eMedicine Specialties > Obstetrics and Gynecology > General Gynecology
Dysmenorrhea
Updated: Jan 28, 2009
Introduction
Background
Dysmenorrhea is defined as difficult menstrual flow or painful menstruation. The term dysmenorrhea is derived from the Greek words dys, meaning difficult/painful/abnormal, meno, meaning month, and rrhea, meaning flow.
Dysmenorrhea is one of the most common gynecologic complaints in young women who present to clinicians.1 The optimal management of this symptom depends on an understanding of the underlying cause. Dysmenorrhea is classified as primary (spasmodic) or secondary (congestive).2
Primary dysmenorrhea is defined as menstrual pain not associated with macroscopic pelvic pathology (ie, absence of pelvic disease). It typically occurs in the first few years after menarche3 and affects up to 50% of postpubescent females.4
Secondary dysmenorrhea is defined as menstrual pain resulting from anatomic and/or macroscopic pelvic pathology,3,5 such as that seen in women with endometriosis or chronic pelvic inflammatory disease. This condition is most often observed in women aged 30-45 years.
The following risk factors have been associated with more severe episodes of dysmenorrhea:6
- Earlier age at menarche
- Long menstrual periods
- Heavy menstrual flow
- Smoking
- Positive family history
Obesity and alcohol consumption were found to be associated with dysmenorrhea in some (not all) studies.7,8,9 Physical activity and the duration of the menstrual cycle do not appear to be associated with increased menstrual pain.7
Pathophysiology
The etiology and pathophysiology of dysmenorrhea have not been fully elucidated. Nonetheless, the following may be involved.
Primary dysmenorrhea
Current evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin F2alpha (PGF2alpha), a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium.10 The response to prostaglandin inhibitors in patients with dysmenorrhea supports the assertion that dysmenorrhea is prostaglandin mediated. Substantial evidence attributes dysmenorrhea to prolonged uterine contractions and decreased blood flow to the myometrium.
Elevated prostaglandin levels were found in the endometrial fluid of women with dysmenorrhea and correlated well with the degree of pain.11 A 3-fold increase in endometrial prostaglandins occurs from the follicular phase to the luteal phase, with a further increase occurring during menstruation.12 The increase in prostaglandins in the endometrium following the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction.5
Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. Significant amounts of leukotrienes have been demonstrated in the endometrium of women with primary dysmenorrhea that does not respond to treatment with prostaglandin antagonists.8,13,14,15,16
The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea.17,18 Vasopressin's role in the endometrium may be related to prostaglandin synthesis and release.
A neuronal hypothesis has also been advocated for the pathogenesis of primary dysmenorrhea. Type C pain neurons are stimulated by the anaerobic metabolites generated by an ischemic endometrium.
Primary dysmenorrhea has also been attributed to behavioral and psychological factors. Although these factors have not been convincingly demonstrated to be causative, they should be considered if medical treatment fails.
Secondary dysmenorrhea
A number of factors may be involved in the pathogenesis of secondary dysmenorrhea. The following pelvic pathologies can lead to the condition:
- Endometriosis
- Pelvic inflammatory disease
- Ovarian cysts and tumors
- Cervical stenosis or occlusion
- Adenomyosis
- Fibroids
- Uterine polyps
- Intrauterine adhesions
- Congenital malformations (eg, bicornate uterus, subseptate uterus)
- Intrauterine contraceptive device
- Transverse vaginal septum
- Pelvic congestion syndrome
- Allen-Masters syndrome
Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.19
Frequency
United States
Dysmenorrhea may affect more than half of menstruating women, and its reported prevalence has been highly variable. A survey of 113 patients in a family practice setting showed a prevalence of dysmenorrhea of 29-44%,20 but prevalence rates as high as 90% in women aged 18-45 years have been reported.1 The use of oral contraceptives (OCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), both of which are effective in ameliorating symptoms of primary dysmenorrhea, may confound the prevalence.
