blood-tinged fluid with a fluid hematocrit under 16% or transvaginal ultrasound revealing only a small amount of free intraperitoneal fluid.
Culdocentesis is very helpful in determining the cause of peritonitis: fresh blood suggests a corpus luteum; chocolate “old” blood, an endometrioma; oily sebaceous fluid, a benign teratoma; purulent fluid, pelvic inflammatory disease (PID) or tubo-ovarian abscess. A skillful reading of transvaginal ultrasound images can help to characterize a cystic structure in the pelvis as a dermoid, endometrioma, corpus luteum, or pelvic abscess and quantify the amount of intraperitoneal fluid.
Management
Orthostasis, significant anemia, hematocrit of the culdocentesis fluid of greater than 16%, or a large amount of free peritoneal fluid on ultrasound suggests significant hemoperitoneum and usually requires surgical management by laparoscopy or laparotomy. Patients who are not orthostatic or febrile, who are not pregnant or anemic, and who have only a small amount of fluid in the cul-de-sac can often be observed in the hospital, without surgical intervention, or even discharged home from the emergency room after observation.
Adnexal Torsion
Torsion (twisting) of the vascular pedicle of an ovary, ovary with cyst, fallopian tube, paratubal cyst, or rarely a pedunculated uterine myoma results in ischemia of the structures distal to the twisted pedicle and acute onset of pain. A benign cystic teratoma is the most common neoplasm to undergo torsion. Because of adhesions, ovarian carcinoma and inflammatory masses such as endometriomas or abscesses rarely undergo torsion. It is unusual for a normal tube and ovary to torque, although a polycystic ovary can undergo torsion. Diagnosis of adnexal torsion is challenging. The clinician must base the diagnosis on history, clinical examination, and additional investigations such as pelvic ultrasound (14). There is no specific size criteria for ovarian torsion, but one study found that 83% of torsion occurred in ovaries that were 5 cm or larger (15).
Symptoms
The pain of torsion is usually severe and constant or, if the torsion is partial and intermit, the pain can wax and wane. The onset of the torsion and subsequent abdominal pain frequently coincides with activity such as lifting, exercise, or intercourse. Autonomic reflex responses (e.g., nausea, emesis, tachycardia, and apprehension) are usually present.
Signs
Mild temperature elevation, tachycardia, and leukocytosis may accompany the necrosis of tissue. Pregnancy test is negative unless there is a co-existent pregnancy. The diagnosis must be suspected in any woman with acute pain and unilateral adnexal mass.
On examination, the localized direct and rebound tenderness can be noted in the lower quadrant(s). Another important sign is the presence of a large pelvic mass on bimanual examination.
Diagnosis
The process of torsion occludes the lymphatic and venous drainage of the involved adnexa; therefore, the torqued viscus rapidly increases in size and can be easily palpated on examination or visualized by ultrasound. However, the presence of Doppler blood flow to the ovary on ultrasound does not definitely rule out torsion.
Management
Adnexal torsion must be treated surgically. The adnexa may be untwisted and a cystectomy performed if appropriate. Even if it appears that necrosis occurred, there is evidence that it remains functional and sparing the adnexa can preserve its hormonal and reproductive function (16). Treatment can be accomplished by laparoscopy or laparotomy, depending on the size of the mass.
Acute Salpingo-oophoritis and Pelvic Inflammatory Disease
The diagnosis and management of acute salpingo-oophoritis and PID are discussed in Chapter 18 (17,18)
Symptoms
All cases of PID are polymicrobial, involving gram-negative and -positive aerobic and anaerobic bacteria; however, PID initiated by Neisseria gonococcus or chlamydia is manifested by the acute onset of pelvic pain that increases with movement, fever, purulent vaginal discharge, and sometimes nausea and emesis. Subclinical PID can be seen with chlamydial salpingo-oophoritis, with more insidious symptoms that can be confused with the symptoms of irritable bowel syndrome. Bacterial vaginosis has been commonly associated with PID (19).
Signs
Elevated temperature and tachycardia are typical. Abdominal examination may show distention and decreased bowel sounds caused by secondary ileus. Direct and rebound abdominal tenderness with palpation are marked. The most important signs of acute salpingo-oophoritis are cervical motion tenderness and bilateral adnexal tenderness. Evaluation of the pelvis may be difficult because of pain and guarding, but lack of a discrete mass or masses differentiates acute salpingo-oophoritis from tubo-ovarian abscess or torsion. Right upper quadrant can be a distinct sign of PID-related perihepatitis involving the liver capsule and peritoneal surfaces, called Fitz-Hugh–Curtis syndrome.
Diagnosis
Leukocytosis and elevated erythrocyte sedimentation rate (ESR), a nonspecific, although more sensitive, sign of inflammation, are found in patients with acute PID. Pregnancy test is usually negative because PID as co-existent intrauterine pregnancy (IUP) is rare. If the pregnancy test is positive, an infected or very inflamed ectopic pregnancy, or instrumented IUP or infected, incomplete abortion should be suspected. Appendicitis and diverticulitis can be mistaken for PID. Laparoscopy can be useful if the diagnosis is uncertain. The Centers for Disease Control and Prevention guidelines for diagnosing PID state that PID should be suspected and treatment started if the patient is at risk for PID and she has uterine, cervical, or adnexal motion tenderness without any apparent cause (19a). Findings that support the diagnosis include cervical or vaginal mucopurulent discharge, elevated ESR or C-reactive protein (CRP), laboratory confirmation of gonorrhea or chlamydia, oral temperature of 38.3°C or higher, or white blood cells on wet mount of vaginal secretions or culdocentesis fluid. Most specific criteria for the diagnosis include endometritis on endometrial biopsy, laparoscopic evidence of PID (tubal edema, erythema, and purulent discharge), or thickened, fluid-fluid [MB1]fallopian tubes on pelvic ultrasound or magnetic resonance imaging (MRI).
Tubo-Ovarian Abscess
Tubo-ovarian abscesses, a complication of acute salpingo-oophoritis, are usually unilateral and multilocular (20). The symptoms and signs are similar to those of acute salpingitis. A ruptured tubo-ovarian abscess is a life-threatening surgical emergency because gram-negative endotoxic shock can develop rapidly.
Signs
Vital signs reveal fever, tachycardia, and low blood pressure if the patient is septic. Tubo-ovarian abscesses can often be palpated on bimanual examination as firm, exquisitely tender, bilateral fixed masses. The abscesses can be palpated or “point” in the pelvic cul-de-sac and are appreciated on rectovaginal examination. Approximately 90% of patients will have abdominal or pelvic pain and 60% to 80% will present with fever and/or leukocytosis (21).
Diagnosis
The diagnostic imaging of choice for tubo-ovarian abscesses is ultrasound. CT with and without contrast can be used to establish the diagnosis. The differential diagnosis of a unilateral mass includes tubo-ovarian abscess and adnexal torsion, ectopic pregnancy, endometrioma, leaking ovarian cyst, and periappendiceal or diverticular abscess. If physical and ultrasound examination results are not definitive, laparoscopy or laparotomy must be performed.
Management
Tubo-ovarian abscesses should always be treated as an inpatient, and conservative medical therapy with broad spectrum antibiotics can be attempted (see Chapter 18). In one study, this yielded a treatment success rate of 75% (22). If the patient is persistently febrile or not improving clinically, CT or ultrasound-guided drainage of the abscesses should be undertaken. CT-guided percutaneous drainage can be achieved transabdominally or transvaginally. Drainage along with intravenous antibiotics is considered first-line therapy (23). If fertility is not desired, bilateral salpingo-oophorectomy and hysterectomy will provide definitive therapy.
A ruptured tubo-ovarian abscess rapidly leads to diffuse peritonitis, evidenced by tachycardia and rebound tenderness in all four quadrants of the abdomen. With endotoxic shock, hypotension and oliguria ensue, and the result can be fatal. Exploratory laparotomy with resection of infected tissue is mandatory (24) (see Chapter 18).
Uterine Leiomyomas
Leiomyomas (fibroids) are uterine smooth muscle tumors, as discussed in detail in Chapter 15. Discomfort may be present when myomas are in the broad ligament or encroaching on adjacent bladder, rectum, or supporting ligaments of the uterus. The discomfort is usually reported as noncyclic pressure or pain symptoms and less often, urinary frequency, dysmenorrhea, dyspareunia, or constipation. There is no association between degree of pain and fibroid volume or number (25).
Acute pelvic pain caused by uterine leiomyomas is rare but can develop if the myoma undergoes degeneration or torsion (26). Degeneration of myomas occurs secondary to loss of blood supply, usually attributable to rapid growth associated with pregnancy. In a nonpregnant woman, degenerating uterine leiomyoma is often a misdiagnosis, because it can be confused with subacute salpingo-oophoritis. A pedunculated subserosal leiomyoma can undergo torsion with ischemic necrosis and can be associated with pain similar to that of adnexal torsion. When a submucous leiomyoma becomes pedunculated within the endometrial cavity, the uterus contracts forcefully as if to expel a foreign body and the resulting pain is similar to that of labor. The cramping pain is usually associated with vaginal hemorrhage.
Signs
Vital signs are usually normal, although a low-grade temperature and mild tachycardia can be present with degeneration. Abdominal or bimanual examination and ultrasound reveal an irregular solid mass or masses arising from the uterus. If degeneration occurs, the inflammation can cause abdominal tenderness in response to palpation and mild localized rebound tenderness.
Diagnosis and Management
With degeneration there is usually leukocytosis. Ultrasound can distinguish adnexal from uterine etiology of an eccentric mass. If diagnosis is still uncertain, a pelvic MRI is more accurate (27). The fibroid can be excised laparoscopically; however, surgery is not mandatory. A submucous leiomyoma with pain and hemorrhage should be excised transcervically with hysteroscopic guidance.
Endometriosis-Related Acute Pain
In women with endometriosis, endometrial glands and stroma implant outside the uterine cavity, most commonly at the cul-de-sac, ovaries, or pelvic visceral and parietal peritoneum. Each menstrual cycle potentially results in further proliferation, causing inflammation, scarring, fibrosis, and adhesion formation. Women with endometriosis often experience dysmenorrhea, dyspareunia, and dyschezia, irregular bleeding, or subfertility. Acute pain attributable to endometriosis is usually premenstrual and menstrual; if nonmenstrual acute generalized pain occurs, a ruptured endometrioma (chocolate endometriotic cyst within the ovary) should be considered. The management of endometriosis is discussed under dysmenorrhea and chronic pelvic pain (see also Chapter 17).
Diagnosis
The abdomen is often tender in one or both the lower quadrants. Significant distention or rebound tenderness may be present if there is there is a ruptured endometrioma. Bimanual and rectovaginal examinations can reveal a fixed, retroverted uterus with tender nodules in the uterosacral region or thickening of the cul-de-sac. An adnexal mass, if present, usually is fixed to the broad ligament and cul-de-sac. The clinical diagnosis of endometriosis is accurate approximately 50% of the time. Definitive diagnosis is made by laparoscopy or laparotomy. In the setting of chronic pain symptoms, as noted above, with an acute exacerbation a leaking endometrioma should be suspected. If there is a characteristic mass on ultrasound, laparoscopy is indicated.
