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 hours 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.
Etiology of Dysmenorrhea
Dysmenorrhea can be
Primary (more common)
Secondary (due to pelvic abnormalities)
Symptoms of primary dysmenorrhea cannot be explained by structural gynecologic disorders. Pain is thought to result from uterine contractions and ischemia, probably mediated by prostaglandins (eg, prostaglandin F2-alpha, 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:
Passage of menstrual tissue through the cervix
High levels of prostaglandin F2-alpha in menstrual fluid
A narrow cervical os
A malpositioned uterus
Lack of exercise
Anxiety about menses
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:
Early age at menarche
Long or heavy menstrual periods
A family history of dysmenorrhea
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 of secondary dysmenorrhea 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 Inflammatory Disease (PID) Pelvic inflammatory disease (PID) is a polymicrobial infection of the upper female genital tract: the cervix, uterus, fallopian tubes, and ovaries; abscess may occur. PID may be sexually transmitted... read more , pelvic congestion, intrauterine adhesions, psychogenic pain, and intrauterine devices Intrauterine Device (IUDs; IUD) In the US, 12% of women who use contraception use intrauterine devices (IUDs); IUDs are becoming more popular because of their advantages over oral contraceptives: IUDs are highly effective... read more (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.
Evaluation of Dysmenorrhea
Clinicians can identify dysmenorrhea based on symptoms. They then determine whether dysmenorrhea is primary or secondary.
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
The age at which symptoms began
Their nature and severity
Factors that relieve or worsen symptoms (including the effects of contraceptives)
Degree of disruption of daily life
Effect on sexual activity
Presence of pelvic pain unrelated to menses
Response to acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs)
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 or other traumatic events.
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.
The following findings are of particular concern:
New or sudden-onset pain
Evidence of peritonitis
Interpretation of findings
Red flag findings suggest a cause of pelvic pain other than dysmenorrhea.
Primary dysmenorrhea is suspected if
Symptoms begin soon after menarche or during adolescence.
Secondary dysmenorrhea is suspected if
Symptoms begin after adolescence.
Patients have known causes, including uterine adenomyosis, fibroids, a tight cervical os, a mass protruding from the cervical os, or, particularly, endometriosis.
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.
Treatment of Dysmenorrhea
Underlying disorders are treated.
Symptomatic treatment of dysmenorrhea 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 B1, vitamin E, and zinc, 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 hours 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 months.
Most dysmenorrhea is primary.
Check for underlying structural pelvic lesions.
Usually, before doing other tests, do ultrasonography to check for structural gynecologic disorders.
An NSAID or an NSAID plus a low-dose oral contraceptive is usually effective.