Primary dysmenorrhea peaks in late adolescence and the early 20s.21 The incidence falls with increasing age and with increasing parity. The prevalence and severity of dysmenorrhea in parous women are reportedly significantly lower in many7,22,23 but not all1 studies. No significant difference with respect to prevalence and severity of dysmenorrhea was found between nulligravid women and those in whom pregnancy had been terminated by either spontaneous or induced abortion.7
In an epidemiologic study of an adolescent population (aged 12-17 y), Klein and Litt reported a prevalence of dysmenorrhea of 59.7%.24 Of patients reporting pain, 12% described it as severe; 37%, as moderate; and 49%, as mild. Dysmenorrhea caused 14% of patients to miss school frequently. Although black adolescents reported no increased incidence of dysmenorrhea, they were absent from school more frequently (23.6%) than whites (12.3%), even after adjusting for socioeconomic status.
International
The prevalence of dysmenorrhea worldwide is similar to that in the US, with rates ranging from 15.8-89.5%, with higher prevalence rates reported in adolescent populations.25,26,27,7,28,22,29,30
Mortality/Morbidity
Dysmenorrhea can disrupt personal life and is a significant public health problem associated with substantial economic loss related to work absences. Ten percent of women with the condition have severe pain that can be incapacitating. In the United States, the annual economic loss has been estimated at 600 million work hours and 2 billion dollars.31
Race
No data suggest that race affects the incidence of dysmenorrhea.
Sex
See Frequency.
Age
See Frequency.
Clinical
History
- History is critical in establishing the diagnosis of dysmenorrhea and should include an assessment of the onset, duration, type, and severity of pain. A thorough menstrual history is also essential and should include the age at menarche, cycle regularity, cycle length, last menstrual period, and duration and amount of menstrual flow.
- Determine factors that exacerbate or ameliorate the symptoms and the degree of disruption to school, work, and social activities.
- Consider gravidity and parity status, previous pelvic infections, dyspareunia, infertility, and pelvic surgeries, injuries, and procedures.
- Also assess symptoms such as nausea, vomiting, bloating, diarrhea, and fatigue, which may be observed in patients with dysmenorrhea.
- Consider sexual history, including the choice of contraceptive methods. If used, establish the effect of OCs on relieving or exacerbating the condition. Moreover, discuss the use of other agents that affect dysmenorrhea pain.
- A family history may be helpful in differentiating endometriosis from primary dysmenorrhea.32 The history should include questions pertaining to sexual abuse because this is reportedly associated with dysmenorrhea and chronic pelvic pain.33
- In summary, a complete history should include the following:
- Age at menarche
- Menstrual frequency, length of period, estimate of the menstrual flow, and presence or absence of intermenstrual bleeding
- Associated symptoms
- Severity of pain and its relationship to the menstrual cycle
- Impact on physical and social activity
- Progression of symptom severity
- Sexual history
- Primary dysmenorrhea should be distinguished from secondary dysmenorrhea on the basis of clinical features.
- Primary dysmenorrhea almost invariably occurs in ovulatory cycles and usually appears within a year after menarche. In classic primary dysmenorrhea, the pain begins with the onset of menstruation (or just shortly before) and persists throughout the first 1-2 days. The pain is described as spasmodic and superimposed over a background of constant lower abdominal pain, which radiates to the back or anterior and/or medial thigh.
- Associated general symptoms, such as malaise, fatigue (85%), nausea and vomiting (89%), diarrhea (60%), lower backache (60%), and headache (45%), may be present with primary dysmenorrhea. Dizziness, nervousness, and even collapse are also associated with dysmenorrhea.
- The clinical features of primary dysmenorrhea include the following:
- Onset shortly after menarche
- Usual duration of 48-72 hours (often starting several hours before or just after the menstrual flow)
- Cramping or laborlike pain
- Often unremarkable pelvic examination findings (including rectal)
- A different pattern of pain is observed with secondary dysmenorrhea that is not limited to the onset of menses; this is usually associated with abdominal bloating, pelvic heaviness, and back pain. Typically, the pain progressively increases during the luteal phase until it peaks around the onset of menstruation.