Gastrointestinal Tract Causes of Acute Pelvic Pain
Appendicitis
The most common intestinal source of acute pelvic pain in women is appendicitis. Lifetime incidence in the United States is 7%, and it is the most common cause of emergent abdominal surgery(28). The symptoms and signs of appendicitis can be similar to those of PID, but the nausea and emesis are often more prominent with appendicitis.
Symptoms
The first symptom of appendicitis is typically diffuse abdominal pain, periumbilical pain, followed by anorexia, nausea, and vomiting. Within a matter of hours, the pain generally shifts to the right lower quadrant. Fever, chills, emesis, and obstipation (no flatus or stool per rectum) may ensue. However, this classic symptom pattern is often absent. Atypical abdominal pain can occur when the appendix is retrocecal or entirely within the true pelvis (which occurs in 15% of the population). In this setting, tenesmus and diffuse suprapubic pain may occur.
Signs
A low-grade fever is generally present, but the temperature may be normal. High temperatures are typically seen with appendiceal perforation. Local tenderness is usually elicited on palpation of the right lower quadrant (McBurney point). The appearance of severe generalized muscle guarding, abdominal rigidity, rebound tenderness, right-sided mass, tenderness on rectal examination, positive psoas sign (pain with forced hip flexion or passive extension of hip), and obturator signs (pain with passive internal rotation of flexed thigh) indicate appendicitis. The pelvic examination usually does not show cervical motion or bilateral adnexal tenderness, but right-sided unilateral adnexal area tenderness can be present.
Diagnosis
Many patients with acute appendicitis have normal total leukocyte counts but a left shift is usually present. Ultrasound examination of the pelvic organs is normal, whereas the appendix may appear abnormal on ultrasound or CT with contrast. CT with oral contrast with normal filling of the appendix rules out appendicitis. Diagnostic laparoscopy can be useful to rule out other sources of pelvic pathology, but it may be difficult to visualize the appendix sufficiently to rule out early appendiceal inflammation, so appendectomy can be indicated if the diagnosis is uncertain.
Management
Initial management is intravenous administration of fluids, strict restriction of any oral intake, and preoperative antibiotics followed by laparoscopy or laparotomy. Surgery with a false-positive rate of 15% is considered acceptable and is preferable to prolonged observation with the risk of rupture and peritonitis. Not only is a ruptured appendix life threatening, but it can have profound consequences for the fertility of women of reproductive age. With the advent of imaging, negative appendectomy rates are less than 10% (29).
Acute Diverticulitis
Acute diverticulitis is a condition in which there is inflammation of a diverticulum or outpouching of the wall of the colon, usually involving the sigmoid colon. Diverticulitis typically affects postmenopausal women but can occur in women during their 30s and 40s.
Symptoms
The severe, left lower quadrant pain of diverticulitis can occur following a long history of symptoms of irritable bowel (bloating, constipation, and diarrhea), although diverticulosis usually is asymptomatic. Diverticulitis is less likely to lead to perforation and peritonitis than is appendicitis. Fever, chills, and constipation typically are present, but anorexia and vomiting are uncommon.
Signs
Bowel sounds are hypoactive and are substantially decreased with peritonitis related to a ruptured diverticular abscess. Abdominal examination reveals distention with left lower quadrant tenderness on direct palpation and localized rebound tenderness. Abdominal and bimanual rectovaginal examinations may reveal a poorly mobile, doughy inflammatory mass in the left lower quadrant. Leukocytosis and fever are common. Stool guaiac may be positive as a result of inflammation of the colon or microperforation.
Diagnosis and Management
CT with and without contrast is an important adjunct to history and physical examination (30). It will reveal a swollen, edematous bowel and can rule out an abscess. A barium enema is contraindicated. Diverticulitis is initially managed medically with intravenous administration of fluids, strict restriction of oral intake, and broad-spectrum intravenous antibiotics. A diverticular abscess, obstruction, fistula, or perforation requires general surgical intervention.
Intestinal Obstruction
The most common causes of intestinal obstruction in women are postsurgical adhesions, hernia formation, inflammatory bowel disease, or carcinoma of the bowel or ovary.
Symptoms
Intestinal obstruction is heralded by the onset of colicky abdominal pain followed by abdominal distention, vomiting, constipation, and obstipation. Higher and more acute obstruction results in early vomiting. Colonic obstruction presents with a greater degree of abdominal distention and obstipation. Vomiting first consists of gastric contents, followed by bile, then material with feculent odor, depending on the level of obstruction.
Signs
Fever is often present in the late stages. At the onset of mechanical obstruction, bowel sounds are high pitched and maximal during an episode of colicky pain. As the obstruction progresses, bowel sounds decrease and, when absent, suggest ischemic bowel. Marked abdominal distention often ensues.
Diagnosis and Management
An upright abdominal x-ray series shows a characteristic gas pattern, distended loops of bowel, and air fluid levels; and it helps to determine whether obstruction is partial or complete (no colonic gas seen). CT can be useful. White blood cell count will be elevated in patients with ischemic bowel. Complete obstruction requires surgical management, whereas partial obstruction often can be managed with intravenous fluids, bowel rest, and selective use of nasogastric suction. The cause of the obstruction should be determined and treated if possible. Underlying GI or reproductive tract malignancy may be present.
Urinary Tract Causes of Acute Pelvic Pain
Ureteral colic due to ureteral lithiasis is caused by a sudden increase in intraluminal pressure and associated inflammation. Urinary tract infections producing acute pain include cystitis and pyelonephritis. The most common microbes causing urinary tract infections are Escherichia coli followed by Proteus, Klebsiella, and Pseudomonas (31).
Symptoms and Signs
The pain of lithiasis is typically severe and crampy; it can radiate from the costovertebral angle to the groin. Hematuria is often present. Urinary tract infection (UTI) comprises bladder or kidney infection. Cystitis is associated with dull suprapubic pain, urinary frequency, urgency, dysuria, and occasionally hematuria. Pyelonephritis is associated with flank and costovertebral angle (CVA) pain, although lateralizing lower abdominal pain occasionally is present. Urethritis due to chlamydia or gonorrhea infection can have similar symptoms to those of a UTI. These infections must be ruled out if relevant.
Diagnosis
Diagnosis of stone can be made by urinalysis revealing red blood cells and demonstration of the stone via abdominal ultrasound, CT urography, or intravenous pyelography (uric acid stones may not be detected by CT).There is pain with firm pressure over the costovertebral angle in the case of lithiasis or pyelonephritis. Peritoneal signs are absent. Suprapubic tenderness may accompany cystitis.
The diagnosis of UTI is based on RUA revealing bacteria and leukocytes with or without leukocyte esterase and nitrites, in the absence of squamous epithelial cells. Findings can subsequently be confirmed by culture.The diagnostic thresholds for white blood cell count (WBC) and vaginal squamous cells vary with each laboratory. An elevated number of squamous cells in the urinary specimen suggests contamination of the urine specimen with vaginal secretions and can result in false-positive urine analysis and culture.
Management
Expectant medical treatment consists of oral hydration or intravenous fluids (if the patient is unable to tolerate oral intake), antibiotics for UTI, and pain control. Surgical management, such as lithotripsy or open surgery, is an option for renal and urethral lithiasis. Nonpregnant women (and pregnant women who are afebrile with a normal WBC count) with pyelonephritis and all women with cystitis can be treated on an outpatient basis. Nonpregnant women with pyelonephritis can be treated with a 14-day course of a fluoroquinolone or trimethoprim/sulfamethoxazole (some recommend one intravenous dose of a third-generation cephalosporin before discharging patients with oral antibiotics) (see Chapter 18) (32). Caution should be used with trimethoprim/sulfamethoxazole given rising resistance patterns. It is important to follow up urine culture sensitivities and treat accordingly. If there is no improvement, raising concerns for patient compliance, inability to tolerate oral medications and fluids, or whether the patient may be immunocompromised as related to AIDS, intravenous drug use/abuse, diabetes, pregnancy, or chronic steroid use, then the patient should be hospitalized and given intravenous antibiotics.
Tuberculosis should be excluded as a cause of pyelonephritis if the characteristic sterile pyuria is present and the patient’s condition does not improve with antibiotics.
Acute Pelvic Pain: Summary
All women of reproductive age with acute pelvic pain should have a complete blood count with differential, ESR, urinalysis, and a sensitive qualitative urine or serum pregnancy test. If not diagnosed expeditiously, an acute process can often result in significant morbidity or mortality. For patients who have chronic pelvic pain and develop acute exacerbation, it is important to rule out a superimposed acute process. Symptoms of fever, chills, diaphoresis, abnormal vaginal bleeding, dizziness, syncope, emesis, significant diarrhea, obstipation, dysuria, hematuria, and hematochezia, and/or signs of elevated temperature, tachycardia, orthostasis, abdominal distention, abnormal bowel sounds, ascites, peritonitis, or abnormal pregnancy are all indicative of an acute process.
Laboratory tests for the evaluation of acute pelvic pain include a CBC with differential, erythrocyte sedimentation rate, clean catch midstream RUA, gonorrhea and chlamydia nucleic acid amplification testing (NAAT) from cervix or urine, and urine or serum pregnancy test. The sedimentation rate is nonspecific, but often is the only abnormal laboratory finding in women with subacute PID. If the pregnancy test is positive, a quantitative β-human chorionic gonadotropin (βhCG) should be ordered. Other studies that are recommended include transvaginal pelvic ultrasound, or if imaging is not available, culdocentesis. The fluid from culdocentesis can be sent for hematocrit if bloody fluid is obtained or Gram stain with culture if the fluid is purulent. The presence of a mass in the cul-de-sac precludes culdocentesis. CT with and without contrast, abdominal x-rays, or upper or lower Gastrografin studies help rule out gastrointestinal pathology when gastrointestinal symptoms predominate. CT is useful for evaluation of retroperitoneal masses or abscesses related to the gastrointestinal tract. Pelvic MRI can be diagnostic if the pelvic ultrasound cannot determine whether a mass is uterine or adnexal.
Diagnostic laparoscopy is reserved for establishing the diagnosis in patients who have acute abdomen of uncertain cause, for elucidating the nature of an ambiguous adnexal mass, or for delineating whether a pregnancy is intrauterine or extrauterine (if ultrasound results and βhCG are equivocal). Visualization is hampered if diagnostic laparoscopy is performed for a large pelvic mass (>12 cm) and is relatively contraindicated in patients with peritonitis, severe ileus, or bowel obstruction. In these settings, laparotomy is preferable. The majority of patients with pelvic pain and a normal pelvic ultrasound have improvement or resolution of symptoms with conservative therapy and do not require surgical intervention (33).
Cyclic Pain: Primary and Secondary Dysmenorrhea
Dysmenorrhea is a common gynecologic disorder affecting as many as 60% of menstruating women (34). Primary dysmenorrhea refers to menstrual pain without pelvic pathology, whereas secondary dysmenorrhea is defined as painful menses associated with underlying pathology. Primary dysmenorrhea usually appears within 1 to 2 years of menarche, when ovulatory cycles are established. The disorder affects younger women but may persist into their 40s. Secondary dysmenorrhea usually develops years after menarche and can occur with anovulatory cycles. The differential diagnosis of secondary dysmenorrhea is outlined in Table 16.3 (2).
