Pelvic Pain and Dysmenorrhea
BS. Nguyễn Hồng Anh
KEY POINTS
1 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.
2 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), or pregnancy-related pain.
3 Chronic pelvic pain (CPP) is a multifaceted disorder characterized by changes in the processing of afferent signaling in the pelvic organs, the surrounding somatic tissues, the spinal cord, and the brain. The shared thoracolumbar and sacral innervations of the pelvic structures and the upregulation processing of neural input in the central nervous system account for the multiplicity of somatic and psychological symptoms experienced by women with CPP.
4 A thorough history and physical examination are important for successful management of acute and chronic pain. The ancillary laboratory and diagnostic procedures performed to assess acute, life-threatening processes differ from those focused on chronic pain conditions. CPP requires a multidisciplinary approach for diagnosis and management.
DEFINITIONS
[1] 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 (CPP) is defined as pain of greater than 3 months in duration, localized to the anatomic pelvis, and sufficiently severe to cause functional disability or necessitate medical care (2).
Whereas acute pain is generally associated with autonomic reflex responses, such as nausea, emesis, diaphoresis, and apprehension, these autonomic reflex responses are not present in women with CPP. Acute pain is often 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 CPP often involves changes in modulation or “upregulation” of normally nonpainful stimuli. Pain is out of proportion to the degree of tissue damage (3,4). Chronic pain is characterized by physiologic, affective, and behavioral responses that differ from those associated with acute pain (44). 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 (CNS) and the persistence of chronic pain (5–8). Genetic predisposition, adverse environmental pressures, and hormonal milieu are thought to increase the vulnerability and predisposition for chronic pain disorders (9).
ACUTE PAIN
The differential diagnosis of acute pelvic pain is outlined in Table 12-1.
Assessing the character of the pain helps create a differential diagnosis. [1] 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 the 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 12-1 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, 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. The innervations of the pelvic organs are outlined in Table 12-2. 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 referred to the same dermatomes (10).
Table 12-2 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;
L1–L2
Pudendal, inguinal,
genitofemoral, posterofemoral
cutaneous
Upper vagina, cervix, uterine corpus, inner third of fallopian tubes, broad ligament, upper bladder, 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. Fundamental to correct diagnosis is an accurate history. 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, 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 (dizziness, syncope, abdominal distention, and right upper quadrant or shoulder pain). Document any past medical and surgical history, and current medications.
Baseline laboratory studies will include, at minimum, a complete blood count (CBC) with differential, clean catch midstream 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
[2] 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 32).
Symptoms
Ectopic pregnancies can implant anywhere other than inside the uterus including the abdomen, cervix, ovary, or cornua of the uterus. Nearly all ectopic pregnancies (98%) are found within the fallopian tube, which will be discussed in this section (11).
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 intraabdominal blood collection transverses the right colic gutter and irritates the diaphragm (C3–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, after sitting for 3 minutes, and finally after standing for 3 minutes. If the systolic blood pressure decreases by 20 mmHg or the diastolic blood pressure decreases by 10 mmHg 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 the motion of the cervix. Adnexal tenderness is present, usually more pronounced on the side of the ectopic pregnancy, and a mass may be palpated. Positive pregnancy test and transvaginal ultrasound are usually confirmatory. Ultrasound findings can include an adnexal mass, pseudosac in the endometrium, and an extrauterine sac with a yolk sac within the embryo in the fallopian tube. If the patient has intraabdominal bleeding, peritoneal free fluid can be seen on the ultrasound. The diagnostic approach and the medical and surgical management of ectopic pregnancy are discussed in Chapter 32 (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 the 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.
Normal menstrual cycles produce follicles which mature to release an ovum,which becomes the corpus luteum that eventually involutes. When the follicle does not rupture to release an ovum it can become a follicular or physiologic cyst and continue to grow. Likewise, the corpus luteum fails to involute and continues to grow after ovulation. Both of these can become hemorrhagic cysts. Uncomplicated ruptured ovarian cysts which are hemodynamically stable can be managed with close observation, hospitalization, or repeat imaging.
[2] A hemorrhagic cyst can become symptomatic, causing worsening vital signs, and require surgery. 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 lifethreatening.
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 as a result of the persistently functioning corpus luteum. The onset of pain is usually sudden and is associated with increasing pelvic pain, which becomes generalized abdominal pain and dizziness or syncope with the 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, CBC, and, if orthostasis is present, type and screening should be ordered. Leukocytosis is uncommon. The hematocrit is decreased if active bleeding is present. If orthostasis is absent and the peripheral hematocrit is relatively normal, clinically significant hemoperitoneum is unlikely. Culdocentesis was used historically to support findings by aspirating clear, blood tinged, or purulent fluid in helping with diagnosis. It has largely been replaced by improvements in pelvic imaging, image-guided aspiration, or diagnostic laparoscopy.
A skillful reading of transvaginal ultrasound images can help 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, 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, not pregnant or anemic, and have only a small amount of fluid in the cul-de-sac can often be observed in the hospital, with surgical intervention, or discharged home from the emergency room after observation.
Adnexal Torsion
[2] 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). In the pediatric population, the clinician should be aware that torsion can happen with no ovarian lesion or mass.
Symptoms
The pain of torsion is usually severe and constant or, if the torsion is partial and intermittent, the pain can wax and wane. The onset of the torsion and subsequent abdominal pain frequently coincides with activities 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 coexistent
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. The presence of
Doppler blood flow to the ovary on ultrasound does not definitely rule out torsion.
CT has been shown to have low overall sensitivity and is not recommended for
the workup for suspected ovarian torsion in one meta-analysis (16) However, in
another case-control study, CT was not shown to be significantly different from
ultrasound in identifying ovarian torsion (17).
The ovarian torsion composite index (OT-CI) is a scoring system that combines
clinical and radiologic findings to accurately predict ovarian torsion. Scores
greater than or equal to 3 had 100% sensitivity and 65.3% specificity and could
be considered for surgical interventions (18).
The diagnosis of ovarian torsion is challenging as clinical symptoms are
neither sensitive nor specific and there are no definitive criteria with
imaging. Surgical diagnosis (laparoscopy or laparotomy) remains the
606diagnostic and therapeutic method of choice if there is suspicion of ovarian
torsion.
