Dysmenorrhea—colicky pain in the lower abdomen and pelvis around the time of menses—is a common condition that disturbs the lives and families of the women who suffer from it. Severe pain and discomfort often lead to absenteeism from work or school, resulting in an overall reduction in productivity and enormous economic loss.
Dysmenorrhea can be classified as primary or secondary, depending on its cause. Secondary dysmenorrhea results from a known pathologic process occurring within the pelvis. Primary dysmenorrhea does not have an anatomic cause.
Because many women seek help for this disorder, the physician should be sensitive to the concerns of each patient and provide a treatment that is specific to each patient’s needs. The goal of therapy is to enable the patient to resume her daily life without the fear of being disabled by pain.
Primary Dysmenorrhea
The prevalence of primary dysmenorrhea is between 40% and 90%, with an average of 75%. It occurs predominantly in women younger than 25 years.
Pathogenesis
Primary dysmenorrhea results from tissue hypoxia and ischemia. An elevation in the basal tone of the uterus, combined with an increase in contraction strength and frequency, leads to vasospasm and a reduction in uterine blood flow.1 Increased levels of prostaglandin F2a (PGF2a), leukotrienes, and vasopressin are responsible for these alterations [see Figure 1].2 It is important to note that this abnormality in prostaglandin production occurs only in endometrial tissue that has been exposed to both estrogen and progesterone.
Diagnosis
Diagnosis of primary dysmenorrhea is based on patient history; results of physical examination are usually normal. Symptoms characteristically begin within 6 to 12 months after menarche, as ovulatory cycles become established. The pain occurs only during ovulatory cycles and lasts about 48 to 72 hours each month. In most patients, the pain starts a few hours before menstruation or at the onset of menstruation.
The degree of pain suffered is variable, but fewer than 15% of women with primary dysmenorrhea have severe pain. Patients with severe pain may also experience other symptoms, such as nausea, vomiting, dizziness, and diarrhea.
Treatment
Treatment of primary dysmenorrhea includes nonsteroidal anti-inflammatory drugs (NSAIDs), oral contraceptives, and transcutaneous electrical nerve stimulation (TENS).3 Other nonpharmacologic approaches that may be effective are the use of a lower abdominal heating pad,4 supplemental vitamin B1 (100 mg daily) or magnesium (400 mg daily),5 and a low-fat vegetarian diet.
NSAIDs inhibit the action of cyclooxygenase and prevent the conversion of arachidonic acid into prostaglandins (PGs). NSAIDs significantly alleviate pain in approximately 75% of patients. The fenamates (e.g., mefenamic acid) are considered the best choice of NSAIDs because they act as antiprostaglandins, preventing both the production of PGs and the binding of the PG to its receptor [see Table 1].7,8 Therapy with NSAIDs should be discontinued if adverse side effects occur.9 Definitive research on the use of cyclooxygenase-2 (COX-2) inhibitors (e.g., celecoxib [Celebrex] or rofecoxib [Vioxx]) in dysmenorrhea has not been completed, but these agents seem promising for this purpose.
Figure 1 Prostaglandin synthesis. (HPETE—hydroperoxyeicosatetraenoic acid)
Table 1 Common Prostaglandin Synthesis Inhibitors
|
Chemical Group |
Derivative |
Usual Dosage |
|
Benzoic acid |
Acetylsalicylic acid (aspirin) |
650 mg p.o. every 4 hr |
|
Fenamates |
Mefenamic acid |
250 mg p.o. every 6 hr |
|
Meclofenamate sodium |
100 mg p.o., t.i.d., for up to 6 days |
|
|
Indoleacetic acid |
Indomethacin |
25-50 mg p.o. every 8 hr |
|
Arylpropionic acid |
Ibuprofen |
400-800 mg p.o. every 4 hr |
|
Naproxen |
250-500 mg p.o. every 12 hr |
|
|
Naproxen sodium |
275-550 mg p.o. every 12 hr |
|
|
Cyclooxygenase-2 (COX-2) inhibitors |
Celecoxib |
200 mg p.o., b.i.d. |
|
Rofecoxib |
50 mg p.o., q.d. |
|
|
Valdecoxib |
20 mg p.o., b.i.d. |
If NSAIDs are ineffective or poorly tolerated, the next step is the use of combined estrogen-progestin oral contraceptives. In a normal menstrual cycle, the progesterone level increases after ovulation and steadily decreases during the luteal phase. As the level of progesterone decreases, lysosomal enzymes within the endometrial cells are released, causing an increase in the production of PGs. Oral contraceptives prevent fluctuations of endogenous progesterone levels, reducing the amount of pain and symptoms associated with primary dysmenorrhea.10 Regular-cycle oral contraceptives are not usually effective for treatment of primary dysmenorrhea; continuous oral contraceptives are preferable. Many patients consider continuous oral contraceptives unnatural but are willing to compromise by taking long-cycle contraceptives, so that they have three or four menses a year [see 16:VI Contraception].
If neither NSAIDs nor oral contraceptives alone alleviate primary dysmenorrhea, the two can be used together. If combination therapy also fails, the patient should be reevaluated and a diagnostic workup initiated for secondary dysmenorrhea.