Table 16.3 Differential Diagnosis of Chronic Pelvic Pain
|
Gynecologic |
Genitourinary |
|
Noncyclic |
Recurrent or relapsing cystourethritis |
|
Adhesions |
Urethral syndrome |
|
Endometriosis |
Interstitial cystitis/bladder pain syndrome |
|
Salpingo-oophoritis |
Ureteral diverticuli or polyps |
|
Ovarian remnant or retained ovary syndrome |
Carcinoma of the bladder |
|
Pelvic congestion |
Ureteral obstruction |
|
Ovarian neoplasm benign or malignant |
|
|
Pelvic relaxation |
Neurologic |
|
Cyclic |
Nerve entrapment syndrome, neuroma, or other neuropathies |
|
Primary dysmenorrhea |
Trigger points |
|
Mittelschmerz |
Musculoskeletal |
|
Secondary dysmenorrhea |
Myofascial pain and trigger points |
|
Endometriosis/adenomyosis |
Congenital anomalies |
|
Uterine or vaginal anomalies with obstruction of menstrual outflow |
Scoliosis and kyphosis |
|
Intrauterine synechiae (Asherman syndrome) |
Spondylolysis |
|
Endometrial polyps or nonhormonal intrauterine device (IUD) |
Spondylolisthesis |
|
Uterine leiomyomata |
Spinal injuries |
|
Pelvic congestion syndrome |
Inflammation |
|
Tumors |
|
|
Osteoporosis |
|
|
Degenerative changes |
|
|
Coccydynia |
|
|
Myofascial syndrome |
|
|
Gastrointestinal |
Systemic |
|
Irritable bowel syndrome |
Fibromyalgia |
|
Ulcerative colitis |
Acute intermittent porphyria |
|
Crohn’s disease |
Abdominal migraine |
|
Carcinoma |
Connective tissue disease including systemic lupus erythematosus |
|
Infection |
Lymphoma |
|
Recurrent partial bowel obstruction |
Neurofibromatosis |
|
Diverticulitis |
|
|
Hernia |
|
|
Abdominal angina |
Primary Dysmenorrhea
The etiology of primary dysmenorrhea includes excessive or imbalanced amount of prostanoids secreted from the endometrium during menstruation. The prostanoids result in increased uterine contractions with a dysrhythmic pattern, increased basal tone and increased active pressure. Uterine hypercontractility, decreased uterine blood flow, and increased peripheral nerve hypersensitivity contribute to pain (35,36). Prostaglandin compounds are found in higher concentrations in secretory endometrium than in proliferative endometrium. The decline of progesterone levels in the late luteal phase triggers lytic enzymatic action, resulting in a release of phospholipids with the generation of arachidonic acid and activation of the cyclo-oxygenase (COX) pathway. The biosynthesis and metabolism of prostaglandins and thromboxane derived from arachidonic acid are depicted in Figure 16.1. Increased synthesis of prostanoids in women with primary dysmenorrhea results in higher uterine tone with high-amplitude contractions causing dysmenorrhea (36). It is theorized that women suffering from dysmenorrhea have up-regulated COX enzyme activity and prostanoid synthase activity. This led to the use of nonsteroidal anti-inflammatory drugs (NSAIDs), which act as COX enzyme inhibitors, for therapy (37).
Symptoms
The pain of primary dysmenorrhea usually begins a few hours before or just after the onset of a menstrual period and may last 48 to 72 hours. The pain is similar to labor, with suprapubic cramping, and may be accompanied by lumbosacral backache, pain radiating down the anterior thigh, nausea, vomiting, diarrhea, and rarely syncopal episodes. The pain of dysmenorrhea is colicky in nature and, unlike abdominal pain that is caused by chemical or infectious peritonitis, is relieved by abdominal massage, counter-pressure, or movement of the body.
Signs
On examination, the vital signs are normal. The suprapubic region may be tender to palpation. Bowel sounds are normal, and there is no upper abdominal tenderness and no abdominal rebound tenderness. Bimanual examination at the time of the dysmenorrheic episode often reveals uterine tenderness; severe pain does not occur with movement of the cervix or palpation of the adnexal structures. The pelvic organs are normal in primary dysmenorrhea.
Diagnosis
To diagnose primary dysmenorrhea, it is necessary to clinically rule out underlying pelvic pathology and confirm the cyclic nature of the pain. During the pelvic examination, the size, shape, and mobility of the uterus; the size and tenderness of adnexal structures; and the nodularity or fibrosis of uterosacral ligaments or rectovaginal septum should be assessed. NAAT for gonorrhea and chlamydia and if relevant, CBC and ESR, help rule out endometritis and subacute PID. Pelvic ultrasound should be performed if symptoms do not resolve with NSAIDs. If no abnormalities are found, a tentative diagnosis of primary dysmenorrhea can be established. Laparoscopy is not necessary at this point.
Management
Prostaglandin synthase inhibitors, also called nonsteroidal anti-inflammatory agents, are effective for the treatment of primary dysmenorrhea (38). The inhibitors should be taken up to 1 to 3 days before or, if menses are irregular, at the first onset of even minimal pain or bleeding and then continuously every 6 to 8 hours to prevent reformation of prostaglandin by-products. The medication should be taken for the first few days of menstrual flow. A 4- to 6-month course of therapy is warranted to determine whether the patient will respond to treatment. Changes in dosages and types of NSAIDs should be attempted if initial treatment is not successful. The medication may be contraindicated in patients with gastrointestinal ulcers or bronchospastic hypersensitivity to aspirin. Side effects are usually mild and include nausea, dyspepsia, diarrhea, and occasionally fatigue.
Hormonal contraceptives are indicated for primary dysmenorrhea unresponsive to NSAIDs or for patients with primary dysmenorrhea who have no contraindications to hormonal contraceptive and who desire contraception. Hormonal contraceptive agents (such as combined estrogen and progestin) or progesterone only oral contraceptives (either cyclic or continuous regimens), transdermal patch, vaginal ring, injectable progestin preparations, or levonorgestrel-releasing intrauterine devices are more effective than placebo alone and result in less absence from work or school (39). Continuous or extended cycle combined oral contraceptive pills are just as efficacious for this pain syndrome (40). Hormonal contraceptives inhibit ovulation, decrease endometrial proliferation, and create an endocrine milieu similar to the early proliferative phase of the menstrual cycle, when prostaglandin levels are lowest. Decreased prostaglandin levels result in less uterine cramping.
If the patient does not respond to this regimen, hydrocodone or codeine may be added for 2 to 3 days per month; before addition of the narcotic medication, psychological factors should be evaluated, and diagnostic laparoscopy to rule out pathology should be considered.
Nonpharmacologic pain management, in particular heat, acupuncture, or transcutaneous electrical nerve stimulation (TENS), may be useful (41–43). Acupuncture is thought to excite receptors or nerve fibers, blocking pain impulses through interactions with mediators like serotonin and endorphins. The perception of pain signals is altered with TENS. It does not directly affect uterine contractions. Abdominal electrical or chemical heating pads are effective in treating primary dysmenorrhea. A Cochrane review evaluated seven randomized controlled trials that used herbal and dietary therapies such as vitamins, minerals proteins, herbs, and fatty acids for relief of dysmenorrhea. There are insufficient data to support any herbal or vitamin regimen (42).
Methods used only rarely to treat primary dysmenorrhea include surgical laparoscopic uterine nerve ablation and presacral neurectomy and hysterectomy (44).
Secondary Dysmenorrhea
Secondary dysmenorrhea is cyclic menstrual pain that occurs in association with underlying pelvic pathology. The pain of secondary dysmenorrhea often begins 1 to 2 weeks before menstrual flow and persists until a few days after the cessation of bleeding. Underlying causes include endometriosis, adenomyosis, subacute endometritis and pelvic inflammatory disease, copper intrauterine devices (IUDs), ovarian cysts, congenital pelvic malformations, and cervical stenosis. Whereas the diagnosis of primary dysmenorrhea is based on history and presence of a normal pelvic examination and ultrasound, the diagnosis of secondary dysmenorrhea may require review of a pain diary to confirm cyclicity and, in addition to a transvaginal ultrasound examination, laparoscopy and/or hysteroscopy may be indicated.
The most common cause of secondary dysmenorrhea is endometriosis, followed by adenomyosis and nonhormonal intrauterine devices. NSAIDs and hormonal contraceptives are less likely to provide pain relief in women with secondary dysmenorrhea than in those with primary dysmenorrhea. The differential diagnosis of secondary dysmenorrhea is outlined in Table 16.3. The management of secondary dysmenorrhea is treatment of the underlying disorder.
Adenomyosis
Adenomyosis is defined as presence of endometrial stroma and glands within the myometrium, at least one low-power field from the basis of the endometrium, whereas endometriosis is characterized by ectopic endometrium appearing within the peritoneal cavity. Adenomyosis, endometriosis, and uterine leiomyomas frequently coexist. Although occasionally noted in women in their younger reproductive years, the average age of symptomatic women is usually older than 40 years. Increasing parity, early menarche, and shorter menstrual cycles may all be risk factors according to one study (45–47).
Symptoms
Symptoms typically associated with adenomyosis include excessively heavy or prolonged menstrual bleeding, dyspareunia, and dysmenorrhea. Symptoms often begin up to 2 weeks before the onset of a menstrual flow and may not resolve until after the cessation of menses.
Signs
The uterus is typically diffusely enlarged, although usually less than 14 cm in size, and is often soft and tender, particularly at the time of menses. Mobility of the uterus is not restricted, and there is no associated adnexal pathology (48).
Diagnosis
Adenomyosis is a clinical diagnosis. Imaging studies including pelvic ultrasound or MRI, although helpful, are not definitive. Because of the cost of MRI and negligible improvement in diagnostic accuracy, this study is not recommended routinely. In women with diffuse uterine enlargement and negative pregnancy test results, secondary dysmenorrhea may be attributed to adenomyosis; however, the pathologic confirmation of suspected adenomyosis can be made only at the time of hysterectomy.
Management
The management of adenomyosis depends on the patient’s age and desire for future fertility. Relief of secondary dysmenorrhea caused by adenomyosis can be ensured after hysterectomy, but less invasive approaches can be tried initially. NSAIDs, hormonal contraceptives, and menstrual suppression using oral, intrauterine, or injected progestins or gonadotropin-releasing hormone agonists are all useful. Treatment follows the same protocol as treatment for endometriosis. Uterine artery embolization can be effective (49).
Endometriosis
In women with endometriosis, endometrial glands and stroma are found outside the uterine cavity, especially at the cul-de-sac, ovaries, and pelvic visceral and parietal peritoneum. Given that confirmation requires visual diagnosis, the prevalence of endometriosis is unknown. It is thought to occur in approximately 10% of the general female population, 15% to 20% of infertile women, and more than 30% of women with chronic pelvic pain. In some cases, regression can occur spontaneously (50). (See the section below on endometriosis under the heading of chronic pelvic pain and also Chapter 17.)
Symptoms
Patients typically complain of severe dysmenorrhea and cyclic pelvic pain that starts up to 2 weeks prior to menses. The pain can be sharp or pressurelike, localized to the midline or involving the lower abdomen, back, and rectum. Other symptoms include deep thrust dyspareunia, subfertility, irregular bleeding despite ovulatory cycles, and nongynecologic symptoms such as cyclic dyschezia, urinary urgency, frequency, bloating, and rarely hematochezia or hematuria.