Management
Adnexal torsion must be treated surgically. The adnexa may be untwisted
and a cystectomy performed if appropriate. Even when it appears that
necrosis occurred, there is evidence that it remains functional and sparing
the adnexa can preserve its hormonal and reproductive function. 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 pelvic
inflammatory disease (PID) are discussed in Chapter 15.
Symptoms
[2] All cases of PID are polymicrobial, involving gram-negative and grampositive aerobic and anaerobic bacteria. 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 salpingooophoritis, with more insidious symptoms that can be confused with the
symptoms of irritable bowel syndrome (IBS) (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 (TOA) 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 coexistent with
intrauterine pregnancy (IUP) is rare. If the pregnancy test is positive, an infected
607or 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 (CDC) 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 motion, or adnexal tenderness without any apparent
cause (20). 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 (WBCs) on wet mount of vaginal secretions. One study showed
that an ESR >19.5 mm per 1/2 h and CRP >11.5 mg/L were predictors of TOA
where below these cutoffs were predictors of PID without TOA (21). Most
specific criteria for the diagnosis include endometritis on endometrial biopsy,
laparoscopic evidence of PID (tubal edema, erythema, and purulent discharge), or
thickened, fluid-filled fallopian tubes on pelvic ultrasound or magnetic resonance
imaging (MRI).
Tubo-Ovarian Abscess
[2] TOA, a complication of acute salpingo-oophoritis, is usually bilateral but
can be unilateral (20). The symptoms and signs are similar to those of acute
salpingitis. A ruptured TOA 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. TOAs can often be palpated on bimanual examination as firm, exquisitely
tender, bilateral fixed masses. The abscesses can be palpated or “pointed” 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.
Diagnosis
The diagnostic imaging of choice for TOAs is ultrasound. CT with and without
contrast can be used to establish the diagnosis (22). The differential diagnosis of a
unilateral mass includes TOA 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
608TOAs should always be treated as an inpatient, and conservative medical
therapy with intravenous broad-spectrum antibiotics can be attempted (see
Chapter 15) (23). If the patient is persistently febrile or not improving clinically,
CT or ultrasound-guided drainage of the abscesses should be undertaken. CTguided percutaneous drainage can be achieved transabdominally or
transvaginally. Drainage along with intravenous antibiotics is considered first-line
therapy (23,24). If fertility is not desired, bilateral salpingo-oophorectomy (BSO)
and hysterectomy will provide definitive therapy.
[2] A ruptured TOA 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 (see
Chapter 15).
According to the CDC, women should show clinical improvement in
regards to pelvic pain and vital signs within 3 days of initiation of therapy. If
there is no improvement, additional diagnostics should be performed, such as
diagnostic laparoscopy and other imaging for alternative diagnoses. Women who
receive a diagnosis of chlamydia or gonorrhea should be retested 3 months after
treatment and their partner should also be treated (20).
Uterine Leiomyomas
Leiomyomas (fibroids) are uterine smooth muscle tumors, as discussed in detail
in Chapter 11. 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 (25). There is no association between the degree of pain and
fibroid volume or number (26). A retrospective review of patients who had [2]
symptomatic fibroids were diagnosed with histology-proven endometriosis (27).
Acute pelvic pain caused by uterine leiomyomas is rare but can develop if
the myoma undergoes degeneration or torsion (27). Rare cases of uterine
rupture have been documented which require prompt treatment (28).
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
609labor. 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 (29). The fibroid can be excised
laparoscopically; however, surgery is not mandatory. A submucosal 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
endometrial cyst within the ovary) should be considered. The management of
endometriosis is discussed under dysmenorrhea and CPP (see also Chapter 13).
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 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
[2] 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 (30). 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. The mean platelet volume has been shown to be
helpful in diagnosis; a decrease in MPV was noted with patients with acute
appendicitis (31). 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
611rule 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.
A ruptured appendix is life-threatening and can have profound consequences
for the fertility of women of reproductive age. With the advent of imaging,
negative appendectomy rates are less than 10% (32).
Acute Diverticulitis
[2] 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. Hemodynamic instability can be
seen with perforation.
Diagnosis and Management
CT with and without contrast is an important adjunct to history and physical
examination (33). 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
612intake, 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, inflammatory bowel disease, or carcinoma of the bowel or
ovary.
Symptoms
[2] 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. Initially vomiting 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.
WBC 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. A water-soluble contrast such as Gastrografin has been
shown to be therapeutic and shown in studies to improve bowel function,
decreased hospital stay, and lower rate of surgery (34). 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 resulting from ureteral lithiasis is caused by a sudden increase
in intraluminal pressure and associated inflammation. Urinary tract infections
(UTIs) producing acute pain include cystitis and pyelonephritis. The most
common microbes causing UTIs are Escherichia coli followed by Proteus,
613Klebsiella, and Pseudomonas (35).
Symptoms and Signs
[2] The pain of lithiasis is typically severe and crampy; it can radiate from
the costovertebral angle (CVA) to the groin. Hematuria is often present. 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 CVA pain, although
lateralizing lower abdominal pain occasionally is present. Urethritis caused by
chlamydia or gonorrhea infection can have similar symptoms to those of a UTI.
These infections must be ruled out, if relevant.
Diagnosis
The 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 CVA 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 significant
squamous epithelial cells. Findings can subsequently be confirmed by
culture. The diagnostic thresholds for 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 sources recommend one intravenous
dose of a third-generation cephalosporin before discharging patients with oral
antibiotics) (see Chapter 15) (36). Caution should be used with
trimethoprim/sulfamethoxazole given the 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
614tolerate 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
[1] All women of reproductive age with acute pelvic pain should have a CBC
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 CPP 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,
hematochezia, and signs of elevated temperature, tachycardia, orthostasis,
abdominal distention, abnormal bowel sounds, ascites, peritonitis, or abnormal
pregnancy are all indicative of an acute process.
[1] Laboratory tests for the evaluation of acute pelvic pain include a CBC with
differential, ESR, 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. [1] 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. 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.
[1] 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
615(37).
CYCLIC PAIN: PRIMARY AND SECONDARY DYSMENORRHEA
[3] Dysmenorrhea is a common gynecologic disorder affecting as many as
60% of menstruating women (38). 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 12-3.
Primary Dysmenorrhea
[3] 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 (39). 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 cyclooxygenase (COX) pathway. The
biosynthesis and metabolism of prostaglandins and thromboxane derived from
arachidonic acid are depicted in Figure 12-1. Increased synthesis of prostanoids
in women with primary dysmenorrhea results in higher uterine tone with highamplitude contractions causing dysmenorrhea (40). It is theorized that women
suffering from dysmenorrhea have upregulated 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 (41).
