This chapter deals primarily with APGO Educational Topic Areas:
TOPIC 39 CHRONIC PELVIC PAIN
TOPIC 46 DYSMENORRHEA
Students should be able to define chronic pelvic pain as well as primary and secondary dysmenorrhea and list common etiologies. They should be able to outline a basic approach to initial evaluation and management of these disorders. They should also appreciate the associated psychological and social issues.
Clinical Case
A 17-year-old virginal woman complains of cyclic, sharp, crampy, lower abdominal pain that begins on the first day of her menstrual flow and lasts 2 to 3 days. Her periods are regular and heavy with clots. Pelvic examination is normal.
Dysmenorrhea is defined as painful menstruation. This is often sufficiently severe that it prevents a woman from performing normal activities. It may also be accompanied by other symptoms, including diarrhea, nausea, vomiting, headache, and dizziness. Dysmenorrhea may be caused by a clinically identifiable cause (secondary dysmenorrhea) or by an excess of prostaglandins, leading to painful uterine muscle activity (primary dysmenorrhea). The term chronic pelvic pain refers to noncyclic pelvic pain (not solely associated with menstruation) that lasts for 6 months or more.
For most patients, diagnosis of dysmenorrhea or chronic pelvic pain is made by careful evaluation through history and physical examination. In some instances, evaluation using other modalities, including laparoscopy, may be needed. Once the diagnosis is established, therapies may be instituted.
DYSMENORRHEA
Primary and secondary dysmenorrhea are a source of recurrent disability for a significant number of women in their early reproductive years. It is uncommon for primary dysmenorrhea to occur during the first three to six menstrual cycles, when regular ovulation is not yet well established. The incidence of primary dysmenorrhea is greatest in women in their late teens to early twenties and declines with age. Secondary dysmenorrhea becomes more common as a woman ages, because it accompanies the rising prevalence of causal factors. Childbearing does not affect the occurrence of either primary or secondary dysmenorrhea.
Etiology
Primary Dysmenorrhea
Primary dysmenorrhea is caused by excess prostaglandin F2α (PGF2α) produced in the endometrium. Prostaglandin production in the uterus normally increases under the influence of progesterone, reaching a peak at, or soon after, the start of menstruation. With the onset of menstruation, formed prostaglandins are released from the shedding endometrium. Prostaglandins are potent smooth muscle stimulants that cause intense uterine contractions, resulting in intrauterine pressures that can exceed 400 mm Hg and baseline intrauterine pressures in excess of 80 mm Hg (normal baseline is about 20 mm Hg). PGF2α also causes contractions in smooth muscle elsewhere in the body, resulting in nausea, vomiting, and diarrhea (Table 32.1). In addition to the increase in prostaglandins from endometrial shedding, necrosis of endometrial cells provides increased substrate arachidonic acid from cell walls for prostaglandin synthesis. Besides PGF2α, prostaglandin E2 (PGE2) is also produced in the uterus. PGE2, a potent vasodilator and inhibitor of platelet aggregation, has been implicated as a cause of primary menorrhagia.
Secondary Dysmenorrhea
Secondary dysmenorrhea is caused by structural abnormalities or disease processes that occur outside the uterus, within the uterine wall, or within the uterine cavity (Box 32.1). Common causes of secondary dysmenorrhea include endometriosis (the presence of endometrial glands and stroma outside of the uterus), adenomyosis (the presence of ectopic endometrial tissue within the myometrium), adhesions, pelvic inflammatory disease (PiD), and leiomyomata (uterine fibroids).
BOX 32.1 Causes of Secondary Dysmenorrhea
Extrauterine causes
Endometriosis
Tumors (benign and malignant)
Inflammation
Adhesions
Psychogenic (rare)
Nongynecologic causes
Intramural causes
Adenomyosis
Leiomyomata
Intrauterine causes
Leiomyomata
Polyps
Intrauterine contraceptive devices
Infection
Cervical stenosis and cervical lesions
Diagnosis
Patients with primary dysmenorrhea present with recurrent, month-after-month, spasmodic lower abdominal pain that occurs on the first 1 to 3 days of menstruation. Dyspareunia is generally not found in patients with primary dysmenorrhea and, if present, should suggest a secondary cause.