- The following may indicate secondary dysmenorrhea19,34 :
- Dysmenorrhea occurring during the first or second cycles after menarche, which may indicate congenital outflow obstruction
- Dysmenorrhea beginning after the age of 25 years
- Pelvic abnormality with physical examination: Consider endometriosis, pelvic inflammatory disease, pelvic adhesions, and adenomyosis.
- Little or no response to therapy with NSAIDs, OCs, or both
Physical
- A pelvic examination is indicated at the initial evaluation, which should be carefully performed in order to exclude uterine irregularities, cul-de-sac tenderness, or nodularity that may suggest endometriosis, pelvic inflammatory disease, or a pelvic mass.
- Women with primary dysmenorrhea usually have normal findings on examination.
- Pelvic pathology may be found during pelvic examination in women with secondary dysmenorrhea, although normal findings do not exclude the condition.
- Women with endometriosis who present with secondary dysmenorrhea have physical findings approximately 40% of the time.35,36
- Patients presenting with secondary dysmenorrhea may have unique and specific findings on physical examination that correspond to their particular pathologies.
Causes
- Causes of secondary dysmenorrhea include the following:
- Intrauterine contraceptive devices
- Adenomyosis
- Uterine myoma (fibroids)
- Uterine polyps
- Adhesions
- Congenital malformation of the müllerian system
- Cervical strictures or stenosis
- Ovarian cysts
- Pelvic congestion syndrome
- Allen-Masters syndrome
- Mittelschmerz (midcycle ovulation pain)
- Psychogenic pain
Differential Diagnoses
| Abortion | Irritable Bowel Syndrome |
| Ectopic Pregnancy | Ovarian Cysts |
| Endometriosis | Pelvic Inflammatory Disease |
| Inflammatory Bowel Disease | Urinary Tract Infection, Females |
Other Problems to Be Considered
The most important differential diagnosis of primary dysmenorrhea is secondary dysmenorrhea.
Workup
Laboratory Studies
- No tests are specific to the diagnosis of primary dysmenorrhea. Diagnosis is made based on clinical findings.
- The following can be performed to exclude organic causes of dysmenorrhea:
- Cervical culture to exclude sexually transmitted diseases
- WBC count to exclude infection
- Human chorionic gonadotropin level to exclude ectopic pregnancy
- Sedimentation rate
- Cancer antigen 125 (CA-125) assay: This has limited clinical value in evaluating women with dysmenorrhea because of its relatively low negative predictive value.
Imaging Studies
- Noninvasive studies may include abdominal and transvaginal ultrasound. (Other more-invasive studies, including hysterosalpingography, may be required.)
- Pelvic ultrasound scans are indicated to evaluate for situations such as ectopic pregnancy, ovarian cysts, fibroids, and intrauterine contraceptive devices. This is a highly sensitive test for detecting pelvic masses.
- Hysterosalpingograms are used to exclude endometrial polyps, leiomyomas, and congenital abnormalities of the uterus.
- Intravenous pyelograms are indicated if uterine malformation is confirmed as a cause or contributing factor for the dysmenorrhea.
Procedures
- Other more-invasive studies, including laparoscopy, hysteroscopy, and dilatation and curettage, may be required.
- Laparoscopic examination is the single most useful procedure. It involves a complete diagnostic survey of the pelvis and reproductive organs to ascertain the presence of any pathology that may account for the clinical symptoms.
- Hysteroscopy and dilatation and curettage may be indicated to evaluate intrauterine pathology found on imaging.
- An endometrial biopsy may be indicated if endometritis is considered likely.
Treatment
Medical Care
- Grading dysmenorrhea according to severity of pain and limitation of daily activity may help guide the treatment strategy.
- In addition to pain relief, other mainstays of treatment include reassurance and education.
Surgical Care
- Surgery is generally not indicated for patients with primary dysmenorrhea.