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
616nature and, unlike abdominal pain that is caused by chemical or infectious
peritonitis, is relieved by abdominal massage, counterpressure, or movement of
the body.
Table 12-3 Differential Diagnosis of Chronic Pelvic Pain
Gynecologic Genitourinary
Noncyclic Recurrent or relapsing cystourethritis
Adhesions
Urethral syndrome
Endometriosis
Interstitial cystitis/painful bladder
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
Neurologic
Pelvic relaxation
Nerve entrapment syndrome,
neuroma, or other neuropathies
Cyclic Trigger points
Primary dysmenorrhea Musculoskeletal
Mittelschmerz Myofascial pain and trigger points
Secondary dysmenorrhea Low-back pain syndrome
Endometriosis/adenomyosis Congenital anomalies
Uterine or vaginal anomalies with
obstruction of menstrual outflow
Scoliosis and kyphosis
617Intrauterine synechiae (Asherman
syndrome)
Spondylolysis
Endometrial polyps or nonhormonal
intrauterine device (IUD)
Spondylolisthesis
Uterine leiomyomata Spinal injuries
Pelvic congestion syndrome Inflammation
Gastrointestinal Tumors
Irritable bowel syndrome Osteoporosis
Ulcerative colitis Degenerative changes
Crohn disease Coccydynia
Carcinoma Myofascial syndrome
Infection Systemic
Recurrent partial bowel obstruction Fibromyalgia
Diverticulitis Acute intermittent porphyria
Hernia Abdominal migraine
Abdominal angina Connective tissue disease including
systemic lupus erythematosus
Lymphoma
Neurofibromatosis
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
[3] To diagnose primary dysmenorrhea, it is necessary to clinically rule out
618underlying pelvic pathology and confirm the cyclic nature of the pain.
History taking is important to rule out abnormal uterine bleeding, presence of
dyspareunia, or nonmidline focal pelvic pain that can point to other causes of
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.
FIGURE 12-1 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.)
Management
[3] Prostaglandin synthase inhibitors, also called NSAIDs, are effective for
the treatment of primary dysmenorrhea (42). The inhibitors should be taken
620up to 1 to 3 days before or, if menses are irregular, at the first onset of
minimal pain or bleeding and continuously every 6 to 8 hours to prevent
reformation of prostaglandin byproducts. 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 have been shown to be equally effective to
NSAIDs. They are indicated for patients with primary dysmenorrhea who
have no contraindications to hormonal contraceptives and who desire
contraception. Hormonal contraceptive agents (such as combined estrogen
and progestin) or progesterone-only oral contraceptives (OCs) (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 (43). Continuous or extended cycle combined OC pills are just as
efficacious for this pain syndrome (44). 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.
Treatment with both NSAIDs and hormonal contraception may be more
effective than either one alone. If the patient does not respond to this regimen
for 2 to 3 months, 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 (45–47).
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. There is insufficient data to support any herbal or
vitamin regimen.
Methods rarely used to treat primary dysmenorrhea include surgical
laparoscopic uterine nerve ablation and presacral neurectomy and hysterectomy
(48).
Secondary Dysmenorrhea
[3] 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. [3] Underlying causes include
endometriosis, adenomyosis, subacute endometritis and PID, copper intrauterine
devices (IUDs), ovarian cysts, congenital pelvic malformations, and cervical
stenosis. Whereas the diagnosis of primary dysmenorrhea is based on the 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 transvaginal ultrasound examination, laparoscopy, and hysteroscopy may be
indicated.
[3] 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 12-3. The
management of secondary dysmenorrhea is treatment of the underlying disorder.
Endometriosis
[3] 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. They can occur outside the pelvis such as
the bowel, diaphragm, and even the pleural cavity. There are several theories
of pathogenesis, but none explains all the different types of endometriosis. 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
CPP. In some cases, regression can occur spontaneously (see the section on
endometriosis under the heading of chronic pelvic pain and Chapter 13) (49).
Symptoms
Patients typically complain of severe dysmenorrhea and cyclic pelvic pain
that starts up to 2 weeks prior to menses. Symptoms depend on the site of
endometriosis. The pain can be sharp or pressure-like, 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. Patients with thoracic
endometriosis can have symptoms of chest pain, pneumothorax, and hemothorax
622that coincides with menses (50).
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. Abdominal wall
endometriosis implants can present with a cyclically painful discrete abdominal
mass on examination.
Diagnosis
Diagnosis of endometriosis is categorized by nonsurgical or surgical
diagnosis. The clinical, or nonsurgical, diagnosis of endometriosis is accurate in
approximately 50% of cases. Though a definitive diagnosis of endometriosis
cannot be made on imaging studies, endometriomas are generally distinguishable
from hemorrhagic corpus lutea by the appearance on ultrasound. Homogeneous
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 or surgical diagnosis is
made by direct operative visualization either laparoscopically or via
laparotomy with histologic confirmation. 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 Caused by Endometriosis: Pharmacologic
Medications can be used to reduce the cyclic hormonal stimulation of these
lesions and eventually decidualize or atrophy the lesions. Surgical resection
of endometriosis has surgical risks but can reduce pain by removing
implants. One study showed short-term improvement in dyspareunia and quality
of sex life in patients up to 12 months after radical resection of endometriosis
(53). Given the excellent response rate, relatively low cost, and fair tolerability
623with medical 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 combined estrogen–
progestin formulations with or without NSAIDs (54). Both cyclic and
continuous combined OCs can be used with equal efficacy (55). Most studies
used OCs containing low-dose estrogen and more androgenic progestins; newergeneration progestins are also effective. Continuous rather than cyclic OC
regimens can be tried, without a hormonal break or with menstruation every 3
months. Two reviews have shown that continuous OCs may be more effective at
reducing pain symptoms than cyclic regiments in maintaining symptoms after
initial surgery (56,57).
Second-line medical therapy involves high-dose progestins or
gonadotropin-releasing hormone (GnRH) analogs. 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 (58). High-dose medroxyprogesterone acetate and
norethindrone acetate are equally effective to the GnRH analogs (59). 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 (60). Etonogestrel implants are
shown to be as effective as medroxyprogesterone acetate (61).