Symptoms
In patients with primary dysmenorrhea, the pain is often diffusely located in the lower abdomen and suprapubic area, with radiation around or through to the back. The pain is described as “coming and going,” or similar to labor. This pain is frequently accompanied by moderate-to-severe nausea, vomiting, and diarrhea. Fatigue, low backache, and headache are also common. Patients often assume a fetal position in an effort to gain relief, and many report having used a heating pad or hot water bottle in an effort to decrease their discomfort.
In patients with secondary dysmenorrhea, the pain often lasts longer than the menstrual period. It may start before menstrual bleeding begins, become worse during menstruation, then persist after menstruation ends. Secondary dysmenorrhea often starts later in life than primary dysmenorrhea.
History
The specific complaints that an individual patient reports are determined by the underlying abnormality. Therefore, a careful medical history often suggests the underlying problem and helps direct further evaluations. Complaints of heavy menstrual flow combined with pain suggest uterine changes such as adenomyosis, leiomyomata, or polyps. Pelvic heaviness or a change in abdominal contour should raise the possibility of large leiomyomata or intra-abdominal neoplasia. Fever, chills, and malaise suggest infection. A coexisting complaint of infertility may suggest endometriosis or chronic PID or its sequelae.
Assessment
For patients with dysmenorrhea, the physical examination is directed toward uncovering possible causes of secondary dysmenorrhea. A pelvic examination may reveal asymmetry or irregular enlargement of the uterus, suggesting leiomyomata. Uterine leiomyomata are easily recognizable on bimanual examination by the irregular contour of the uterus and rubbery solid consistency of the fibroids. Adenomyosis may cause a tender, symmetrically enlarged, “boggy” uterus. Adenomyosis is supported by the exclusion of other causes of secondary dysmenorrhea, but definitive diagnosis can be made only by histologic examination of a hysterectomy specimen. Painful nodules in the posterior cul-de-sac and restricted motion of the uterus should suggest endometriosis (see Chapter 31). Restricted motion of the uterus is also found in cases of pelvic scarring from adhesions or inflammation. Thickening and tenderness of the adnexal structures caused by inflammation may suggest this diagnosis as the cause of secondary dysmenorrhea. Cultures or other tests of the cervix for Neisseria gonorrhoeae and Chlamydia trachomatis should be obtained if infection is suspected. In some patients, a final diagnosis may not be established without invasive procedures, such as laparoscopy.
In evaluating the patient thought to have primary dysmenorrhea, the most important differential diagnosis is that of secondary dysmenorrhea. Although the patient’s history is often characteristic, primary dysmenorrhea should not be diagnosed without a thorough evaluation to eliminate other possible causes.
Physical finding of patients with primary dysmenorrhea should be normal. There should be no palpable abnormalities of the uterus or adnexa, and no abnormalities should be found on speculum or abdominal examinations. Patients examined while experiencing symptoms often appear pale and diaphoretic, but the abdomen is soft and nontender, and the uterus is normal.
Therapy
Primary dysmenorrhea is an appropriate diagnosis for patients with dysmenorrhea in whom no other clinically identifiable cause is apparent. Patients with primary dysmenorrhea generally experience exceptional pain relief through the use of nonsteroidal anti-inflammatory drugs (NSAiDs), which are prostaglandin synthetase inhibitors. Other useful components of therapy for primary dysmenorrhea include the application of heat; exercise; psychotherapy and reassurance; and, on occasion, endocrine therapy (i.e., oral contraceptives to induce anovulation and pain relief [see Chapter 26]).
Nonsteroidal Anti-inflammatory Drugs
Ibuprofen, naproxen, and mefenamic acid are commonly prescribed NSAIDs for primary dysmenorrhea. For a time, selective cyclooxygenase inhibitors (COX-2 inhibitors) were becoming the NSAID of choice because of their targeted action. However, these drugs are now rarely used because of their potential association with life-threatening cardiovascular and gastrointestinal (GI) effects. Studies suggest that continuous low-level topical heat therapy can provide pain relief comparable to that offered by NSAID therapy without the systemic side effects that may occur with these drugs. Therapy with NSAIDs is generally so successful that, if some response is not evident, the diagnosis of primary dysmenorrhea should be reevaluated.
