Dysmenorrhea refers to pain and cramping during menses. When severe, it can interfere with normal daily functioning. It is the most common menstrual complaint, affecting 50-90% of women worldwide. Severe symptoms occur in 2-29% of studied populations. Despite its prevalence, dysmenorrhea is often underreported and undertreated, with significant impact on a woman’s quality of life.
Primary dysmenorrhea is menstrual pain and cramping that occur in the absence of any underlying pelvic pathology. Women with primary dysmenorrhea have a significantly reduced quality of life, poorer mood, and poorer sleep when compared with women with pain-free menstrual cycles.
Primary dysmenorrhea presents after the onset of ovulatory menstrual cycles, usually beginning within 6-12 months of menarche, though prevalence declines with age. After ovulation and in the absence of conception, a female’s progesterone level will decline. The decline in her progesterone level triggers the release of leukotrienes and prostaglandins within the uterus. The prostaglandins constrict blood flow to the uterus and deprive the uterus of oxygen. The reduced blood flow and the reduced oxygen result in abdominal pain and cramping.
The pain often begins 24-48 hours before the start of menses and usually subsides within 12-72 hours. The pain is typically midline but may also radiate to the back or thighs. Accompanying symptoms may include nausea, vomiting, diarrhea, fatigue, headache, and respiratory difficulties.
Secondary dysmenorrhea is caused by pelvic disease such as endometriosis, uterine fibroids, adenomyosis, pelvic inflammatory disease, pelvic adhesions, and cervical stenosis. The pain of secondary dysmenorrhea usually begins earlier in the menstrual cycle and continues beyond the end of menses. Further symptoms may be present depending on the underlying pathology. While secondary causes can manifest at any age, they typically present well after menarche, often as late as the fourth or fifth decade of life.
The following factors have been associated with primary dysmenorrhea. Due to the presence of confounding variables and possible selection bias, however, further studies are needed to firmly establish these risk factors. Risk factors for secondary dysmenorrhea depend on the underlying pelvic pathology.
Age. Symptoms are particularly frequent during adolescence.
Body mass index (BMI). Increased prevalence with BMI < 20 or BMI > 30.
Prolonged, irregular, or heavy menses.
History of pelvic inflammatory disease.
Family history of dysmenorrhea.
Nulliparity or lower parity.
Primary dysmenorrhea is a diagnosis of exclusion. A complete history including menstrual, gynecologic, psychosocial, and dietary factors, as well as a physical examination, is necessary. Abdominal, pelvic, and rectal examinations may not be indicated in younger patients. Typically, when the history and physical examination support the diagnosis of primary dysmenorrhea and the pain responds to nonsteroidal anti-inflammatory drugs (NSAIDs) or oral contraceptives, no further evaluation is necessary. However, when symptoms begin in an older woman, an abdominal, pelvic, and/or rectal examination would be indicated to evaluate for an underlying disorder. Laboratory testing is typically not necessary, but pregnancy should be ruled out in sexually active women.
Laboratory testing may include pregnancy testing, sexually transmitted disease evaluation, urinalysis, and complete blood count.
Cultures for gonorrhea and chlamydia are generally indicated, but negative cultures do not exclude pelvic infection.
Imaging studies may include pelvic and vaginal ultrasound.
Laparoscopy is not typically indicated, as the history, examination, and imaging typically identify the cause of pain. However, this procedure may be indicated for the diagnosis of and treatment of endometriosis and as therapy for fibroids, adhesions, ovarian cysts, and other abdominal or pelvic pathologies.
Primary dysmenorrhea is best treated with a multidisciplinary approach that may include medical, nonmedical, lifestyle, and nutritional interventions.
Nutritional interventions, such as a low-fat, vegan diet, are described below (see Nutritional Considerations).
Regular exercise may be helpful. In unblinded trials, women who exercise appear to have less severe menstrual symptoms compared with women who do not exercise. The regular practice of yoga may also reduce cramps and improve distress. Physical activity decreases blood estrogen concentrations, which would be expected to decrease the risk of dysmenorrhea. The effects of exercise on stress level and weight are also plausible mechanisms for decreased pain.
Smoking cessation may be helpful.
Acupuncture and transcutaneous electrical nerve stimulation (TENS) may be beneficial. Limited evidence from controlled trials indicates that acupuncture produces significantly better pain relief compared with sham acupuncture, and decreases the use of pain medications. Acupressure provides pain relief similar to that of nonsteroidal anti-inflammatory drugs (NSAIDs) when compared with sham acupressure treatment.