GnRH agonist and add-back treatment can be used as pharmacologic
treatments for endometriosis (62). 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 addback therapy with norethindrone acetate 2.5 to 5 mg daily with or without lowdose estrogen (0.625 mg of conjugated estrogen or 1 mg of 17 β-estradiol) (62).
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.
624Androgenic hormones such as danazol are thought to inhibit the
luteinizing hormone surge and steroidogenesis and may have antiinflammatory 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.
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 being used as adjunctive
therapy with medical therapies in refractory cases (63). A 2008 review of
eight studies evaluated AIs for management of endometriosis and found that AIs
combined with progestins or OCs or GnRH analogs decreased mean pain scores
and lesion size and improved the quality of life. In the only randomized controlled
trial (97 women) evaluated in this meta-analysis, AI (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 the spine or hip bone density (64).
Management of Endometriosis: Surgical
Laparoscopy and laparotomy are appropriate for some patients, and can be
considered for treatment in the management of secondary dysmenorrheal
pain related to endometriosis that is unresponsive to hormonal agents (see
also Chapter 13). 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 CPP 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% (65). A meta-analysis found that there was
no difference in pain levels when comparing patients with surgical and medical
management of endometriosis (66). Given these findings, the risks and benefits of
surgical management should be thoroughly discussed with patients when coming
up with a treatment plan.
In women who no longer desire fertility with severe secondary
dysmenorrhea, hysterectomy with BSO and removal of endometriosis lesions
is the preferred treatment. Hysterectomy without BSO results in a higher rate of
625disease 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 denervation procedures (65). Although reoperation 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 further
surgical procedure at least 20%. Hysterectomy with BSO decreased the need for
reoperation to treat pelvic pain by sixfold. Postoperative medical treatment with
OCs can be effective (67). Reoperation 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 13). These lesions can be surgically challenging for laparoscopic
resection. Hormonal therapy can be effective. One study reviewed hormonal
therapy in 217 patients: 68 in 5 observational studies, 59 in a cohort study, and 90
in a randomized controlled trial (68). The study compared AI, vaginal danazol,
GnRH agonist, intrauterine progestin, and two estrogen–progestin combinations,
transvaginally or transdermally, and an oral progestin. With the exception of an
AI 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.
Adenomyosis
[3] Adenomyosis is defined as the 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 (69–71).
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
626may not resolve until after the cessation of menses. Patients may present with
CPP.
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 (72).
Diagnosis
Adenomyosis is a clinical diagnosis. Definitive diagnosis can only be made
histologically. 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.
Transvaginal ultrasound has been shown to have an accuracy rate of 68% to 86%
in diagnosing adenomyosis. The accuracy decreases in women who have
coexisting fibroids or who have focal adenomyosis (73). 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 GnRH agonists are all useful.
Treatment follows the same protocol as treatment for endometriosis. Uterine
artery embolization can be effective (74).
CHRONIC PELVIC PAIN
[3] CPP is defined as pelvic pain that persists in the same location for greater
than 6 months’ duration, causing functional disability or requiring
treatment. 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. CPP
affects 12% to 20% of women in the United States. The differential diagnosis of
CPP is outlined in Table 12-3. [3] Nongynecologic causes of pain, such as IBS,
interstitial cystitis (IC)/bladder pain syndrome (BPS), abdominal wall or
pelvic floor myofascial syndrome, or neuropathy, are frequently overlooked
627but common causes of CPP. This can in part explain why 60% to 80% of
patients undergoing laparoscopy for CPP have no intraperitoneal pathology (2).
Patients with CPP are often anxious and depressed. Their marital, sexual,
social, and occupational lives are disrupted. While some patients with CPP
present with psychiatric comorbidities, some women develop secondary
symptoms as a result of CPP. 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 (75).
CPP states are characterized by upregulation of CNS responsiveness to
peripheral stimuli. [3] 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 CNS 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 (5–7,76).
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 (77). 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 upregulation 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.
[3] 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 (8). 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
628[4] 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 12-4). 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. [4] 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 IBS and IC/BPS. 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 or reproduced (78).
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 12-3.
1. [4] 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 gynecologic, 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 (79–81). 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.
Table 12-4 Pain History Mneumonic
OLD CAARTS Pain History
Onset When and how did pain start? Did it change over time?
Location Localize specifically. Can you put a finger on it?
Duration How long does it last?
Characteristic Cramping, aching, stabbing, burning. “like lightening,”
tingling, itching
Alleviating/Aggravating
factors
What makes it better (medication, stress reduction,
heat/ice, position change) or worse (specific activity,
stress, menstrual cycle)?
Associated symptoms Gynecologic (dyspareunia, dysmenorrhea, abnormal
bleeding, discharge, infertility), GI (constipation,
diarrhea, bloating, gas, rectal bleeding), GU (frequency,
dysuria, urgency, incontinence), neurologic (specific
nerve distribution)
Radiation Does it move to other areas (dermatomal)?
Temporal What time of day (elation to menstrual cycle and
activities of daily living)?
Severity Scale of 0–10
GI, gastrointestinal; GU, genitourinary.
From Rapkin AJ, Howe CN. Chronic pelvic pain: A review. Part 2. In: Family Practice
Recertification. Monroe Township, New Jersey: Medical World Communications,
2006;28:59–67.
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 (2,82,83). 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.
[4] 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 during these maneuvers (84). 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 (84). 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 pathologies, such as
benign or malignant ovarian cysts, uterine leiomyomas of a 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
13.
[4] Endometriosis can be demonstrated in 15% to 40% of patients undergoing
laparoscopy for CPP. Endometriosis is a surgical diagnosis based on
identification and histology of characteristic lesions (85). Endometriosis produces
a low-grade inflammatory reaction; over time this results in adhesions between
confluent pelvic organs (86). However, the cause of the pain is not well
established. [4] There is no correlation between the location of disease and
pain symptoms. (87,88). 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.
631Similarly, 40% to 60% of patients have no tenderness on examination
regardless of stage (88). Deeply infiltrating endometriosis lesions that involve
the rectovaginal septum and the bowel, ureters, and bladder are strongly
associated with pain (86,89,90) Pelvic adhesions related to endometriosis are a
predictor of pelvic pain (91). 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 CNS sensitization and persistence of pain even after surgical
therapy (92–94).