Presacral Neurectomy
In the rare patient who does not respond to medical and other therapy and whose pain is so severe as to be incapacitating, presacral neurectomy may be a consideration. The procedure involves surgical disruption of the “presacral nerves,” the superior hypogastric plexus, which is found in the retroperitoneal tissue from the fourth lumbar vertebra to the hollow over the sacrum. The risk of intraoperative complications, including injury to adjacent vascular structures and long-term sequelae such as chronic constipation, limits the use of this surgical procedure.
Combined Oral Contraceptives
combined oral contraceptives can be useful in patients who do not desire childbearing and who do not have contraindications to their use. They work by suppressing ovulation and stabilizing estrogen and progesterone levels, with a resultant decrease in endometrial prostaglandins and spontaneous uterine activity. Oral contraceptives may be taken in the traditional 28-day cycle, or in an extended fashion that increases the interval between menses. The continuous use of oral contraceptives to eliminate menses can often eliminate dysmenorrhea altogether. Depot medroxyprogesterone acetate (Depo Provera), long-acting implantable progesterone contraceptives (Nexplanon), and progesterone intrauterine delivery systems (Mirena), though not designed for treatment of dysmenorrhea, have all been shown to decrease it.
Therapy for Secondary Dysmenorrhea
For secondary dysmenorrhea, when a specific diagnosis is possible, therapy directed at the underlying condition is most likely to succeed. Specific treatments for many of these diagnoses are discussed in their respective chapters. When definitive therapy cannot be used—for example, in the case of a patient with adenomyosis who wishes to preserve fertility— symptomatic therapy in the form of analgesics or modification of the menstrual cycle may be effective.
CHRONIC PELVIC PAIN
Chronic pelvic pain is a common disorder that represents significant disability and utilization of resources. Estimates suggest that 15% to 20% of women ages 18 to 50 years have chronic pelvic pain that lasts longer than 1 year. Although there is no generally accepted definition of chronic pelvic pain, one proposed definition is noncyclic pain lasting for more than 6 months that localizes to the anatomic pelvis, anterior abdominal wall at or below the umbilicus, the lumbosacral back, or the buttocks and is of sufficient severity to cause functional disability or lead to medical care. Chronic pelvic pain may be caused by diseases of the reproductive, genitourinary, and GI tracts (Box 32.2 and Table 32.2). Other potential somatic sources of pain include the pelvic bones, ligaments, muscles, and fascia. Sometimes there is no clear etiology for the pain.
Assessment
The successful evaluation and treatment of chronic pelvic pain require time and a patient, caring physician. Effective management of this disease is dependent on a good physician–patient relationship, and the therapeutic effects of the relationship itself should not be overlooked. Taking the history and physical examination offer a time in which the physician may both gather information and establish a trusting rapport. The evaluation should begin with the presumption that there is an organic cause for the pain. Even in patients with obvious psychosocial stress, organic pathology can and does occur. Only when other reasonable causes have been ruled out should psychiatric diagnoses such as somatization, depression, or sleep and personality disorders be entertained.
BOX 32.2 Gynecologic Conditions That May Cause or Exacerbate Chronic Pelvic Pain, by Level of Evidence
Level Aa
• Endometriosisb
• Gynecologic malignancies (especially late stage) • Ovarian retention syndrome (residual ovary syndrome)
• Ovarian remnant syndrome
• Pelvic congestion syndrome
• Pelvic inflammatory diseaseb
• Tuberculous salpingitis
Level Bc
• Adhesionsb
• Benign cystic mesothelioma
• Leiomyomatab
• Postoperative peritoneal cysts
Level cd
• Adenomyosis
• Atypical dysmenorrhea or ovulatory pain
• Adnexal cysts (nonendometriotic)
• Cervical stenosis
• Chronic ectopic pregnancy
• Chronic endometritis
• Endometrial or cervical polyps
• Endosalpingiosis
• Intrauterine contraceptive device
• Ovarian ovulatory pain
• Residual accessory ovary
• Symptomatic pelvic relaxation (genital prolapse)
aLevel A: good and consistent scientific evidence of causal relationship to chronic pelvic pain.
bDiagnosis frequently reported in published series of women with chronic pelvic pain.
cLevel B: limited or inconsistent scientific evidence of causal relationship to chronic pelvic pain.
dLevel C: causal relationship to chronic pelvic pain based on expert opinions.