Signs
Bimanual and rectovaginal examinations may reveal uterosacral nodularity and focal tenderness. Fibrosis resulting from endometriosis can cause a fixed retroverted uterus or laterally deviated cervix or uterus. Bimanual examination can demonstrate a fullness consistent with ovarian cystic endometrioma. Patients can have focal uterosacral or broad ligament area tenderness.
Diagnosis
The clinical diagnosis of endometriosis is accurate in approximately 50% of cases. Though a definitive diagnosis of endometriosis cannot be made on image studies, endometriomas are generally distinguishable from hemorrhagic corpus lutea by the appearance on ultrasound. Homogenous hemorrhagic appearing cysts that fail to resolve after one to two menstrual cycles are suspicious for endometriomas. CA125 can be elevated but is a nonspecific and nonsensitive marker for endometriosis. Definitive diagnosis is made by direct operative visualization either laparoscopically or via laparotomy. Active red flame, or colorless vesicles or petechial lesions usually indicate early disease, while powder-burn, fibrotic lesions suggest more longstanding lesions. Suspicious findings should be biopsied for confirmation. Deep infiltrating lesions and peritoneal windows are most often found within the posterior cul-de-sac, especially at the uterosacral ligaments, and may cause pain by penetrating the many nerve endings in this area (51). Patients with endometriosis have nerve fibers in their endometrial tissue, and studies show endometrial biopsy is a potential but as yet unproven diagnostic tool. A double-blind study of 99 women undergoing laparoscopy and endometrial biopsy for evaluation of endometrial nerve fibers found that the biopsy was just as effective as laparoscopy for diagnosing endometriosis (52).
Management of Secondary Dysmenorrhea Due to Endometriosis: Pharmacologic
Medications can be used to reduce the cyclic hormonal stimulation of these lesions and eventually decidualize or atrophy the lesions. No studies directly compared medical versus surgical management of endometriosis. However, given the excellent response rate, relatively low cost, and fair tolerability with hormonal therapy, an expert consensus panel recommended that women with suspected endometriosis who are not actively trying to conceive and who do not have an adnexal mass start with first-line medical management before laparoscopy. First-line treatment consists of a trial of NSAIDs with or without combined estrogen-progestin formulations (53). Both cyclic and continuous combined oral contraceptives (OCs) can be used with equal efficacy (54). Most studies used OCs containing low-dose estrogen and more androgenic progestins; however, newer generation progestins are also effective. For women who continue to have dysmenorrhea after using hormonal contraceptives in a cyclical fashion, continuous OCs regimen can be tried, without a hormonal break or with menstruation every 3 months.
Second-line medical therapy involves high-dose progestins or gonadotropin-releasing hormone (GnRH) analogues. This can be initiated for refractory symptoms or for patients with contraindication to estrogen. Progestins alone are associated with few metabolic concerns and are safe and inexpensive alternatives to surgical intervention. Progestins or progestins plus estrogen effectively manage pain symptoms in approximately three-quarters of the women with endometriosis (55). High-dose medroxyprogesterone acetate and norethindrone acetate are equally effective to the GnRH analogues (56). Progestins should be given at a dose to achieve amenorrhea, then the dose can be tapered to control symptoms.
A randomized controlled trial comparing levonorgestrel intrauterine system (LNG-IUS) with depot GnRH for the treatment of endometriosis-related chronic pain found that both were effective treatments (57).
Androgenic hormones such as danazol are thought to inhibit the luteinizing hormone surge and steroidogenesis and may have anti-inflammatory effects. These medications increase free testosterone, resulting in possible side effects such as deepening of voice, weight gain, acne, and hirsutism. Vaginal danazol in lower doses may be effective.
GnRH agonist and add-back treatment can be used as pharmacologic treatments for endometriosis (58). A randomized-controlled trial of GnRH agonist therapy for 6 months in cases of confirmed endometriosis showed decreased size of endometriotic lesions and pain symptoms. Side effects are related to the hypoestrogenic state and include vasomotor symptoms, mood swings, vaginal dryness, decreased libido, myalgias, and, eventually, bone loss. These side effects can be reduced with supplemental calcium and hormonal add-back therapy with norethindrone acetate 2 to 5 mg daily with or without low-dose estrogen (0.625 mg of conjugated estrogen or 1 mg of 17 β-estradiol) (58). Given the side effects, GnRH agonists usually are not used for more than 8 to 12 months, but with add-back hormones and/or bisphosphonate, GnRH therapy can be considered for use for more than 1 year. Recurrence of symptoms after discontinuation of GnRH agonist ranges from 36% to 70% 5 years after completion of treatment.
Aromatase p-450 and prostaglandin E2 (PgE2) pathways are thought to be involved in the genesis of endometriotic implants. Aromatase plays an important role in estrogen biosynthesis by catalyzing the conversion of androstenedione and testosterone to estrone and estradiol. Although aromatase activity is not detectable in normal endometrium, it is found in eutopic endometrium and endometriotic lesions. Thus, aromatase inhibitors (AIs) are now being used as adjunctive therapy with medical therapies in refractory cases (59). A 2008 review of eight studies evaluated AIs for management of endometriosis and found that AIs combined with progestins or OCs or GnRH analogues decreased mean pain scores and lesion size and improved quality of life. In the only randomized controlled trial (97 women) evaluated in this meta-analysis, aromatase inhibitor (anastrozole) in combination with GnRH agonist significantly improved pain (P <0.0001) compared with GnRH agonist alone at 6-month follow-up, and there was no significant reduction in spine or hip bone density (60).
Management of Endometriosis: Surgical
Laparoscopy and laparotomy are appropriate and for some patients, they are the preferred treatment for the management of secondary dysmenorrheal pain related to endometriosis that is unresponsive to hormonal agents (see also Chapter 17). Excellent operative skill is required to manage endometriosis surgically. Endometriotic lesions should be ablated or resected. Endometriomas must be removed with their capsule. Resection of endometriomas by ovarian cystectomy improves pain and fertility in women with chronic pelvic pain and endometriosis when compared to fenestration, drainage, and coagulation. In a randomized controlled trial of laser ablation for minimal to moderate endometriosis, over 90% of women felt improved at 1-year follow-up, and 87% of women with stage III to IV endometriosis were satisfied with the results at 1-year follow-up. Recurrent pain after 24 months is close to 50% (61).
In women who no longer desire fertility with severe secondary dysmenorrhea, hysterectomy with bilateral salpingo-oophorectomy (BSO) and removal of endometriosis lesions is the preferred treatment. Hysterectomy without BSO results in a higher rate of disease recurrence and a 30% reoperation rate. The risk of recurrent endometriosis with hormone replacement is small if combined estrogen-progestin preparations are used and unopposed estrogen is avoided.
There are limited data regarding outcomes for repeated conservative surgical procedures, including pelvic denervating procedures (61). The authors conclude that although re-operation is often considered the best option, the long-term outcome appears suboptimal with a cumulative probability of recurrent pain between 20% and 40% and of a further surgical procedure of at least 20%. Hysterectomy with BSO decreased the need for re-operation to treat pelvic pain by sixfold. Postoperative medical treatment with OCs can be effective (62). Re-operation in a symptomatic patient after previous conservative surgery should take into account the psychological state of the patient, desire for future fertility, and whether the pain responded to prior surgical therapy with at least 1, but preferably 3 to 5 years of pain relief.
Rectovaginal endometriosis is often deeply infiltrating, highly innervated, and associated with severe cyclic pelvic pain and dyspareunia (see also Chapter 17). These lesions can be surgically challenging for laparoscopic resection. Hormonal therapy can be effective. Vercellini et al. (63) reviewed hormonal therapy in 217 patients: 68 in five observational studies, 59 in a cohort study, and 90 in a randomized controlled trial (63). The study compared aromatase inhibitor, vaginal danazol, GnRH agonist, intrauterine progestin, and two estrogen-progestin combinations, transvaginally or transdermally and an oral progestin. With the exception of an aromatase inhibitor used alone, the pain relief with medical therapies was satisfactory over the 6- to 12-month course of the treatment, with 60% to 90% of women reporting substantial decrease or complete relief from pain symptoms.
Chronic Pelvic Pain
Chronic pelvic pain (CPP) is defined as pelvic pain that persists in the same location for greater than 6 months' duration, causing functional disability or requiring treatment (64). CPP is an inclusive, general term that encompasses many more specific causes, ranging from reproductive, gastrointestinal, and urinary tract etiologies to myofascial pain and nerve entrapment syndromes.Chronic pelvic pain affects 12% to 20% of women in the United States. The differential diagnosis of CPP is outlined in Table 16.3. Nongynecologic causes of pain, such as irritable bowel syndrome, interstitial cystitis/bladder pain syndrome, abdominal wall or pelvic floor myofascial syndrome, or neuropathy, are frequently overlooked but common causes of chronic pelvic pain. This can in part explain why 60% to 80% of patients undergoing laparoscopy for chronic pelvic pain have no intraperitoneal pathology (2).
Patients with CPP are often anxious and depressed. Their marital, sexual, social, and occupational lives are disrupted. These patients frequently have poor treatment outcomes from traditionally effective gynecologic and medical therapy and may undergo multiple unsuccessful surgical procedures for pain. About 12% to 19% of hysterectomies are performed for pelvic pain, and 30% of patients who present to pain clinics have had a hysterectomy (65).
CPP states are characterized by up-regulation of central nervous system (CNS) responsiveness to peripheral stimuli. The relationship between the pain and pathology, such as endometriosis, adhesions, or venous congestion, is inconsistent and treatment is associated with pain recurrence. Recent investigations suggest that “plasticity” of the nervous system or alterations in signal processing may be involved in the maintenance of chronic pain states (2,6). Maladaptive changes within the peripheral and central nervous system predispose to allodynia (pain with usually nonpainful stimuli), hyperalgesia (excessive pain with a potentially painful stimulus), widening of the receptive field (pain experienced over a larger territory), and abnormal reflex responses in surrounding musculature (5–7).
The spinal cord is not a simple conduit between the periphery and the brain. It is an important site of “gating” mechanisms, such as excitation, inhibition, convergence, and summation of neural stimuli (66). With visceral tissue injury, a subset of nociceptive C-fibers that are usually dormant, called “silent” afferents, can become activated. The dorsal horn of the spinal cord is then flooded with noxious chemical stimuli that, over time, can lead to up-regulation of the signaling in the dorsal horn and brain, and pain sensation can be persistent and amplified, even after the peripheral pathology has resolved. The dorsal horn neurons demonstrate a number of electrophysiologic changes in this setting, such as the development of spontaneous activity, enlarged receptive fields, and lowered threshold for firing.
In chronic pain states, the pain is no longer adaptive. The initial painful input produces a persistent abnormal state of increased responsiveness called central sensitization (67). It is not known why in some individuals or in certain settings, prolonged stimuli or injury will result in sensitization. Different regions of the CNS are important in modulating the sensory and affective components of the pain response. Pain persistence is fostered by adverse or traumatic early experience, conditioning, fear, arousal, depression, and anxiety.