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 (93). 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 “comorbid” with
other chronic conditions such as IC/PBS, IBS, myofascial pain, fibromyalgia and
vulvodynia, and anxiety disorders. These disorders need to be managed
concurrently.
Adhesions
[4] 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 (95,96). 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 (97). 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 (98–
100). One randomized controlled trial that did not consistently demonstrate a
significant long-term reduction in pain did find some improvement if the
632adhesions were dense and involved the small bowel (101). In a nonrandomized
study of patients who underwent adhesiolysis for pelvic pain, 41% of patients still
had residual abdominal symptoms during a 15 year follow up (102).
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 (103). 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
(2,104).
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 CPP, 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
carboxymethyl cellulose have been shown in meta-analysis studies to be effective
for prevention of adhesion reformation (105). 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 (106–110). 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. This study
demonstrated that women with CPP had a larger mean ovarian vein diameter,
633delayed disappearance of contrast medium, and greater ovarian plexus congestion
compared to controls. The existence of this condition is controversial as this
condition does not have definitive diagnostic criteria (110).
Pelvic congestion syndrome results from compression of the left renal vein at
the origin of the superior mesenteric artery (also known as “nutcracker
syndrome”). This leads to pelvic venous congestion.
Signs and Symptoms
[4] 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 (110). 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
Diagnosis can be made clinically. However, imaging can be used to help
diagnosis and aid in therapy. Transuterine venography or MRI are the
primary method for diagnosis, although other modalities, such as pelvic
ultrasound and laparoscopy, may disclose varicosities (106,110). Because of the
cost and possible side effects of treatment, further management should be based
on related symptoms and not solely 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 salpingooophorectomy (106–110). Low-estrogen, progestin-dominant continuous OCs,
high-dose progestins, and GnRH analogs often provide pain relief (107).
Hormonal suppression should be the initial mode of treatment for women with
suspected pelvic congestion. Medroxyprogesterone acetate, 30 mg daily, is useful
(108). Goserelin acetate (3.5 mg a month for 6 months) has been shown to be
effective in treating pelvic congestion in pelvic venography improvements and in
symptom improvement (107). 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 (109,110). Technically more invasive,
transcatheter embolotherapy selectively catheterizes the ovarian and internal iliac
veins, followed by contrast venography and embolization. This treatment showed
634some 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 (110).
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 15).
Ovarian Remnant and Residual Ovary Syndromes
[4] In a reproductive-aged patient who has had a BSO, with or without a
hysterectomy, for severe endometriosis or PID, CPP may be caused by ovarian
remnant syndrome (111). 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. This can be seen
in patients with endometriosis in which ovarian implants are left in place.
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
635tissue. 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 BSO 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 (111). 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. Imaging with pelvic ultrasound can be used if pelvic mass is found
on exam.
Management
Patients who are not candidates for, or decline, surgery can be managed
through medical treatment such as high-dose progestins or OCs, which
usually provides good results. Patients 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 (112). 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 (113,114).
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 (111). 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. [4] 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 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
636and visualization of colonic mucosa when appropriate.
Irritable Bowel Syndrome
[4] 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 CPP. An estimated
35% of patients with CPP have a concurrent diagnosis of IBS (115,116). Women
who had a hysterectomy for CPP are twice as likely to have IBS. Women are at a
slightly higher risk of IBS than men (117). The pathophysiology of IBS appears
to be influenced by CNS sensitization and decreased descending inhibition, which
ultimately leads to visceral hypersensitivity. Visceral hypersensitivity and
abnormal reflex responses, demonstrated in both animal and human studies, result
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
(118,119).
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, diarrheapredominant, and pain-predominant (alternating bowel habits) depending on their
main symptoms. The new Rome IV criteria for diagnosis (Table 12-5) 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 the
form and appearance of stool (120).
Table 12-5 Rome IV Criteria for Irritable Bowel Syndrome
Recurrent abdominal pain for at least 1 day per week (on average) for the previous 3
months with onset of symptoms at least 6 months before the diagnosis and associated
with two of three features:
1. Related to defecation
2. Associated with a change in frequency of stool
6373. 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 (TCAs). 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 (117–119). Multidisciplinary
therapy addresses the cognitive, affective, and behavioral components of the pain.
Therapy may decrease the intensity of nociceptor stimulation and change the
patient’s interpretation of the meaning of pain (119).
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 TCAs can alleviate the pain of IBS as shown in a
number of randomized controlled trials. TCAs can 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 coexisting depression. Selective serotonin reuptake
inhibitors (SSRIs) and serotonin/norepinephrine reuptake inhibitors (SNRIs)
638were 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 (117–119).
Urologic Etiology
[4] CPP of urologic origin may be related to recurrent cystourethritis,
urethral syndrome, sensory urgency of uncertain cause, and IC/PBS. 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
(121). 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 evolve into the initial stages of IC/PBS.
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.
According to the American Urological Association, these symptoms must be
present for at least 6 weeks.
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 RUA and culture should be
obtained to rule out UTI. Urine cytology can help exclude malignancy or
hematuria. A postvoid residual can easily be done in clinic to check for urinary
retention. 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 ureaplasma, chlamydia, candida,
639trichomonas, 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 be a manifestation of IC/PBS.
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 UTIs. 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 (PT), 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
(122). Psychological support is very important in this group of women.
Management requires a multidisciplinary approach, as is true of CPP in
general.
Interstitial Cystitis/Bladder Pain Syndrome or Painful Bladder Syndrome
IC/BPS 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 (123).
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 “IC” refers
to patients who have PBS symptoms, but who also have “typical cystoscopic
and histologic features” during bladder hydrodistention (123).
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 (124). This theoretical mechanism is based on the
fact that many IC sufferers are sensitive to certain foods and beverages.
Immunologic mechanisms were proposed because abnormal mast cell activity,
640increased substance P–expressing nerve fibers and increased nerve growth factor,
were all found in bladder biopsies of IC-affected individuals (124). Autoimmune
mechanisms may be responsible in some individuals given that there is a higher
incidence of systemic lupus erythematosus, allergies, inflammatory bowel and
IBD, 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 (125).
Symptoms
Symptoms include pain and 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 (125).
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.
Definitions and diagnostic criteria continue to change. In 2011, the American
Urological Association defined criteria as an unpleasant sensation perceived
to be related to the urinary bladder, associated with lower urinary tract
symptoms of more than 6 weeks’ duration, in the absence of infection or
other identifiable causes.