History
As with the evaluation of any pain, attention must be paid to the description and timing of the symptoms involved. The history should include a thorough medical, surgical, menstrual, and sexual history. Specific questions regarding associated symptoms, provocative and palliative factors, and timing may help delineate the organ system from which the pain originates. Inquiries should be made into the patient’s home and work status, social history, and family history (past and present). The patient should be questioned about sleep disturbances and other signs of depression as well as a past history of physical and sexual abuse. Studies have found a significant correlation between a history of abuse and chronic pain. If a history of abuse is obtained, the patient should also be screened for any current physical or sexual abuse.
Physical Examination
Physical examination of patients with chronic pain is directed toward uncovering possible causative pathologies. The patient should be asked to indicate the location of the pain as a guide to further evaluation and to provide some indication of the character of the pain. If the pain is localized, the patient will point to a specific location with a single finger; if the pain is diffuse, the patient will use a sweeping motion of the whole hand. Maneuvers that duplicate the patient’s complaint should be noted, but undue discomfort should be avoided to minimize guarding, which would limit a thorough examination. carnett sign or tensing of the abdominal wall while raising the legs or chin in the supine position can help identify myofascial pain, which should increase with these maneuvers involving the rectus muscles. Visceral pain will decrease or remain unchanged with these maneuvers. Additionally, care should be taken to examine for muscle spasm pain induced by the obturator internus muscle (abduct and internally rotate leg against pressure) and the levator ani muscles (tighten pelvic floor as if to stop urine or Kegel exercise).
Differential Diagnosis
Many of the same conditions that cause secondary dysmenorrhea may cause chronic pain states. As in the evaluation of patients with dysmenorrhea, cervical cultures should be obtained if infection is suspected. For most patients, a reasonably accurate differential diagnosis can be established through the history and physical examination. The wide range of differential diagnoses possible in chronic pelvic pain lends itself to a multidisciplinary approach, which might include psychiatric evaluation or testing. Consultation with social workers, physical therapists, gastroenterologists, anesthesiologists, orthopedists, and others should be considered. The use of imaging technologies or laparoscopy may also be required to determine a diagnosis. However, in approximately one third of patients with chronic pelvic pain who undergo laparoscopic evaluation, no identifiable cause is found. Nevertheless, two thirds of these patients have potential causes identified where none was apparent before laparoscopy.
Conditions That Increase the Risk of Chronic Pelvic Pain
Common disorders in women with chronic pelvic pain are PID, irritable bowel syndrome (iBS), interstitial cystitis, endometriosis, and adhesions. However, it is sometimes difficult to pinpoint a specific cause of chronic pelvic pain. Many women with chronic pelvic pain have more than one disease that might lead to pain.
Pelvic Inflammatory Disease
Approximately 18% to 35% of women who have had PID will develop chronic pelvic pain. The exact mechanism is unknown, but may involve chronic inflammation, adhesive disease, and the coexistence of psychosocial factors. PID is discussed in more detail in Chapter 29.
Irritable Bowel Syndrome
IBS occurs in 50% to 80% of women with chronic pelvic pain. The diagnosis of IBS is defined by the Rome III criteria: Symptoms of recurrent abdominal pain or discomfort and a marked change in bowel habit for at least 6 months, with symptoms experienced on at least 3 days of at least 3 months. Two or more of the following must apply: 1) pain is relieved by a bowel movement, 2) onset of pain is related to a change in frequency of stool, or 3) onset of pain is related to a change in the appearance of stool. IBS is often usefully subcategorized for purposes of treatment depending on the predominant complaint: pain, diarrhea, constipation, or alternating constipation and diarrhea. The pathophysiology of the syndrome is not clearly identified, but factors proposed to be involved include altered bowel motility, visceral hypersensitivity, psychosocial factors (especially stress), an imbalance of neurotransmitters (especially serotonin), and infection (often indolent or subclinical). A history of childhood sexual or physical abuse is highly correlated with the severity of symptoms experienced by those with IBS.