Evaluation of Chronic Pelvic Pain
On the first visit, a thorough pain history should be performed, taking into consideration the nature of each pain symptom: location, radiation, severity, aggravating and alleviating factors; effect of menstrual cycle, stress, work, exercise, intercourse, and orgasm; the context in which pain arose; and the social and occupational toll of the pain (Table 16.4). A visual or verbal analog pain scale to record pain severity 0 through 10 and stating “no pain” and “worst possible pain” is important in assessing the severity of pain and comparing the changes in severity over subsequent visits. The evaluation should include a comprehensive questionnaire that addresses depression, anxiety, emotional, physical and sexual trauma, quality of life, and criteria to assist with the diagnosis of irritable bowel syndrome and interstitial cystitis or bladder pain syndrome. The International Pelvic Pain Society published a comprehensive pain assessment tool in order to facilitate the history and physical examination, which can be found on the International Pelvic Pain Society’s Web site and reprinted and reproduced (68).
Table 16.4 Pain History Mneumonic
Diagrams of a woman’s abdomen, back, and genital area should be used to help the patient define the location of pain (2). The patient should be questioned about symptoms specific to the types of pathology listed in Table 16.3.
1. Genital (abnormal vaginal bleeding, abnormal vaginal discharge, dysmenorrhea, dyspareunia, sub-fertility, sexual functioning)
2. Enterocoelic (constipation, diarrhea, flatulence, hematochezia, and relationship of pain to times of altered bowel function or form and pain relief with bowel movements)
3. Musculoskeletal/neuropathic (physical trauma—surgical or injury, exacerbation with exercise or postural changes, weakness, numbness, lancinating pain)
4. Urologic (urgency, frequency, nocturia, hesitancy, dysuria, hematuria, incontinence)
5. Psychological (previous diagnoses, hospitalizations, and medications, current depression, anxiety, panic, including suicidal ideation, past and current emotional, physical, or sexual trauma)
Record a thorough gynecological, medical, and surgical history; medication, ethanol, or recreational drug intake; prior evaluations for pain with outcome; and review prior operative and pathology reports. Prior physical, emotional, and sexual trauma or abuse should be ascertained (69–71). The attitude of the patient and her family toward the pain, resultant behavior of the patient and her family, and current upheavals in the patient’s life should be discussed. The part of the history relating to sensitive issues may have to be revisited after establishing rapport with the patient.
Whatever the original cause of the pain, when pain has persisted for any length of time, it is likely that other psychosocial factors are now contributing to the maintenance of the pain. Pain is commonly accompanied by anxiety and depression, and these conditions need to be carefully assessed and treated (2,72,73). In a typical gynecologic setting, referral to a psychologist or psychiatrist for parallel evaluation can evoke resistance. The inference is drawn that the referring physician is ascribing the pain to psychological causes. The patient needs to understand the reason for this referral and to be reassured that it is a routine and necessary part of the evaluation. A psychologist is one of the key personnel in a multidisciplinary pain clinic.
A complete physical examination should be performed, with particular attention directed to the abdominal and lumbosacral areas, vulva, pelvic floor, and internal organs via vaginal, bimanual, and rectovaginal examination. The examination should include the Carnett test, which is an evaluation of the painful sites on the abdominal wall before and after tensing of the abdominal muscles (head raised off the table or with bilateral straight leg raise) to differentiate abdominal wall and visceral sources of pain. Abdominal wall pain is augmented and visceral pain is diminished with palpating the tender points after these maneuvers (74). While standing, the patient should be examined for hernias, both abdominal (inguinal and femoral) and pelvic (cystocele and enterocele). An attempt should be made to locate by palpation the tissues that reproduce the patient’s pain. If abdominal wall sources of pain are noted, it is useful to block these areas with injection of local anesthetics and then perform the pelvic examination (74). Neuropathic symptoms (sharp or lancinating or electrical pain, burning, or tingling sensations) should be localized to the peripheral nerve subserving the involved area.
Reproductive Tract
The most common findings noted at the time of laparoscopy for CPP are endometriosis and adhesions. Patients with other gynecologic pathology, such as benign or malignant ovarian cysts, uterine leiomyomas of size sufficient to encroach on supporting ligaments or other somatic structures, or significant pelvic relaxation should be evaluated and treated in a manner that is appropriate for the underlying condition. Pain associated with these latter conditions is generally not severe, and appropriate surgical management is therapeutic.
Endometriosis
See the section on secondary dysmenorrhea above and for a more thorough discussion of the diagnosis and management of endometriosis refer to Chapter 17.
Endometriosis can be demonstrated in 15% to 40% of patients undergoing laparoscopy for chronic pelvic pain. Endometriosis is a surgical diagnosis based on identification and histology of characteristic lesions (75). Endometriosis produces a low-grade inflammatory reaction; over time this results in adhesions between confluent pelvic organs (76). However, the cause of the pain is not well established. There is no correlation between the location of disease and pain symptoms (77,78). There appears to be no relationship between the incidence and severity of pain or the stage of the endometriotic lesions, and as many as 30% to 50% of patients have no pain regardless of stage. Similarly, 40% to 60% of patients have no tenderness on examination regardless of stage (78). Deeply infiltrating endometriosis lesions that involve the rectovaginal septum and the bowel, ureters, and bladder are strongly associated with pain (76,79,80). Pelvic adhesions related to endometriosis are a predictor of pelvic pain (81). Vaginal and uterosacral deep lesions are associated with dyspareunia and dyschezia.
Prostaglandin E and F2α production from explants of petechial lesions present in mild, low-stage disease was found to be significantly greater than from the explants of powder-burn or black lesions, which are more common in patients with higher-stage endometriosis. Prostaglandin and cytokine production may account for severe pain in some patients with mild disease. More importantly, endometriotic implants acquire a vascular and nerve supply that may contribute to peripheral and central nervous system sensitization and persistence of pain even after surgical therapy (82–84).
Endometriosis-related pain syndrome is a new and evolving concept that is defined as pain that does not respond adequately to appropriate medical and surgical therapy, especially in the setting of minimal or mild disease. In this situation, neural plasticity results from central sensitization, hypothetically initiated by the peripheral inflammatory insult (83). The disease is no longer just the endometriosis, but is fostered by the alterations in the peripheral and CNS. Endometriosis-related pain syndrome is often co-existent or “co-morbid” with other chronic conditions such as bladder pain syndrome/interstitial cystitis (BPS/IC), irritable bowel syndrome (IBS), myofascial pain, fibromyalgia and vulvodynia, and anxiety disorders. These disorders need to be managed concurrently.
Adhesions
Adhesions noted at the time of laparoscopy may be in the same general region of the abdomen as the source of the pelvic pain; however, neither the specific location (i.e., adnexa structures, parietal, visceral peritoneum, or bowel) nor density of the adhesions correlates consistently with the presence of pain symptoms (85,86). In one nonrandomized, noncontrolled study of adhesion lysis, a subgroup of women with anxiety, depression, multiple somatic symptoms, and social and occupational disruption responded poorly to adhesiolysis. The group without these characteristics had significant improvement in pain (87). Prospective randomized controlled trials do not support adhesiolysis for women with CPP. A randomized controlled trial of laparoscopic adhesiolysis showed an improvement in both the groups (i.e., laparoscopy with and laparoscopy without lysis of adhesions), suggesting a large placebo effect (88–90). One randomized controlled trial that did not consistently demonstrate a significant long-term reduction in pain did find some improvement if the adhesions were dense and involved the small bowel (91).
Most women with adhesions had a prior surgical procedure with possible injury to abdominal wall nerves, such as the iliohypogastric or ilioinguinal nerves, and those are more likely to be the cause of the pain. The abdominal wall must be carefully evaluated for myofascial or nerve injury, or entrapment, as the source of pain before assuming that adhesions contribute to the genesis of pain.
Diagnosis
Diagnostic laparoscopy is recommended if GI, GU, and myofascial and neuropathic causes are ruled out or treated and the results of the psychological evaluation are negative. Mini-laparoscopy using local anesthesia and conscious sedation is used to perform “conscious pain mapping,” whereby specific adhesions are tweaked and pelvic pain response is recorded (92). In an observational study of 50 women using local anesthesia, manipulation of appendiceal and pelvic adhesions contributed to pelvic pain. However, lysis of these adhesions did not improve outcomes over traditional laparoscopic therapy (2,11).
Management
The causal role of adhesions in the genesis of pelvic pain is uncertain, and surgery will lead to further adhesion formation and perhaps organ injury. Therefore, lysis is not recommended unless there is intermittent partial bowel obstruction or infertility. Although some observational studies showed that laparoscopic lysis of adhesions can alleviate chronic pelvic pain, randomized controlled trials have not revealed any long-term benefit. If surgery is performed, barrier materials such as oxidized regenerated cellulose or hyaluronic acid with carboxymethylcellulose can be used for prevention of adhesion re-formation. Repeated surgical procedures for lysis of adhesions are not indicated.
Pelvic Congestion
Pelvic congestion syndrome involves congestion or dilation of uterine and/or ovarian venous plexuses (93–97). First proposed in the 1950s, this condition was a suggested result of emotional stress that could lead to smooth muscle spasm and congestion of ovarian and uterine pelvic venous plexuses. A subsequent blind study was undertaken to compare results of transuterine venography in patients with unexplained CPP and negative laparoscopy with controls (97). This study demonstrated that women with CPP had a larger mean ovarian vein diameter, delayed disappearance of contrast medium, and greater ovarian plexus congestion compared to controls. The existence of this condition is controversial.
Signs and Symptoms
Pelvic congestion affects women of reproductive age. Typical symptoms include bilateral lower abdominal and back pain that is increased with standing for long periods, secondary dysmenorrhea, dyspareunia, abnormal uterine bleeding, chronic fatigue, and irritable bowel symptoms (97). Pain usually begins with ovulation and lasts until the end of menses. The uterus is often bulky, and the ovaries are enlarged with multiple functional cysts. The uterus, parametria, and uterosacral ligaments are tender.
Diagnosis
Transuterine venography is the primary method for diagnosis, although other modalities, such as pelvic ultrasound, magnetic resonance imaging, and laparoscopy, may disclose varicosities (93). Because of the cost and possible side effects of treatment, further management should be based on related symptoms and not simply on the presence of varicosities.
Management
Treatment of suspected pelvic congestion ranges from the less invasive hormonal suppression and cognitive behavioral pain management to the more invasive ovarian vein embolization or hysterectomy and salpingo-oophorectomy (93–97). Low-estrogen, progestin-dominant continuous oral contraceptives, high-dose progestins, and GnRH analogues often provide pain relief (94). Hormonal suppression should be the initial mode of treatment for women with suspected pelvic congestion. Medroxyprogesterone acetate, 30 mg daily, is useful (95). A multidisciplinary approach incorporating psychotherapy, behavioral pain management, or both is highly recommended. Percutaneous transcatheter embolization can be considered for women who do not respond to medical or hormonal therapy (96,97). Technically more invasive, transcatheter embolotherapy selectively catheterizes the ovarian and internal iliac veins, followed by contrast venography and embolization. This treatment showed some promise in small uncontrolled studies, but larger randomized controlled trials are necessary to validate its benefits. For women who have completed their childbearing, hysterectomy with oophorectomy is a reasonable option if multidisciplinary management has failed (97).
Subacute Salpingo-oophoritis
Patients with salpingo-oophoritis usually present with symptoms and signs of acute infection. Atypical or partially treated infection may not be associated with fever or peritoneal signs. Subacute or atypical salpingo-oophoritis is often a sequel of chlamydia or mycoplasma infection. Abdominal tenderness, cervical motion, and bilateral adnexal tenderness are typical of pelvic infection (see Chapter 18).