National Institutes of Health (NIH) Consensus Criteria for diagnosis of IC
states that patients must have at least two of the following: (1) pain on bladder
filling relieved by emptying; (2) pain in suprapubic, pelvic, urethral, vaginal, or
perineal region; (3) glomerulations on endoscopy or decreased compliance on
cystometrogram (126).
Patients can be evaluated with cystoscopy with hydrodistention 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 (127);
it is debatable whether a positive potassium test is definitive for IC or if a positive
test is a manifestation of bladder hyperalgesia (126).
Management
641Although there is no definitive cure for IC/PBS, 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 PT. These first-line
treatments are individually specific. For example, studies have shown that the
foods that can cause irritation differ between individuals (128). Urinary
alkalinization can be useful (129). 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, urinary frequency, and neuropathic pain,
respectively (129). Oral pentosan polysulfate sodium (PPS) is the only U.S. Food
and Drug Administration (FDA)-approved oral therapy for IC and is modestly
beneficial (129,130). Pentosan polysulfate is a heparin-like 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 (131). Dimethyl sulfoxide (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 (132).
Hydrodistention of the bladder to maximum capacity under epidural anesthesia
has been used to treat ICS/PBS and has shown to be helpful in improving
symptoms (133,134).
Sacral neuromodulation is an invasive, yet promising, technique under
investigation for treatment of refractory IC (135). Sacral neuromodulation is not
FDA approved for IC, and larger studies are required to confirm efficacy.
Treatments that require more data to support safety and efficacy include
intravesical instillation of GAGs and intradetrusor botulinum toxin.
Neurologic and Musculoskeletal Causes
Nerve Entrapment
[4] Abdominal cutaneous nerve injury or entrapment of the iliohypogastric
or ilioinguinal nerves can occur with transverse suprapubic laparotomy
incisions or laparoscopy incisions placed inferior to the anterior superior
iliac spine. Injury can follow heavy lifting or traumatic injury, such as with a
motor vehicle accident. The ilioinguinal (thoracic 12, lumbar 1 and lumbar 2,
642T12, 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
(136). Localized pain in the L1–L2 dermatome lateral to the rectus muscle
immediately following surgery should be evaluated expeditiously, as removal
of the offending fascial suture will be curative. Neuropathic pain may not
begin until weeks after surgery or even years following surgery, following
vigorous abdominal wall stress with lifting or reinjury.
Femoral nerve injury can result when deep lateral retractor blades
compress the nerve between the blade and the lateral pelvic side wall (137).
Femoral nerve damage results in an inability to flex at the hip joint or to extend at
the knee.
Symptoms of nerve entrapment or injury include sharp, burning, aching pain,
and paresthesia in the dermatomal distribution of the involved nerve. With nerve
entrapment, hip flexion and exercise or activity exacerbates pain and rest or
infiltration with a local anesthetic relieves pain. The pain is usually judged as
coming from the abdomen, not the skin (138).
Pudendal neuropathy can result from vaginal surgery (especially with
lateral mesh attachments), childbirth, exercise, and chronic constipation or
pelvic floor muscle abnormalities. Vulvar surgical procedures including
episiotomies, laser hair removal, and Bartholin gland removal can lead to
injury of the vestibular, rectal, or clitoral nerves, terminal branches of the
pudendal nerve (139).
Nantes criteria for pudendal nerve entrapment in and around the Alcock canal
are: (1) pain in the sacral 2–4 dermatomal area innervated by the pudendal nerve
(i.e., ipsilateral clitoris/ penis, distal urethra, labia/scrotum, perineum, and anus);
(2) pain is increased while sitting; (3) patient is not awakened by pain; (4) no
sensory loss on clinical examination (sensory deficits are suggestive of a sacral
nerve root lesion); (5) resolution of pain with administration of pudendal nerve
block (140). Entrapment can potentially be relieved by surgical release but
neuralgia caused by nerve injury will not recover from surgery. It is not possible
with examination or imaging to completely differentiate pudendal entrapment
from neuralgia related to nerve injury.
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 at the rectus margin, medial and inferior to the anterior iliac
spine. Carnett test will be positive with increased pain over the area of entrapment
or injury. Carnett test involves palpation of the tender area followed by
643repalpation during an abdominal wall tensing maneuver, that is abdominal crunch
(3/4 “sit up”) or bilateral straight leg raise. Abdominal wall pain is more severe
with palpation during muscle contraction in the setting of L1, L2 nerve
entrapment, injury, hernia, or myofascial pain. For the pudendal nerve, the
maximal tenderness is near the ischial spine and the Alcock canal.
A tentative diagnosis or neuropathy 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 the following weeks.
Management
Many patients may require no further intervention after a series of weekly nerve
blocks and avoiding activities that lead to compression of the nerve. Many
patients require PT or medications that downregulate nerve firing. Medications
for neuropathic pain include topical local anesthetics, oral anticonvulsants, or
antidepressants. PT can be helpful in cases of pudendal neuropathy involving
abnormal functioning of levator or obturator internus muscles. If injection and
other pharmacologic approaches produce only limited pain relief and there are no
contributory visceral or psychological factors, surgical decompression of the
involved nerve may be recommended.
Myofascial Pain
Myofascial pain of the abdominal wall or pelvic floor muscles are commonly
overlooked in the evaluation of CPP. [4] Myofascial pain syndrome (MPS)
consists of pain originating from muscle trigger points in the skeletal muscle
and fascia. By definition, a myofascial trigger point is a “hyperirritability
focus within a tender, taut band-like hardness within one or more skeletal
muscles or the associated fascia” (141). Intra-abdominal pathology, muscular
overload, and direct trauma can result in the development of trigger points but are
not required for development or perpetuation.
Depending on the study, 13% to 75% of women with CPP have myofascial
pelvic tenderness and/or trigger points (142). Pelvic floor muscle pain can result
from surgical trauma, poor posture, severe constipation, or viscerosomatic
reflex responses. The muscles sharing thoracolumbar and sacral nerve supply
with the reproductive, gastrointestinal, and urinary systems can lead to pelvic
floor and abdominal wall muscle pain (143). Trigger points can develop in
muscles in the zone of the referred pain from the underlying organ and in turn the
trigger point can lead to abdominal fullness, bloating, swelling, and gas. IC/PBS,
IBS, endometriosis, and vulvodynia are associated with pelvic floor dysfunction
and trigger points and many women with these diagnoses have, or will develop,
644generalized chronic myofascial pain and fibromyalgia (143). Trigger points in the
lower rectus abdominis between the umbilicus and symphysis can develop in
women with severe dysmenorrhea.