Secondary Dysmenorrhea
The pain associated with secondary dysmenorrhea is the direct result of a pathologic process. Unlike primary dysmenor-rhea, secondary dysmenorrhea varies with regard to the patient’s age at onset and the causative condition. Some of the conditions that can cause secondary dysmenorrhea include en-dometriosis, adenomyosis, pelvic adhesions and infection, pelvic congestion, cervical stenosis, psychological stress, and psychological disturbances.
Endometriosis
Endometriosis is the presence of endometrial glands and stroma outside the uterus [see 16:X Endometriosis]. Approximately 7% of women in the United States suffer from this disorder. Endometriosis causes intra-abdominal hemorrhage, fi-brosis, and adhesion formation. Consequently, dyspareunia, infertility, and pelvic pain occur.11
The pain usually begins 2 to 3 days before menses and worsens during menstruation. Tender nodules along the uterosacral ligament, a posteriorly fixed uterus, and enlarged cystic ovaries are characteristic findings; however, results of physical examination are often normal. Definitive diagnosis requires direct visualization during laparoscopy, with or without a tissue biopsy.
Treatment may entail either medical intervention or surgery. Oral contraceptives, intramuscular injection of leuprolide acetate depot, oral danazol, or high-dose progestins (oral or intramuscular) are all beneficial in suppressing the endometrial implants and relieving the symptoms of pain.
Adenomyosis
Adenomyosis is the presence of ectopic endometrial glands and stroma in the myometrium of the uterus. Unlike the ec-topic glands in endometriosis, the ectopic glands in adeno-myosis do not undergo monthly cyclical changes.
Symptoms of adenomyosis classically include dysmenorrhea and menorrhagia (heavy menstrual bleeding). As the disease progresses, so does the dysmenorrhea. On physical examination, the uterus is soft, globular, and uniformly enlarged. Typically, the uterus is tender just before and during menstruation.
Diagnostic aids include pelvic sonography, magnetic resonance imaging, and hysterosalpingography. Unfortunately, most cases go undiagnosed until histologic evaluation is made at the time of a hysterectomy.
Treatment starts with medical suppression of ovarian function and culminates in hysterectomy if symptoms do not abate. Thermal balloon ablation of the endometrium, which is an effective treatment for some patients with dysmenorrhea from other causes,12 does not work in adenomyosis.
Cervical stenosis
When menstrual flow is impeded at the level of the internal cervical os, intrauterine pressure increases and pelvic pain occurs. A narrow or stenotic os may be a congenital abnormality or the result of trauma, infection, or surgery.
The diagnosis of cervical stenosis should be considered in women who have a history of hypomenorrhea and severe pelvic pain during menses or if the diameter of the external cervical os is less than 5 mm.
During the physical examination, the physician should attempt to pass a uterine sound into the endometrial cavity. Inability to document a clear passage through the cervical canal warrants further investigation. Diagnostic workup with hyster-osalpingography may reveal a narrow cervical canal.
Treatment consists of dilating the cervical canal with laminaria tents or performing a formal dilatation and curettage (D and C) under anesthesia. These procedures have limited therapeutic benefit and need to be repeated frequently. Complete resolution of symptoms typically occurs with pregnancy and vaginal delivery, which therefore is considered the ultimate therapy.
Pelvic inflammatory disease
Most pelvic infections are caused by Chlamydia, Neisseria gonorrhoeae, and mixed microbial organisms. Pelvic anatomy is often distorted as a consequence of dense adhesion formation. During menstruation, adhesion edema and venous congestion result in severe pelvic pain and discomfort. This pain may eventually become chronic.
Patients at risk for pelvic inflammatory disease (PID) include current or past users of intrauterine devices (IUDs) and women with more than one sexual partner. The workup includes cervical cultures, endometrial biopsy, and pelvic sonography.
Treatment of the dysmenorrhea associated with PID includes NSAIDs for pain management and antibiotics for acute infection. Surgery can be offered to patients with chronic pain and to those with a known tubo-ovarian abscess or hydrosalpinx. Although lysis of adhesions can be performed, results are usually poor because recurrence is high.
Pelvic congestion syndrome
Engorgement and thrombosis of the pelvic veins are another cause of dysmenorrhea.13 The pooling of blood in the pelvic vasculature results in a burning and throbbing pain. The pain is characteristically worse at night and after prolonged periods of standing. Bimanual examination often reveals a uterus that is mildly enlarged and tender to the touch. The diagnosis of pelvic congestion syndrome is made almost exclusively during laparoscopic evaluation.
Although the underlying cause of pain is not well understood, treatment often entails NSAIDs and psychological therapy. New treatment approaches that utilize uterine artery embolization show promising results. Hysterectomy should be reserved for patients who do not respond to other therapeutic modalities.
Other causes of chronic pelvic pain
Secondary dysmenorrhea can also be caused by psychological problems, including stress, tension, and abnormal conditioned behavior. For these patients, resolution of symptoms is best achieved through lifestyle and behavior modification. Chronic pelvic pain, rather than acute pain, is more common among women with psychological disorders.
Patients who have pain for more than 6 months are considered to have chronic pelvic pain. In addition to a gynecologic cause of the pelvic pain, the physician should always consider other causes. The basic workup should include gastrointestinal, urologic, musculoskeletal, and psychological evaluations. Once a diagnosis has been established, treatment should focus on correcting the underlying disorder. Treatment should be initiated with medical therapy. If this fails, more aggressive treatment can be attempted, including presacral neurectomy or a laparoscopic uterine nerve ablation (LUNA) procedure.14-16