Ovarian Remnant and Residual Ovary Syndromes
In a reproductive-aged patient who has had a bilateral salpingo-oophorectomy, with or without a hysterectomy, for severe endometriosis or PID, chronic pelvic pain may be caused by ovarian remnant syndrome. This syndrome results from residual ovarian cortical tissue that is left in situ after a difficult dissection in an attempt to perform an oophorectomy. This tissue can become encased in adhesions and result in painful cysts. Often, the patient had multiple pelvic operations with the uterus and adnexa removed sequentially. Laparoscopic oophorectomy, combined with a difficult dissection, is a strong risk factor.
Residual ovary syndrome is uncommon considering the number of women undergoing hysterectomy with ovarian preservation. Theoretically, after a hysterectomy with one or both ovaries intentionally left in situ, adhesions develop and encase the ovaries, then cyclical expansion of the ovaries can result in pain and, in some cases, a tender persistent mass.
Symptoms
The patient usually reports lateralizing pelvic pain, often cycling with ovulation or the luteal phase that is described as sharp and stabbing or constant, dull, and nonradiating, occasionally with associated genitourinary or gastrointestinal symptoms. Symptoms tend to arise 2 to 5 years after initial oophorectomy. A tender mass in the lateral region of the pelvis is pathognomonic. The patient may report deep dyspareunia, constipation, or flank pain.
Diagnosis
Ultrasonography usually confirms a mass with the characteristics of ovarian tissue. The accuracy of ultrasound can be improved by treating the patient with a 5- to 10-day course of clomiphene citrate, 100 mg daily, to stimulate follicular development. In a patient who has had bilateral salpingo-oophorectomy and is not taking hormone therapy,estradiol and follicle-stimulating hormone (FSH) assays reveal a characteristic premenopausal picture (FSH <40 mIU/mL and estradiol >20 pg/mL), although on occasion the remaining ovarian tissue may not be active enough to suppress FSH levels (98). The patient may have a persistent estrogenized state based on the vulvar and vaginal examination and lack postmenopausal symptoms such as hot flashes, night sweats, and mood changes. Medical therapy that suppresses ovarian function can be diagnostic and therapeutic.
Management
Initial medical treatment with high-dose progestins or oral contraceptives usually provides good results. Patients also experience pain relief with a GnRH agonist, although these medications are impractical for long-term therapy. Those who achieve relief with GnRH agonists also experience relief with subsequent surgery (99). Laparoscopic examination usually is not productive because the ovarian mass may be missed or adhesions may prevent accurate diagnosis. A few articles documented successful laparoscopic treatment of this condition (100,101). Removal of the remnant ovarian tissue is necessary for treatment, and the corrective surgery tends to be arduous, with risks of cystotomy, enterotomy, and postoperative small bowel obstruction (98). Surgical pathology usually reveals the presence of ovarian tissue, sometimes with endometriosis, corpus lutea or follicle cysts, and fibrous adhesions. Clomiphene citrate can be used 7 to 10 days before surgery to induce folliculogenesis, allowing ovarian tissue to be more easily detected.
Gastroenterologic Etiology
The uterus, cervix, and adnexa share visceral innervation with the lower ileum, sigmoid colon, and rectum. These pain signals travel through sympathetic nerves to spinal cord segments T10 to L1. It is often difficult, therefore, to determine whether lower abdominal pain is of gynecologic or enterocoelic origin. Skillful medical history and examination are necessary to distinguish gynecologic from gastrointestinal causes of pain.Inflammatory bowel disease, such as Crohn’s disease or ulcerative colitis, infectious enterocolitis, intestinal neoplasms, appendicitis, and hernia must be ruled out with appropriate history and physical examination, complete blood cell count, and stool cultures and visualization of colonic mucosa when appropriate.
IBS is one of the more common causes of lower abdominal pain and may account for up to 60% of referrals to the gynecologist for chronic pelvic pain. An estimated 35% of patients with chronic pelvic pain have a concurrent diagnosis of IBS (102,103). Women who had a hysterectomy for chronic pelvic pain are twice as likely to have IBS. The pathophysiology of IBS appears to be influenced by central nervous system sensitization and decreased descending inhibition, which ultimately leads to the visceral hypersensitivity. Visceral hypersensitivity and abnormal reflex responses, demonstrated in both animal and human studies, results in an increased intensity of pain, lowered threshold for sensation, and an enlarged viscera-somatic region of pain referral, all of which lead to the IBS symptoms (104,105).
Symptoms
The predominant symptom of IBS is abdominal pain. Other symptoms include abdominal distention, excessive flatulence, alternating diarrhea and constipation, increased pain before a bowel movement, decreased pain after a bowel movement, and pain exacerbated by events that increase gastrointestinal motility, such as eating, stress, anxiety, depression, and menses. The pain is usually intermittent, occasionally constant, cramp-like, and more likely to occur in the left lower quadrant. The patient with IBS can be placed into one of three categories: constipation-predominant, diarrhea-predominant, and pain-predominant (alternating bowel habits) depending on their main symptoms. The new Rome III criteria for diagnosis (Table 16.5) includes at least 3 days of recurrent abdominal pain or discomfort per month over the past 3 months with at least two of the following features: relief with defecation, onset associated with change in stool frequency, or onset associated with change in form and appearance of stool (106).
Table 16.5 Rome III Criteria for Irritable Bowel Syndrome
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At least 3 days per month of recurrent abdominal pain or discomfort for the previous 3 months, has associated with two of three features: |
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1. Relieved with defecation; and/or 2. Onset associated with a change in frequency of stool; and/or 3. Onset associated with a change in form (appearance) of stool. |
Signs
On physical examination, the findings of a palpable tender sigmoid colon or discomfort during insertion of the finger into the rectum and hard feces in the rectum are suggestive of IBS.
Diagnosis
The diagnosis of IBS is usually based on history and physical examination, and although suggestive, especially in young women, the findings are not specific. A CBC, thyroid function study, stool sample to test for white cells and occult blood, and sigmoidoscopy or colonoscopy or barium enema are usually required, particularly in older individuals and in young individuals who have not responded to initial treatment. The results of these studies are all normal in patients with IBS.
Management
Treatment consists of reassurance, education, stress reduction, bulk-forming agents and other symptomatic treatments, and low-dose tricyclic antidepressants. A multidisciplinary management approach consisting of medical and psychological approaches is recommended. Patients should eliminate triggers in their diet, such as food containing lactose, sorbitol, alcohol, fat, and fructose. Products that contain caffeine can cause abdominal bloating, cramping, and more frequent bowel movements. After the patient has tried these lifestyle changes, if she remains symptomatic, a short-term trial of antispasmodics such as dicyclomine or hyoscyamine can be given (105). Multidisciplinary therapy addresses the cognitive, affective, and behavioral components of the pain. Therapy may decrease the intensity of nociceptor stimulation as well as change the patient’s interpretation of the meaning of pain (105).
Antispasmodic agents relax the smooth muscle and reduce contractility of the gastrointestinal tract. While antispasmodics and laxatives may produce symptomatic relief of bowel symptoms, the pain symptoms of IBS may respond to antidepressants. Low-dose tricyclic antidepressants (TCAs) can alleviate the pain of IBS as shown in a number of randomized controlled trials. TCAs can also reduce excessive gastrointestinal contractility and are approved for use as antispasmodics. TCAs may be used for women with moderate to severe pain, who were refractory to other therapies. Although the dose to achieve the analgesic response is much lower than that used for antidepressive effects, TCAs may be increased to higher dosages in patients with co-existing depression. Selective serotonin reuptake inhibitors (SSRIs) and serotonin/norepinephrine reuptake inhibitors (SNRIs) were used successfully in the treatment of IBS and can be used in those patients failing TCA treatment or those who are depressed or are unable to tolerate the side effects of TCAs.
Urologic Etiology
Chronic pelvic pain of urologic origin may be related to recurrent cystourethritis, urethral syndrome, sensory urgency of uncertain cause, and interstitial cystitis/bladder pain. With an appropriate diagnostic workup, infiltrating bladder tumors, ureteral obstruction, renal lithiasis, and endometriosis can easily be ruled out as possible causes.
Urethral Syndrome
Urethral syndrome is defined as a symptom complex including dysuria, frequency and urgency of urination, suprapubic discomfort, and often dyspareunia in the absence of any abnormality of the urethra or bladder(107). The cause of urethral syndrome is uncertain and is attributed to a subclinical infection, urethral obstruction, and psychogenic and allergic factors. The symptoms of urethral syndrome may actually evolve into the initial stages of interstitial cystitis.
Symptoms
Urinary urgency, frequency, suprapubic pressure, and other less frequent symptoms such as bladder or vaginal pain, urinary incontinence, postvoid fullness, dyspareunia, and suprapubic pain are commonly observed.
Signs
Physical and neurologic examinations should be performed. Anatomic abnormalities, including pelvic relaxation, urethral caruncle, and hypoestrogenism, should be evaluated. The patient should be evaluated for vaginitis. The urethra should be carefully palpated to detect purulent discharge.
Diagnosis
A clean catch or catheterized urine specimen for routine urinalysis and culture should be obtained to rule out urinary tract infection. As indicated, urethral and cervical studies for chlamydia should be obtained, and a wet prep for vaginitis should be performed. Urethral syndrome should be considered if infection is ruled out, the evaluation does not disclose vulvovaginitis, and no allergic phenomenon causing contact dermatitis of the urethra can be detected. The possibility of ureoplasma, chlamydia, candida, trichomonas, gonorrhea, and herpes should be eliminated. Cystoscopic evaluation should be performed to rule out urethral diverticulum, stones, and cancer. Pelvic floor muscles should be evaluated, as spasm of these muscles can lead to urethral pain and tenderness. The urethral pain can also be a manifestation of bladder pain syndrome.
Management
Various forms of therapy are suggested for urethral syndrome. Those patients in whom no infectious agent is present but who have sterile pyuria may respond to a 2- to 3-week course of doxycycline or erythromycin. Long-term, low-dose antimicrobial prophylaxis often is used in women with urgency and frequency symptoms who had careful documentation of recurrent urinary tract infections. Some of these women may continue to have symptoms when their urine is not infected, and bacterial infection redevelops over time. Posttreatment test of cure cultures are useful. It is recommended that all postmenopausal women with this condition be given a trial of local estrogen therapy for at least 2 months. If there is no improvement after antibiotic or estrogen therapy, physical therapy, and cognitive-behavioral therapy, then urethral dilation can be considered but recent studies are lacking. Positive results were noted with biofeedback techniques. Other treatments including acupuncture and laser therapy proved successful (108). Psychological support is very important in this group of women. Management requires a multidisciplinary approach, as is true of chronic pelvic pain in general.
Interstitial Cystitis/Bladder Pain Syndrome or Painful Bladder Syndrome
Interstitial cystitis (IC)/bladder pain syndrome occurs more often in women than men. Most patients are between 40 and 60 years of age. In 2002, painful bladder disorders were defined by the International Continence Society (ICS) in a set of new recommendations (109). The most widely used definition, painful bladder syndrome (PBS) is described as a clinical syndrome (i.e., a complex of symptoms) consisting of “suprapubic pain related to bladder filling, accompanied by other symptoms, such as increased daytime and nighttime frequency in the absence of proven infection or other obvious pathology.” By comparison, the term “interstitial cystitis” refers to patients who have PBS symptoms, but who also have “typical cystoscopic and histological features” during bladder hydrodistension (109).
