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Primary and secondary dysmenorrhea are a source of recurrent disability for a significant number of women in their early re-
productive years. It is uncommon for primary dysmenorrheato 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 20s and declines with age. Secondary dysmen-orrhea becomes more common as a woman ages, because it accompanies the rising prevalence of causal factors. Childbearing does not affect the occurrence of either pri-mary or secondary dysmenorrhea.
Primary dysmenorrhea is caused by excess prostaglandinF2produced in the endometrium. Prostaglandin produc-tion 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 endome-trium. Prostaglandins are potent smooth-muscle stimu-lants 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. Prostaglandin F2α also causes contractions in smooth mus-cle elsewhere in the body, resulting in nausea, vomiting, and diarrhea (Table 30.1). In addition to the increase in prostaglandins from endometrial shedding, necrosis of endometrial cells provides increased substrate arachi-donic acid from cell walls for prostaglandin synthesis. Besides prostaglandin F2α, prostaglandin E2 is also pro-duced in the uterus. Prostaglandin E2, a potent vasodilator and inhibitor of platelet aggregation, has been implicated as a cause of primary menorrhagia.
Secondary dysmenorrhea is caused by structural ab-normalities or disease processes that occur outside the uterus, within the uterine wall, or within the uterine cavity (Box 30.1). Common causes of secondary dysmen-orrhea include endometriosis (the presence of ectopic endometrial tissue outside of the uterus), adenomyosis (the presence of ectopic endometrial tissue within the myometrium), adhesions, pelvic inflammatory disease, and leiomyomata (uterine fibroids).
Tumors (Benign, Malignant)
Intrauterine contraceptive devices
Cervical stenosis and cervical lesions
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. The patient often illustrates her description with a fist opening and closing. This pain is frequently accompanied by moderate to severe nausea, vomiting, and/or diarrhea. Fatigue, low backache, and headache are also common. Patients often assume a fetal position in an effort to gain re-lief, 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 dur-ing menstruation, then persist after menstruation ends. Secondary dysmenorrhea often starts later in life than primary dysmenorrhea.
The specific complaints that an individual patient has are determined by the underlying abnormality. Therefore, a careful medical history often suggests the underlying prob-lem 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 intraabdomi-nal neoplasia. Fever, chills, and malaise suggest infection. A coexisting complaint of infertility may suggest endo-metriosis or chronic pelvic inflammatory disease.
For patients with dysmenorrhea, the physical examination is directed toward uncovering possible causes of secondary dysmen-orrhea. A pelvic examination may reveal asymmetry orirregular enlargement of the uterus, suggesting leiomy-omata or other tumors. Uterine leiomyomata are easily rec-ognizable on bimanual exam by their smooth contour and rubbery solid consistency. Adenomyosis may cause a ten-der, symmetrically enlarged, “boggy” uterus. This diagno-sis is supported by 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. Restricted motion of the uterus is also found in cases of pelvic scarring from adhesions or inflam-mation. Thickening and tenderness of the adnexal struc-tures caused by inflammation may suggest this diagnosis as the cause of secondary dysmenorrhea. Cultures of the cervix for Neisseria gonorrhoeae and Chlamydia trachoma-tis 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 exam-ined while experiencing symptoms often appear pale and “shocky,” but the abdomen is soft and nontender, and the uterus is normal.
Primary dysmenorrhea is an appropriate diagnosis for patients with dysmenorrhea in whom no other clinically identifiable cause is apparent. Patients with primary dysmenorrhea generallyexperience exceptional pain relief through the use of non-steroidal anti-inflammatory drugs (NSAIDs), which areprostaglandin-synthetase inhibitors. Ibuprofen, naproxen, and mefenamic acid are commonly prescribed NSAIDs for primary dysmenorrhea. For a time, cyclo-oxygenase 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 associ-ation with life-threatening cardiovascular and gastrointesti-nal effects. Recent 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 nonsteroidal anti-inflammatory agents is generally so successful that, if some response is not evident, the diagnosis of primary dysmenorrhea should be reevaluated. Other useful components of therapy for pri-mary dysmenorrhea include the application of heat; exercise; psychotherapy and reassurance; and, on occasion, endocrine therapy, i.e., oral contraceptives to induce anovulation.
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 consider-ation. The procedure involves surgical disruption of the “presacral nerves,” the superior hypogastric plexus, which is found in the retroperitoneal tissue from the fourth lum-bar 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, limit the use of this surgical procedure.
For secondary dysmenorrhea, when a specific diagnosis is possible, therapy directed at the underlying condition is most likely to succeed. 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.
Combined oral contraceptives can be useful inpatients who do not desire childbearing and who do not have contraindications to their use. They work by suppress-ing ovulation and stabilizing estrogen and progesterone lev-els, 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.
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