Dysmenorrhea is uterine pain around the time of menses. Pain may occur with menses or precede menses by 1 to 3 days. Pain tends to peak 24 h after onset of menses and subside after 2 to 3 days. It is usually sharp but may be cramping, throbbing, or a dull, constant ache; it may radiate to the legs.
Headache, nausea, constipation or diarrhea, lower back pain, and urinary frequency are common; vomiting occurs occasionally.
Symptoms of premenstrual syndrome may occur during part or all of menses.
Sometimes endometrial clots or casts are expelled.
Dysmenorrhea can be
Symptoms cannot be explained by structural gynecologic disorders. Pain is thought to result from uterine contractions and ischemia, probably mediated by prostaglandins (eg, prostaglandin F2α, a potent myometrial stimulant and vasoconstrictor) and other inflammatory mediators produced in secretory endometrium and possibly associated with prolonged uterine contractions and decreased blood flow to the myometrium.
Contributing factors may include the following:
Primary dysmenorrhea begins within a year after menarche and occurs almost invariably in ovulatory cycles. The pain usually begins when menses start (or just before) and persists for the first 1 to 2 days; this pain, described as spasmodic, is superimposed over constant lower abdominal pain, which may radiate to the back or thigh. Patients may also have malaise, fatigue, nausea, vomiting, diarrhea, low back pain, or headache.
Risk factors for severe symptoms include the following:
Symptoms tend to lessen with age and after pregnancy.
In about 5 to 15% of women with primary dysmenorrhea, cramps are severe enough to interfere with daily activities and may result in absence from school or work.
Symptoms are due to pelvic abnormalities. Almost any abnormality or process that can affect the pelvic viscera can cause dysmenorrhea.
Common causes of secondary dysmenorrhea include
Less common causes include congenital malformations (eg, bicornuate uterus, subseptate uterus, transverse vaginal septum), ovarian cysts and tumors, pelvic inflammatory disease, pelvic congestion, intrauterine adhesions, psychogenic pain, and intrauterine devices (IUDs), particularly copper- or levonorgestrel-releasing IUDs. Levonorgestrel-releasing IUDs cause less cramping than copper-releasing IUDs.
In a few women, pain occurs when the uterus attempts to expel tissue through an extremely tight cervical os (secondary to conization, loop electrosurgical excision procedure [LEEP], cryocautery, or thermocautery). Pain occasionally results from a pedunculated submucosal fibroid or an endometrial polyp protruding through the cervix.
Risk factors for severe secondary dysmenorrhea are the same as those for primary.
Secondary dysmenorrhea usually begins during adulthood unless caused by congenital malformations.
History of present illness should cover complete menstrual history, including age at onset of menses, duration and amount of flow, time between menses, variability of timing, and relation of menses to symptoms.
Clinicians should also ask about
Review of systems should include accompanying symptoms such as cyclic nausea, vomiting, bloating, diarrhea, and fatigue.
Past medical history should identify known causes, including endometriosis, uterine adenomyosis, or fibroids. Method of contraception should be ascertained, specifically asking about IUD use.
Past surgical history should identify procedures that increase risk of dysmenorrhea, such as cervical conization and endometrial ablation.
Sexual history should include prior or current history of sexual abuse.
Pelvic examination focuses on detecting causes of secondary dysmenorrhea. The vagina, vulva, and cervix are inspected for lesions and for masses protruding through the cervical os. Structures are palpated to check for a tight cervical os, prolapsed polyp or fibroid, uterine masses, adnexal masses, thickening of the rectovaginal septum, induration of the cul-de-sac, and nodularity of the uterosacral ligament.
The abdomen is examined for evidence of peritonitis.
Red flag findings suggest a cause of pelvic pain other than dysmenorrhea.
Primary dysmenorrhea is suspected if
Secondary dysmenorrhea is suspected if
Endometriosis is considered in patients with adnexal masses, thickening of the rectovaginal septum, induration of the cul-de-sac, nodularity of the uterosacral ligament, or, occasionally, nonspecific vaginal, vulvar, or cervical lesions.
Testing aims to exclude structural gynecologic disorders. Most patients should have
Intrauterine and ectopic pregnancy are ruled out by pregnancy testing. If pelvic inflammatory disease is suspected, cervical cultures are done.
Pelvic ultrasonography is highly sensitive for pelvic masses (eg, ovarian cysts, fibroids, endometriosis, uterine adenomyosis) and can locate lost and abnormally located IUDs.
If these tests are inconclusive and symptoms persist, other tests are done, such as the following:
Hysterosalpingography or sonohysterography to identify endometrial polyps, submucous fibroids, or congenital abnormalities
MRI to identify other abnormalities, including congenital abnormalities, or, if surgery is planned, to further define previously identified abnormalities
IV pyelography, but only if a uterine malformation has been identified as causing or contributing to the dysmenorrhea
If results of all other tests are inconclusive, hysteroscopy or laparoscopy can be done. Laparoscopy is the most definitive test because it enables clinicians to directly examine all of the pelvis and reproductive organs and to check for abnormalities.
Symptomatic treatment begins with adequate rest and sleep and regular exercise. A low-fat diet and nutritional supplements such as omega-3 fatty acids, flaxseed, magnesium, vitamin E, zinc, and vitamin B1 are suggested as potentially effective.
Women with primary dysmenorrhea are reassured about the absence of structural gynecologic disorders.
If pain persists, NSAIDs (which relieve pain and inhibit prostaglandins) are typically tried. NSAIDs are usually started 24 to 48 h before and continued until 1 or 2 days after menses begin.
If the NSAID is ineffective, suppression of ovulation with a low-dose estrogen/progestin oral contraceptive may be tried.
Other hormone therapy, such as danazol, progestins (eg, levonorgestrel, etonogestrel, depot medroxyprogesterone acetate), gonadotropin-releasing hormone agonists, or a levonorgestrel-releasing IUD, may decrease dysmenorrheal symptoms.
Periodic adjunctive use of analgesics may be needed.
Hypnosis is being evaluated as treatment. Other proposed nondrug therapies, including acupuncture, acupressure, chiropractic therapy, and transcutaneous electrical nerve stimulation, have not been well-studied but may benefit some patients.
For intractable pain of unknown origin, laparoscopic presacral neurectomy or uterosacral nerve ablation has been efficacious in some patients for as long as 12 mo.