Symptoms
History should investigate overuse, repetitive strains, injuries, and dysfunctional
posturing which can result in myofascial trigger points in the abdominal wall,
back, and pelvic floor. History of IBS, IC/PBS, or endometriosis should prompt a
search for abdominal wall and pelvic floor myofascial pain. Abdominal wall and
pelvic floor myofascial pain is exacerbated by activity, or by stimuli to the
dermatome of trigger points (e.g., full bladder, bowel, luteal phase, or menses;
any stimulation to organs that share the dermatome of the involved nerve) (144).
Signs
Pelvic muscle assessment should include both external and internal muscles. In
addition to testing for tenderness, muscle strength, for which both the squeeze and
lift components are essential, and function testing are important (145).
Unfortunately, techniques for the discovery of pelvic floor trigger points are not
standardized, making it difficult to describe the musculoskeletal system for the
diagnostic workup.
Management
Massage therapy can help relieve the pain in some cases. “Myofascial
release” is a special vigorous message that can be effective (141). Depending
on the location of the myofascial trigger points, pelvic floor PT is indicated
(145,146).
PT entails manual techniques to inactivate trigger points, restore muscle
length, and correct predisposing factors. Pelvic floor PT involves a variety of
muscle relaxation and lengthening exercises to pelvic floor muscles as well as
releasing trigger points by connective tissue release. A retrospective chart review
of 75 women with chronic myofascial pelvic pain noted significantly improved
pain scores proportional to the number of PT visits completed (144). A
randomized study noted 57% patients with CPP benefited from myofascial PT
(147,148). The response rate was significantly greater with PT compared to
therapeutic massage. Sustained pressure with adequate force to a trigger point for
a specified period or injection can inactivate the irritable point (149).
NSAIDs, gabapentin, pregabalin, low-dose TCAs, SNRIs, 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
645four to five biweekly injections, the procedure should be abandoned if longlasting 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 (MPS). 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 (151). Acupuncture
can be effective (152). 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
[4] Fibromyalgia is an MPS, made up of the triad of diffuse pain, fatigue, and
nonrestorative sleep. Women with abdominal wall or pelvic floor myofascial
pain, IC/PBS, and IBS often have comorbid 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
CNS 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
SNRIs, anticonvulsants, and benzodiazepines to improve sleep (150).
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 spondylogenic (related to the axial
skeleton and its structure) pathology (153).
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
646Examination 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 the 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 orthopedic or neurosurgery consult
may be required.
Vulvodynia
[4] Vulvodynia has a prevalence of 15% and is classified as vulvar pain for at
least 3 months without a clear source (154). Specific causes of vulvar pain must
be excluded before a diagnosis of vulvodynia can be made. Specific causes of
vulvar pain that should be ruled out include inflammatory conditions
(dermatitis, dermatoses), malignancy, neuralgia, trauma, iatrogenic causes
(e.g., chemotherapy, radiation, surgery), infection (candida, herpes), and
hormonal deficiency. Factors that can initiate or maintain vulvodynia include
comorbid pain or psychiatric disorders, genetic predisposition to pain or
inflammation, sex steroid hormone deficiency, pelvic floor musculoskeletal
abnormalities, relevant neurologic changes in the pudendal or sacral 2–4 nerves,
and psychosocial issues. Vulvodynia is classified by pain localization, triggers,
and timing of onset. If there is localized pain of the vulvar vestibule
(vestibulodynia) or clitoris (clitorodynia), vulvodynia is classified as localized.
Pain over the entire vulva is called generalized vulvodynia. Mixed vulvodynia
refers to pain that is localized and generalized. Pain is further classified as
provoked which means pain with genital contact or spontaneous, whereby the
pain occurs without contact. Pain can be provoked and spontaneous. If the pain
occurs from the first genital penetration attempt, it is classified as primary. If the
647pain starts after a period of painless genital contact, it is classified as secondary.
The pathophysiology of vulvodynia is unclear but likely complex and
multifactorial. Provoked vestibular pain, the most common type of
vulvodynia, has been hypothesized to start with a chronic inflammatory
process or immunologic challenge such as yeast infection or injury.
Proliferation of nociceptive nerve fibers, increased inflammatory infiltrate
dominated by mast cells, and increased neuroinflammatory neurokines, cytokines,
chemokines, and prostanoids can develop in predisposed individuals (155).
Altered pelvic floor musculature contractility often is associated but may be
etiologic. There is evidence for central and peripheral sensitization with
hypersensitivity to tactile, thermal, and chemical stimuli.
A history and examination are adequate for the diagnosis of vulvodynia.
Patients should be questioned about their medical, psychological, sexual, and pain
history (156). The vulva and vagina should be examined for any lesions,
infections, or dermatoses. A cotton swab is used to test the vestibule for pain
at 12, 2, 5, 6, 7, and 10 o’clock. Pain of at least 4/10 on a numeric rating scale
when the swab is pressed to a depth of 1/3 of the cotton tip for 1 second is
consistent with provoked vestibulodynia. Pelvic floor muscle tone and
tenderness should be ascertained with a single lubricated finger in the vagina. A
wet mount of vaginal discharge should be performed to look for yeast or bacterial
vaginosis and for signs of inflammation (excessive white blood cells) or estrogen
deficiency (multiple parabasal or intermediate cells). Imaging studies can be
considered to diagnose the pain if not limited to vestibule.
The treatment of vulvar pain is multifactorial. Address any underlying
disorder which may be causing the pain such as infection, dermatoses,
psychological, or hormonal issues. Long-term hormonal contraceptives may
contribute to vestibular thinning and pain. Vulvar hygiene is an important part of
the treatment. Patients should be taught to eliminate pads, allergens, fabric
softeners, soaps, and other potentially irritating chemicals. The pharmacologic
treatments of vulvodynia can include topical lidocaine 5%, anticonvulsants
such as gabapentin topical (6% compounded) or oral, TCAs either as a
topical or oral formulation, botulinum toxin injections, hormonal therapy if
estrogen deficiency is noted, and injections of local anesthetic with or without
steroid. Pelvic floor PT is usually recommended for treatment of vulvodynia.