The etiology of IC/PBS is unknown, but several hypotheses exist. A defective glycosaminoglycan (GAG) epithelial layer, which allows irritating substances in the urine to penetrate the urothelium to the subepithelial nerve endings, may be responsible for the syndrome (110). This theoretical mechanism is based on the fact that many IC sufferers have a positive potassium diffusion test and are sensitive to certain foods and beverages. Immunological mechanisms were proposed because abnormal mast cell activity, increased substance P expressing nerve fibers and increased nerve growth factor, were all found in bladder biopsies of IC affected individuals (110). Autoimmune mechanisms may be responsible in some individuals given that there is a higher incidence of systemic lupus erythematosus, allergies, inflammatory bowel and irritable bowel disease, and fibromyalgia in patients with bladder symptoms. Another possible mechanism is central sensitization with altered sympathetic and hypothalamic adrenal axis, substantiated by the existence of “phantom” bladder pain even after surgical removal of the bladder (110).
Symptoms
Symptoms include severe and disabling urinary frequency and urgency, nocturia, and occasional dysuria and hematuria. Suprapubic, pelvic, urethral, vaginal, vulvar, or perineal pain is common and can be relieved to some extent by emptying of the bladder (111).
Signs
Pelvic examination usually reveals anterior vaginal wall and suprapubic tenderness. Pelvic floor muscles are invariably involved, and tender to palpation. Urinalysis may reveal microhematuria without pyuria, although results are usually normal.
Diagnosis
The diagnosis is one of exclusion and is no longer based on cystoscopy. Patients who should be excluded include those younger than 18 years, those with symptoms for less than 9 months, absence of nocturia, frequency less than eight times per day, genitourinary infection (including bacterial cystitis, vaginitis, herpes), radiation- or chemotherapy-induced cystitis, bladder calculi, genitourinary cancers, lack of urgency with bladder filling greater than 350 cm3, involuntary bladder contractions, or relief with antibiotics, antispasmodic, or anticholinergics.
National Institutes of Health (NIH) Consensus Criteria for diagnosis of IC states that patients must have at least two of the following: (i) pain on bladder filling relieved by emptying, (ii) pain in suprapubic, pelvic, urethral, vaginal, or perineal region, (iii) glomerulations on endoscopy or decreased compliance on cystometrogram (111a).
Patients can be evaluated with cystoscopy with hydrodistension and biopsy. Petechial bladder mucosal hemorrhages (glomerulations) are characteristic of IC. The use of a pelvic pain and urgency or frequency symptom scale and a bladder potassium intravesical test can promote early diagnosis; it is still debatable whether a positive potassium test is definitive for interstitial cystitis or if a positive test is a manifestation of bladder hyperalgesia (112).
Management
Although there is no definitive cure for IC/BPS, patients can achieve remission with multidisciplinary therapy. First-line treatments are primarily behavioral modification such as bladder training and stress management, cognitive-behavioral therapy, dietary modifications or restriction of acidic, spicy, and fermented foods, and pelvic floor muscle physical therapy. Urinary alkalinization can be useful (113). TCAs have been efficacious. Amitriptyline 10 mg can be taken at bedtime and titrated as tolerated up to 150 mg or to relief of symptoms. Amitriptyline has antihistaminic, anticholinergic, and sodium channel blocking properties that are potentially therapeutic for opposing the histamine from mast cell degranulation, the urinary frequency, and the neuropathic pain, respectively. Oral pentosan polysulfate sodium (PPS) is the only U.S. Food and Drug Administration (FDA) approved oral therapy for IC and is modestly beneficial (114). Pentosan polysulfate is a heparinlike moiety that resembles the GAG layer, but should not be used with NSAIDs because of the bleeding risk.
Intravesical therapy can be first or second-line. With an intravesical mixture of lidocaine, bicarbonate, and heparin instilled three times a week for 3 weeks, 57% of women reported resolution of pain (115). Dimethylsulfoxide(DMSO) is the only FDA approved intravesical treatment of IC. Intravesical 50% DMSO showed significant symptomatic improvement compared to placebo in two randomized controlled trials. Intravesical solutions containing dissolved PPS showed some promise but are not FDA approved and are under investigation (116).
Sacral neuromodulation is an invasive, yet promising, technique under investigation for treatment of refractory IC (117). Sacral neuromodulation is not FDA approved for IC, and larger studies are required to confirm efficacy.
Neurologic and Musculoskeletal Causes
Nerve Entrapment
Abdominal cutaneous nerve injury or entrapment may occur spontaneously or within weeks to years after transverse suprapubic skin or laparoscopy incisions. The ilioinguinal (T12 and L1, L2) or iliohypogastric (T12 and L1, L2) nerves may become trapped between the transverse and internal oblique muscles, especially when the muscles contract. Alternatively, the nerve may be ligated or traumatized during the surgery (118).
Femoral nerve injury, one of the most commonly injured nerves in gynecologic laparotomy, can result when deep lateral retractor blades compress the nerve between the blade and the lateral pelvic side wall (119). Symptoms of nerve entrapment include sharp, burning, aching pain and paresthesias in the dermatomal distribution of the involved nerve. Femoral nerve damage results in an inability to flex at the hip joint or to extend at the knee (119). With nerve entrapment, hip flexion and exercise or activity exacerbates pain and rest or infiltration with a local anesthetic relieves pain (120). The pain is usually judged as coming from the abdomen, not the skin.
Pudendal neuropathy is another form of nerve pain that can result from vaginal surgery, especially with lateral mesh attachments, childbirth, and even chronic constipation or pelvic floor muscle abnormalities. Vulvar surgical procedures including episiotomies, laser hair removal, and Bartholin’s gland removal may injure branches of the pudendal nerve, namely the vestibular, rectal, or clitoral branches (121).
Nantes criteria for pudendal neuropathy are: (i) pain in the area innervated by the pudendal nerve (i.e., ipsilateral clitoris/penis, distal urethra, labia/scrotum, perineum, and anus); (ii) pain is increased while sitting; (iii) patient is not awakened by pain; (iv) no sensory loss on clinical examination (sensory deficits are suggestive of a sacral nerve root lesion); (v) resolution of pain with administration of pudendal nerve block (122).
Signs
On examination, the point of maximal tenderness or pain should be localized with the fingertip. The maximal point of tenderness in an iliohypogastric or ilioinguinal injury is usually at the rectus margin, medial and inferior to the anterior iliac spine. For the pudendal nerve the maximal tenderness is usually near the ischial spine. A tentative diagnosis can be confirmed by a diagnostic nerve block with 3 to 5 mL of 0.25% bupivacaine. Patients usually report immediate relief of symptoms after injection, and at least 50% of patients experience relief lasting longer than a few hours over a week or two.
Management
Many patients may require no further intervention after a series of weekly nerve blocks, although some patients require physical therapy or the addition of medications that down-regulate nerve firing. If injection successfully produces only limited pain relief and there are no contributory visceral or psychological factors, radiofrequency nerve ablation or surgical decompression of the involved nerve may be recommended. Medication for neuropathic pain, such as topical local anesthetics, anticonvulsants or antidepressants, often is effective.
Myofascial Pain
Myofascial syndrome is documented in about 15% of patients with chronic pelvic pain (120). These patients are noted to have numerous trigger points, hyperirritable areas within a tight band of skeletal muscle or within its fascia (123,124). Trigger points are possibly initiated by pathogenic autonomic reflex of visceral or muscular origin and are painful on compression (124–126). The referred pain of the trigger point occurs in a dermatomal distribution and may be caused by nerves from the muscle or deeper structures sharing a common second-order neuron in the spinal cord. The patient can experience weakness and restriction in range of motion of the affected muscle. Physical therapy is a mainstay (127). Painful trigger points characteristically can be abolished with the injection of local anesthetic into the painful area, and topical lidocaine patches or creams can be useful (123). Trigger points can be present in women with chronic pelvic pain irrespective of presence or type of underlying pathology. In one study, 89% of women with chronic pelvic pain had abdominal, vaginal, or lumbosacral trigger points (123). In the absence of the initial or ongoing organic pathology, various factors are theorized to predispose to the chronicity of the myofascial syndrome, including psychological, hormonal, and biomechanical factors (124). A multidisciplinary approach to myofascial pain must include cognitive behavioral and relaxation approaches.
Symptoms
Abdominal wall and pelvic floor myofascial pain is often exacerbated during the premenstrual period or by stimuli to the dermatome of trigger points (e.g., full bladder, bowel, or any stimulation to organs that share the dermatome of the involved nerve) (125).
Signs
On examination, fingertip pressure on the trigger points evokes local and referred pain. Tensing of the muscles by either straight leg lifting or raising the head off the table or palpation increases the pain. A specific jump sign can be elicited by palpation with fingertip or a cotton swab. An electric (tingling) sensation confirms correct needle placement (123).
Management
Massage therapy can help relieve the pain in some cases. “Myofascial release” is a special vigorous message that can be effective (124). Depending on the location of the myofascial trigger points, pelvic floor physical therapy is indicated (128). Sustained pressure with adequate force to a trigger point for a specified period can inactivate the irritable nerve (129). NSAIDs, gabapentin, pregabalin, low-dose TCAs, and benzodiazepines may be useful in patients requiring pharmacologic interventions. Injection of the trigger point with 3 mL of 0.25% bupivacaine provides relief that usually outlasts the duration of the anesthetic action. After four to five biweekly injections, the procedure should be abandoned if long-lasting relief is not obtained. A 60-patient randomized controlled trial compared lidocaine patch and placebo patch versus anesthetic injection for the treatment of myofascial pain syndrome. The study revealed similar efficacy of anesthetic patch to the gold standard treatment with trigger point injection and was associated with less discomfort than injection therapy (126). Acupuncture can be effective (130). Concomitant with injection at trigger points; relaxation, stress reduction, and cognitive-behavioral pain management should be undertaken, especially if anxiety, depression, history of emotional trauma, physical or sexual abuse, sexual dysfunction, or social or occupational disruption are present.
Fibromyalgia
Fibromyalgia is a myofascial pain syndrome, made up of the triad of diffuse pain, fatigue, and nonrestorative sleep. Women with abdominal wall or pelvic floor myofascial pain, bladder pain syndrome or interstitial cystitis and IBS often have fibromyalgia. Women are affected more commonly than men. To diagnose the syndrome, the patient must have tender points in all four quadrants. The cause is thought to be a central nervous system sensitization that results in abnormal perception of chronic pain. Fibromyalgia is closely associated with chronic fatigue syndrome, a combination of regional myofascial problems including infections and autoimmune disorders or dysautonomias. The management includes education, environmental changes (well-balanced diet, adequate time for sleep, and an environment conducive to restful sleep), exercise and stretching, and counseling or cognitive behavioral therapy for relaxation and maximizing coping mechanisms. Medications used include NSAIDs, low-dose TCAs, selective serotonin/norepinephrine reuptake inhibitors, anticonvulsants, and benzodiazepines to improve sleep (129).
Low-Back Pain Syndrome
In women who experience lower-back pain without pelvic pain, gynecologic pathology rarely is the cause of their pain. However, low-back pain may accompany gynecologic pathology. Back pain may be caused by gynecologic, vascular, neurologic, psychogenic, or spondologenic (related to the axial skeleton and its structure) pathology (131).