NSAIDs (ibuprofen, naproxen) are often effective in treating the pain of primary (and occasionally secondary) dysmenorrhea. Treatment is more effective if begun prior to the expected onset of symptoms and continued throughout menses.
Oral contraceptives are often effective and are commonly used for pain that is refractory to NSAID therapy. Other forms of contraceptives (patches, vaginal ring, and injectable medroxyprogesterone) may also provide symptom relief. Oral contraceptives and an NSAID may be combined if monotherapy with each of these is not effective.
Intrauterine devices with levonorgestrel are also helpful, although devices without hormones may aggravate symptoms.
Calcium channel blockers, nitroglycerin, and nitric oxide, agents that block uterine contractions, and other pharmaceuticals are under investigation for their role in treating dysmenorrhea.
Women who do not respond to therapy (including the nutritional steps described below) within 3-4 cycles should undergo reevaluation for the cause of symptoms. This next step typically includes diagnostic laparoscopy.
Treatment is based on the underlying pathology. NSAIDs and oral contraceptive pills may be useful in some patients.
The rationale for dietary changes in the treatment of dysmenorrhea comes from the observation that diets that are low in fat or high in fiber reduce plasma estrogen concentrations and estrogen activity. Under controlled conditions, high-fiber, low-fat diets have been shown to reduce estradiol levels by 10-25%. A meta-analysis of intervention studies suggested that, overall, studies reducing dietary fat have reduced serum estradiol concentrations by 7.4% in premenopausal women and 23% in postmenopausal women, but that greater reductions in dietary fat were associated with greater reductions in estradiol. Similar findings were evident in a randomized trial of women previously treated for breast cancer. A high-fiber, low-fat diet significantly reduced plasma estradiol concentrations.
Fiber’s ability to reduce plasma estrogens is explained by its ability to interrupt enterohepatic circulation. That is, as estrogens are filtered from the blood by the liver and pass through the bile duct into the intestinal tract, fiber carries them away with the wastes. In the absence of fiber, estrogens can be reabsorbed back into circulation. The mechanism by which lower-fat diets reduce estrogens is not clear.
Reduced estrogen concentrations presumably reduce endometrial thickening. In turn, reduced endometrial thickening may reduce the production of prostaglandins (e.g., PGE2) that cause the uterine muscle contraction and ischemia. Diet can also play a role by helping to suppress the inflammation that contributes to pain perception in patients with dysmenorrhea.
A low-fat, vegan diet has been shown to reduce dysmenorrhea symptoms. In a placebo-controlled crossover trial, a low-fat, vegan diet was shown to increase serum concentrations of sex hormone-binding globulin and reduce dysmenorrhea symptoms. Prior to the diet change, volunteers reported an average of 3.9 days of pain in each cycle, which fell to 2.7 days on a low-fat, vegan diet. In addition, the severity of pain was significantly reduced.
Animal products increase estrogen concentrations, and the arachidonic acid and saturated fat they contain activate inflammatory pathways through upregulating NFκB. Patients with dysmenorrhea have also been found to have higher blood levels of arachidonic acid-derived prostaglandins such as PGE2 and PGF2α. A systematic review of studies on diet and dysmenorrhea concluded from observational and clinical trials that a higher dietary ratio of omega-3 to omega-6 fatty acids and supplementation with omega-3 fatty acids are protective against dysmenorrhea by reducing proinflammatory prostaglandin formation.
Maintain a healthy weight. Although mixed, research has revealed that being underweight or overweight increases the risk for dysmenorrhea. In a study including 9,688 women, women with a BMI < 18.5 were at 34% increased risk of dysmenorrhea, and women with a BMI ≥ 30 were at 22% increased risk, compared with women with a BMI between 18.5 and 29.99. Women with a BMI ≥ 30 who lost weight reduced their risk of dysmenorrhea. Researchers speculate that under- and overweight status lead to menstrual irregularities, which, in turn, increase the risk of dysmenorrhea.
Low-fat, vegan diet. See Basic Diet Orders.
Counseling on stress-reduction techniques.
What to Tell the Family
A patient making dietary changes to improve symptoms of dysmenorrhea will benefit from the support of family members, who are likely to find that the same changes may be beneficial for other health issues.
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