Further treatments include surgery (vestibulectomy) for provoked vestibulodynia,
psychological (cognitive–behavioral, psychotherapy, mindfulness-based
relaxation therapy), EMG biofeedback, and complementary/alternative treatments
such as acupuncture or hypnotherapy (157–161).
Psychological Factors
648[3] Psychological factors that increase pain vulnerability and lower resilience
promote the chronicity of pain (162). The meaning attached to the pain, painrelated catastrophizing, low self-efficacy in managing pain, poor pain coping,
anxiety, negative affect, childhood emotional, physical or sexual traumatic
experiences, and poor social support all play a role in maintaining and amplifying
chronic pain (163–165). Recent investigations are beginning to shed light on how
current and previous psychological, behavioral, and psychosocial factors affect
chronic pain. Crucial are the changes in brain networks concerning reward,
motivation, learning, and pathways descending from the brain to the periphery
that modulate pain (162). [3] There is a close relationship between depression
and pain. The Beck Depression Inventory can be used as a tool for evaluation; a
score over 12 suggests dysphoria and over 18, depression (166). Antidepressants,
particularly SNRIs often relieve depression and pain.
[3] Childhood physical abuse has been noted to be more prevalent in women
with CPP than in those with other types of pain (39% vs. 18.4%) (81). In a
comparison of women with CPP, 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 CPP 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 CPP (167).
Dramatizing the pain is a coping mechanism that is used by pain sufferers to
generate support from others around them (168). This practice, combined with
pain-related anxiety and fear, propagates pain.
Management of Chronic Pelvic Pain
Multidisciplinary Approach
[3] The multidisciplinary management approach recognizes the importance
of cognitive, psychological, and myofascial contributions to chronic pain. The
treatment milieu for women with chronic pain must be therapeutic,
optimistic, and supportive. The patient should be instructed to complete a
daily pain rating form for two menstrual cycles and bring to her subsequent
visit. This form provides the clinician and patient with important information for
pain diagnosis and management. Each day, the average pain level (0 to 10), mood
(0 to 10), vaginal bleeding (yes or no), and briefly, events that trigger pain such as
stress, foods, and physical activities should be recorded. The pain ratings can
encourage the patient’s sense of control and decrease feelings of helplessness.
649Daily recording improves self-efficacy and compliance, and help the patient to
recognize the connection between pain and stressors. The ratings reveal the
relationship of the pain to the menstrual cycle. Cyclical pain associated with
ovulation, premenstrual, or menstrual phase can be improved with hormonal
suppression.
[3] 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 with techniques as mindfulness-based
meditation or yoga. Patients should be instructed in ways to enhance
opportunities for control of pain. Various strategies, including cognitivebehavioral therapy, mindfulness-based relaxation techniques, stress management,
hypnosis, and other psychotherapeutic approaches affect CNS pain networks and
increase descending inhibition of peripheral pain signals. Psychological group
treatment is a very cost-effective approach for helping patients learn stress
reduction techniques and develop coping behavioral mechanisms (169).
Psychotherapy is indicated for women who have pronounced depression, sexual
difficulties, or previous trauma. Acupuncture can be helpful. Myofascial
evaluation can be supplemented by PT evaluation and if appropriate, PT treatment
should be initiated.
Various studies of multidisciplinary pain management in CPP were performed
in the past (170). 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 (171). 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 the quality of life (170).
[3] The following groups of patients should be considered for
multidisciplinary therapy early in the management process: (1) no obvious
pathology; (2) pathology that has an equivocal role in pain production; (3)
poor response to traditionally effective medical or surgical management; (4)
more than one visceral or somatic structure involved in the production of
pain (i.e., more than one “pain generator”); (5) significant stress, anxiety,
posttraumatic stress disorder, or depression; (6) history of past or current
physical, emotional, or sexual trauma. There is a dearth of evidence based on
controlled trials for the treatment of noncyclic pelvic pain (172).
Pharmacologic Interventions
Any patients with dysmenorrhea or pain that worsens in the luteal or
650menstrual phase should be given pre-emptive NSAIDs in adequate doses
and/or hormonal agents to suppress ovulation and/or menses. The choice of
the hormonal agent used to suppress the menstrual cycle will vary with patient
preference, concurrent medical conditions, and side effects.
Patients with neuropathic pain or those with evidence of central
sensitization or myofascial pain benefit from agents that alter neural
processing (173). A low dose of a TCA, most anticonvulsants, and selective
SNRIs are often effective, especially if combined with cognitive-behavioral
therapy or mindfulness. 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 women’s lifestyle (104).
Anticonvulsants such as gabapentin or pregabalin are useful for treatment of
CPP. Gabapentin plus amitriptyline can be more efficacious than amitriptyline
alone (173). The anticonvulsants likely impact pain via blockade of calcium
channels.
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 downregulate neural signaling.
Women with significant depression or anxiety should be treated with an
appropriate therapeutic dose of antidepressant or anxiolytic 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 CPP 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.
Updated opioid guidelines for chronic noncancer pain are available (174,175).
Physical Therapy
PT procedures restore tissue and joint flexibility, improve posture and body
mechanics, restore strength and coordination, reduce nervous system irritability,
651and restore function (175). PT is an important component of the management
of patients with myofascial pain in the abdominal wall, pelvic floor, or lower
back or fibromyalgia (146).
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. 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 CPP than laparoscopy alone (176). A 2007
review revealed that there is insufficient evidence to recommend pelvic nerve
disruption for the treatment of dysmenorrhea (177).
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 (96–102). 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 CPP to 5.8% (178).
[4] Hysterectomy is particularly useful for women who have completed
childbearing and have secondary dysmenorrhea or chronic pain related to
endometriosis, uterine pathology, such as adenomyosis, or pelvic congestion.
However, hysterectomy is generally not indicated for patients with CPP
(179–181). Before recommending hysterectomy for pain or unilateral
adnexectomy for unilateral pain, it is useful to apply the PREPARE mnemonic in
discussions with the patient (182): the Procedure that is being done, Reason or
652indication, 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 (183). Nevertheless, 25% of women in the retrospective
study noted that pain persisted or worsened at 1-year follow-up (183). Persistent
pain in the prospective study was associated with multiparity, prior history of
PID, absence of pathology, and Medicaid payer status. 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 (184).
The American College of Obstetricians and Gynecologists outlined criteria
that should be met before performing a hysterectomy for pelvic pain (185).
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
(186). 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 (186)
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