- In patients with secondary dysmenorrhea, treatment of the underlying pathology may necessitate surgical intervention.
- In refractory cases of dysmenorrhea, laparoscopic presacral neurectomy (PSN) or uterosacral nerve ablation (LUNA) have been efficacious in some patients for as long as 12 months after treatment.37,38,39
Consultations
In patients with refractory symptoms, a multidisciplinary approach may be indicated.
Diet
Both a low-fat vegetarian diet40 and fish-oil supplements41 have been reported to reduce menstrual pain in some women.
Medication
Treatment of primary dysmenorrhea is directed at providing relief from the cramping pelvic pain and associated symptoms (eg, headache, nausea, vomiting, flushing, diarrhea) that typically accompany or immediately precede the onset of menstrual flow. The pelvic pain can be distressing and occasionally radiates to the back and thighs, often necessitating prompt intervention. To date, pharmacotherapy has been the most reliable and effective treatment for relieving dysmenorrhea. Because the pain results from uterine vasoconstriction, anoxia, and contractions mediated by prostaglandins, symptomatic relief can often be obtained from use of agents that inhibit prostaglandin synthesis and have anti-inflammatory and analgesic properties.
NSAIDs and combination OCs are the most commonly used therapeutic modalities for the management of primary dysmenorrhea. These agents have different mechanisms of action and can be used adjunctively in refractory cases. The lack of response to NSAIDs and OCs (or the combination) may increase the likelihood of a secondary cause for dysmenorrhea.
Other therapies for dysmenorrhea have been proposed, but most are not well studied. These include thiamine, vitamin E, omega-3 fatty acids, magnesium, acupuncture, acupressure, various herbal medicines, transdermal nitroglycerin, calcium-channel blockers, beta-adrenergic agonists, antileukotrienes, and transcutaneous electrical nerve stimulation (TENS) units. Use of topical, continuous, low-level heat may be beneficial for some patients.42,43
Treatment of secondary dysmenorrhea involves correction of the underlying organic cause. Specific measures (medical or surgical) may be required to treat pelvic pathology (eg, endometriosis) and to ameliorate the associated dysmenorrhea. Periodic use of analgesic agents as adjunctive therapy may be beneficial.
Nonsteroidal anti-inflammatory drugs
NSAIDs are the most commonly used treatments for dysmenorrhea. NSAIDs decrease menstrual pain by decreasing intrauterine pressure and lowering PGF2alpha levels in menstrual fluid.44,45,46 Because they are used for short periods in otherwise healthy young women, they are generally well tolerated and free of serious toxicity. Gastrointestinal (GI) upset is the most common adverse effect associated with NSAIDs, and patients receiving these medications should be monitored for more serious adverse effects, including GI bleeding and renal dysfunction.
Patients should also be monitored for potential pharmacokinetic and pharmacodynamic drug interactions and possible effects on platelet aggregation. NSAIDs are contraindicated in patients with renal insufficiency, peptic ulcer disease, gastritis, bleeding diatheses, and aspirin hypersensitivity. These agents must be used on a regular basis (as-needed use is not adequate in most patients) for several days. To avoid inadvertent exposure to these agents during early pregnancy, NSAIDs should be started at the onset of menstrual bleeding.
While some NSAIDs have been touted as being particularly effective for dysmenorrhea (especially the fenamates), scientific data to support such claims are sparse and generally weak.47 Moreover, well-designed prospective comparative studies have not been performed. Diclofenac, ibuprofen, ketoprofen, meclofenamate, mefenamic acid, and naproxen are the NSAIDs specifically approved by the US Food and Drug Administration (FDA) for treatment of dysmenorrhea. Aspirin may not be as effective as other NSAIDs, and acetaminophen may be a useful adjunct for alleviating only mild menstrual cramping pain.48,47
NSAIDs that achieve peak serum concentrations within 30-60 minutes and have a faster onset of action (eg, ibuprofen, naproxen, meclofenamate) may be preferred. However, individual patient response varies, and patients may need a trial of several agents before finding one that works. Some NSAIDs (eg, indomethacin) should be avoided because they have a higher incidence of adverse effects.