Interstitial Cystitis
interstitial cystitis is a chronic inflammatory condition of the bladder that is often characterized by pelvic pain, urinary urgency and frequency, and dyspareunia. The proposed etiology is a disruption of the glycosaminoglycanlayer that normally coats the mucosa of the bladder. The interstitial cystitis symptom index predicts the diagnosis of interstitial cystitis and may be used to help determine whether cystoscopy is indicated. Further evaluation can be done with bladder distention with water or intravesical potassium sensitivity testing.
THERAPY
Patients with chronic pelvic pain offer a therapeutic challenge. If possible, care should be directed at a specific cause. The use of analgesics should be on a fixed time schedule that is independent of symptoms.
Medical Therapy
Suppression of ovulation may be useful as either a therapeutic modality or as a diagnostic tool to assist in ruling out ovarian or menstrual processes. Gonadotropin-releasing hormone agonists cause a central downregulation of the ovarian hormones and have been used in the treatment of endometriosis. These agents may also help relieve some of the symptoms of IBS, interstitial cystitis, and pelvic congestion syndrome (in which engorged pelvic blood vessels are purported to cause pelvic aching and pain), all of which are hormonally mediated to some extent.
Patients with symptoms characteristic of IBS should be referred to a gastroenterologist for further evaluation. The use of a food diary to identify and eliminate foods that are associated with symptoms, combined with the nurturing physician–patient relationship to avoid “doctor shopping” and episodic care, is the mainstay of treatment. Limiting caffeine, alcohol, fatty foods, and gas-producing vegetables is often helpful. Lactose or wheat gluten intolerance may be identified by the diary. If constipation is a major symptom, the consumption of 20 to 30 g of fiber or the use of osmotic laxatives such as lactulose is often useful. When diarrhea is a major symptom, antidiarrheals can be useful. Gas pain and cramping may be treated with antispasmodics such as dicyclomine and hyoscyamine.
Treatments for interstitial cystitis include dietary modification, intravesical agents, and oral agents aimed at decreasing inflammation and pain signals. As with IBS, caffeine, alcohol, artificial sweeteners, and acidic foods should be eliminated. Dimethyl sulfoxide is the only drug approved for direct bladder instillation to treat interstitial cystitis, although many physicians treat with a combination of anti-inflammatory and analgesic medications. Oral agents include antihistamines, tricyclic antidepressants, and pentosan polysulfate, a glycosaminoglycan analogue that may help reestablish the disrupted mucosa of the bladder.
Surgical Therapies
Surgical therapies, such as hysterectomy, should be performed only after nongynecologic causes have been ruled out. Hysterectomy is very effective in relieving pain arising from the uterus and may also improve symptoms in women without identifiable uterine pathology.
Other Therapies
Alternate treatment modalities such as transcutaneous electrical nerve stimulation, biofeedback, nerve blocks, laser ablation of the uterosacral ligaments, and presacral neurectomy may be used, as appropriate. Adding psychotherapy to medical treatment of chronic pelvic pain appears to improve response over that of medical treatment alone and should be considered. In some cases, the goal in treatment may not be a cure, that is, elimination of the chronic pain but, rather, successful management of the symptoms to allow maximal function and quality of life.
FOLLOW-UP
Patients being treated for pelvic pain (dysmenorrhea or chronic pain states) should be carefully monitored for success and the possibility of complications from the therapy. Patients on oral contraceptives for the first time should be asked to return for follow-up after 2 months and again after 6 months. Once successful therapy is established, routine periodic health maintenance visits should continue. Patients with chronic pelvic pain should be encouraged to return for follow-up on a periodic basis, rather than only when pain is present, thus avoiding reinforcing pain behavior as a means to an end.
Clinical Follow-Up
This patient’s history is typical of primary dysmenorrhea. Based on this determination, the patient was started on nonsteroidal anti-inflammatory therapy. The patient experienced immediate improvement in her cramps and coincidentally noted a slight reduction in her menstrual flow.
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