Symptoms
Women with low-back pain syndrome often have pain occurring after trauma or physical exertion, in the morning on arising, or with fatigue. Nongynecologic low-back pain can intensify with the menstrual cycle.
Signs
Examination consists of inspection, evaluation with movement, and palpation. Various anatomic structures in the spine should be considered as sources of pain. Muscles, vertebral joints, and discs (including lumbosacral junction, paravertebral sacrospinal muscles, and sacroiliac joints) are common sources of spondylogenic pain that must be examined carefully (2).
Diagnosis
Diagnostic imaging studies performed while the patient is standing, lying, and sitting with maximal flexion can be helpful. An elevated ESR suggests pain of inflammatory or neoplastic origin. Though most patients with acute back pain do not require imaging, plain films can be obtained to evaluate for infection, fracture, malignancy, spondylolisthesis, degenerative changes, disc space narrowing, and prior surgery. For patients who require advanced imaging, MRI without contrast is considered to be the best imaging modality.
Management
Consultation with the patient’s primary care provider should be sought before initiating management for back pain unless the source could be referred gynecologic pain. For more complex cases, an orthopaedic or neurosurgery consult may be required.
Psychological Factors
From a psychological perspective, various factors may promote the chronicity of pain, including the meaning attached to the pain, anxiety, the ability to redirect attention, personality, mood state, past experience, and reinforcement contingencies that may amplify or attenuate pain (132). The Minnesota Multiphasic Personality Inventory (MMPI) studies of women with chronic pelvic pain reveal a high prevalence of a convergence “V” profile (elevated scores on the hypochondriasis, hysteria, and depression scales). Treatment that results in subjective improvement in pain severity and increased activity level produces a significant improvement in personality profile (133).
There is also a close relationship between depression and pain (73). Both give rise to similar behavior, such as behavioral and social withdrawal and decreased activity, and may be mediated by the same neurotransmitters, including norepinephrine, serotonin, and endorphins. The Beck Depression Inventory can be used as a tool for evaluation; a score over 12 suggests dysphoria and over 18, depression (133a). Antidepressants, particularly serotonin norepinephrine reuptake inhibitors (SNRIs) often relieve both depression and pain.
Childhood physical abuse has been noted to be more prevalent in women with chronic pelvic pain than in those with other types of pain (39% vs. 18.4%) (71). In a comparison of women with chronic pelvic pain, women with nonpelvic chronic pain (headache), and pain-free women, a higher lifetime prevalence of major sexual abuse and physical abuse was found in the chronic pelvic pain group. Childhood traumas may lead to an increased vulnerability to psychosocial stress and impaired coping strategies and promote chronicity of pain after an injury.
If patients are taught self-efficacy and adaptive pain coping skills through psychological treatment interventions, pain can be reduced and functioning improved. Cognitive behavioral therapy can be useful in treating chronic pelvic pain (134). Dramatizing the pain is a coping mechanism that is used by pain sufferers to generate support from others around them (135). This practice, combined with pain-related anxiety and fear, propagates pain (133).
Management of Chronic Pelvic Pain
Multidisciplinary Approach
The approach to women with chronic pain must be therapeutic, optimistic, supportive, and sympathetic. The patient should be instructed to complete a daily pain ratings form after her first office visit. This form provides the clinician and patient with important information for pain management. Pain level (0–10), vaginal bleeding, and events that trigger pain such as stress, foods, and certain physical activities are recorded. The pain ratings can encourage the patient’s sense of control and decrease feelings of helplessness. Daily recording improves self-efficacy and compliance, allows for diagnosis of atypical cyclic pain (luteal as opposed to menstrual), and helps the patient to recognize the connection between pain and stressors. The ratings should be reviewed at follow-up visits.
Offering regular follow-up appointments is preferable to asking the patient to return only if pain persists because the latter reinforces pain behavior. Specific pain management skills should be taught using cognitive-behavioral approaches by a psychologist or using such techniques as mindfulness-based meditation or yoga. Patients should be taught ways to enhance opportunities for control of pain. Psychotherapy is indicated for women who have pronounced depression, sexual difficulties, or indications of past trauma. Various strategies, including relaxation techniques, stress management, sexual and marital counseling, hypnosis, and other psychotherapeutic approaches probably increase CNS descending inhibition of peripheral [MB2]pain signals. Psychological group treatment is a very cost-effective approach for helping patients learn stress reduction techniques and develop coping behavioral mechanisms (136). Acupuncture can be helpful (138). Physical therapy evaluation and treatment are important.
Various studies of multidisciplinary pain management were performed. This approach incorporates the skills of the gynecologist, psychologist, and physical therapist, and may include an anesthesiologist for specialized nerve blocks. Retrospective, uncontrolled studies revealed relief of pain in 85% of the participants (137). One prospective randomized study revealed a similar response rate, which was significantly better than that of traditional therapy for pain and associated symptom reduction, improvement of daily functioning, and quality of life (138).
The following groups of patients should be considered for multidisciplinary therapy early in the management process: (i) no obvious pathology, (ii) pathology that has an equivocal role in pain production, (iii) poor response to traditionally effective medical or surgical management, (iv) more than one visceral or somatic structure involved in the production of pain (i.e., more than one “pain generator”), (v) significant stress, anxiety, posttraumatic stress disorder, or depression, (vi) history of past or current physical, emotional, or sexual trauma.
Pharmacologic interventions
Any patients with dysmenorrhea or pain that worsens in the luteal or menstrual phase should be given hormonal agents to suppress ovulation and/or menses, as discussed above.
Patients with neuropathic pain or those with evidence of central sensitization or myofascial pain benefit from agents that alter neural processing. A low dose of a tricyclic antidepressant, various anticonvulsants, or selective serotonin/norepinephrine reuptake inhibitors are often effective, especially if combined with cognitive behavioral therapy. These pharmacologic agents lower the threshold for nerve firing and can help reduce reliance on narcotic pain medication, increasing activity and relieving the impact the pain has on the women’s overall lifestyle (11). Only one small, randomized controlled trial looked at the effect of selective serotonin reuptake inhibitors on pelvic pain, and failed to show a significant difference in pain or functional ability in a short follow-up period (138).
Anticonvulsants such as gabapentin or pregabalin are useful for treatment of chronic pelvic pain. Gabapentin plus amitriptyline was more efficacious than amitriptyline alone (139).
Local anesthetics are sodium channel blockers and they downgrade nerve firing. Ilioinguinal iliohypogastric, pudendal, nerve blocks and trigger point injections can be easily learned by the gynecologist and used liberally where appropriate to down-regulate neural signaling (11).
Women with depression should be treated with an appropriate therapeutic dose of antidepressant medication. Psychiatry can be consulted in this setting.
The role of opioid therapy in chronic pain is controversial and randomized controlled trials are lacking. Long-term management of chronic pelvic pain with narcotic medications is considered a last resort after failure of all other treatment modalities. Opioids should be given on a scheduled basis, and patients should have consistent follow-up with evaluation of the extent of pain relief, level of function, and quality of life. Physicians should carefully document failure of other treatment options and patient counseling. Narcotics should be prescribed only with a narcotic contract. The patient should sign a written contract agreeing to obtain pain medications from only one provider and describing other expectations with respect to treatment. Some other points that the patient should agree to include no early refills or increasing dosage of medication without discussion with the doctor, no alcohol or illegal drugs, random blood or urine drug screens if needed, and psychiatric or psychological evaluation if needed (140).
Physical Therapy
Physical therapy (PT) procedures restore tissue and joint flexibility, improve posture and body mechanics, restore strength and coordination, reduce nervous system irritability, and restore function. PT is an important component of the management of patients with myofascial pain in the abdominal wall, pelvic floor, or lower back (141).
Laparoscopy
Women with disabling pain that is premenstrual and or menstrual and that does not respond to NSAIDs or hormonal contraceptives should be considered for laparoscopic evaluation. Diagnostic laparoscopy is a standard procedure in the evaluation of patients with chronic noncyclic pelvic pain; however, laparoscopy is generally withheld until other nongynecologic somatic or visceral causes of pain are excluded. Nonrandomized retrospective and prospective studies suggest that diagnostic laparoscopy provides a positive psychological effect on the treatment of chronic pelvic pain, but this should not be the main goal of laparoscopy (142). During diagnostic laparoscopy, endometriotic lesions should be excised for biopsy, and if infection is suspected, cultures should be performed. The laparoscopy is essentially a debulking procedure, and all visible endometriosis may not be able to be removed safely; but if possible the implants should be excised or electrocoagulated.
Presacral neurectomy and laparoscopic uterosacral nerve ablation (LUNA) are techniques to interrupt the nerve supply to the uterus. A large study showed that LUNA was no more effective for chronic pelvic pain than laparoscopy alone (143). A Cochrane database review revealed that there is insufficient evidence to recommend pelvic nerve disruption for the treatment of dysmenorrhea (45).
The role of pelvic adhesions in pain is unclear, and the efficacy of lysis of adhesions is even more in doubt. Adhesiolysis, even via laparoscopy, is frequently complicated by adhesion reformation and may not be effective for relief of pain in controlled trials (90,144). Other causes must be treated first, and psychological consultation and management should precede or accompany the lysis of adhesions.
Hysterectomy
Although 19% of hysterectomies are performed to cure pelvic pain, 30% of patients presenting to pain clinics have already undergone hysterectomy without experiencing pain relief. A multidisciplinary approach including a gynecologist, physical therapist, and a psychologist decreased the frequency of hysterectomy in one study from 16.3% of patients with chronic pelvic pain to 5.8% (145).
Hysterectomy is particularly useful for women who have completed childbearing and have secondary dysmenorrhea or chronic pain related to endometriosis, to uterine pathology, such as adenomyosis, or to pelvic congestion. Before recommending hysterectomy for pain or unilateral adnexectomy for unilateral pain, it is useful to apply the PREPARE mnemonic in discussions with the patient (146): the Procedure that is being done, Reason or indication, Expectation or desired outcome of the procedure, Probability that the outcome will be achieved, Alternatives and nonsurgical options, and Risks as well as Expense (see Chapter 3). Hysterectomy for central pelvic pain in women with dysmenorrhea, dyspareunia, and uterine tenderness provided relief of pain in 77% of women in one retrospective study and in 74% of women in one prospective cohort study (147,148). Nevertheless, 25% of women in the retrospective study noted that pain persisted or worsened at 1-year follow-up (147). Persistent pain in the prospective study was associated with multiparity, prior history of PID, absence of pathology, and Medicaid payer status (148). The Maine Women’s Health Study, a prospective cohort study, studied outcomes of 199 women with frequent pain at baseline who underwent hysterectomy. In this cohort, only 11% reported persistent symptoms after their surgery (149).
The American College of Obstetricians and Gynecologists outlined criteria that should be met before performing a hysterectomy for pelvic pain (150). They require at least 6 months of pelvic pain without any otherwise correctable pathology. When deciding on the surgical approach, consideration should be given to a vaginal or laparoscopic hysterectomy over an abdominal approach if there are no extensive adhesions expected or large uterine/fibroid size does not preclude it. There are many studies that confirm less morbidity and shorter hospital stays with vaginal compared with abdominal hysterectomies (151). A prospective study of abdominal versus vaginal versus laparoscopically assisted surgery did not find any statistical difference or worsening of outcomes of urinary or sexual function between the different approaches at 6 months (151).
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