Despite some preliminary data suggesting efficacy in patients with primary dysmenorrhea, the newer cyclooxygenase-2 (COX-2) inhibitors have not been demonstrably superior to conventional NSAIDs.49 However, these agents may be used in patients who cannot tolerate other NSAIDS or in whom these agents are contraindicated. COX-2–derived prostanoids nonetheless appear to be involved in the pathophysiology of primary dysmenorrhea.50
NSAIDs that inhibit type I prostaglandin synthetase and suppress the production of cyclic endoperoxides (eg, fenamates, COX-2–selective agents, propionic acids, indole acetic acids) alleviate dysmenorrhea symptoms by decreasing endometrial and menstrual fluid prostaglandin concentrations.
Naproxen (Naprosyn, Aleve, Anaprox)
Available in both prescription and nonprescription doses. Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis.
Dosing
Adult
500 mg PO followed by 250 mg PO q6-8h or 500 mg q12h; not to exceed 1.25 g/d
Pediatric
Not established
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of antihypertensives; may decrease diuretic effects of loop and thiazide diuretics; may increase PT when taking anticoagulants (instruct patients to watch for signs/symptoms of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; history of asthma, urticaria, or allergic-type reactions to aspirin or other NSAIDS; treatment of perioperative pain in setting of coronary artery bypass graft surgery
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant/antiplatelet therapy; discontinue if a rash occurs
Ibuprofen (Advil, Motrin, Nuprin)
Available in both prescription and nonprescription doses. Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis.
Dosing
Adult
400 mg PO q4-6h; not to exceed 3.2 g/d
Pediatric
Not established
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of antihypertensives; may decrease diuretic effects of loop and thiazide diuretics; may increase PT when taking anticoagulants (instruct patients to watch for signs/symptoms of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; history of asthma, urticaria, or allergic-type reactions to aspirin or other NSAIDS; treatment of perioperative pain in setting of coronary artery bypass graft surgery
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant/antiplatelet therapy; discontinue if a rash occurs
Diclofenac (Cataflam, Voltaren)
Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis.
Dosing
Adult
100 mg PO initially then 50 mg PO tid; not to exceed 150 mg/d
Pediatric
Not established
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of antihypertensives; may decrease diuretic effects of loop and thiazide diuretics; may increase PT when taking anticoagulants (instruct patients to watch for signs/symptoms of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; history of asthma, urticaria, or allergic-type reactions to aspirin or other NSAIDS; treatment of perioperative pain in setting of coronary artery bypass graft surgery
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant/antiplatelet therapy; discontinue if a rash occurs
Ketoprofen (Orudis, Actron, Oruvail)
Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in the decrease of prostaglandin synthesis. Smaller initial dosages are particularly indicated in the elderly and in those with renal or liver dysfunction. Doses greater than 75 mg do not improve therapeutic response and may be associated with a higher incidence of adverse effects.
Dosing
Adult
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
Pediatric
Not established
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of antihypertensives; may decrease diuretic effects of loop and thiazide diuretics; may increase PT when taking anticoagulants (instruct patients to watch for signs/symptoms of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; history of asthma, urticaria, or allergic-type reactions to aspirin or other NSAIDS; treatment of perioperative pain in setting of coronary artery bypass graft surgery
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during concomitant anticoagulant/antiplatelet therapy; discontinue if a rash occurs
Meclofenamate sodium
Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis. Higher incidence of diarrhea compared with other NSAIDS.
Dosing
Adult
100 mg PO tid for up to 6 d; not to exceed 300 mg/d
Pediatric
Not established
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of antihypertensives; may decrease diuretic effects of loop and thiazide diuretics; may increase PT when taking anticoagulants (instruct patients to watch for signs/symptoms of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; active GI bleeding; ulcer disease
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Diarrhea may occur (reduce dose or discontinue use);
caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant/antiplatelet therapy; discontinue if a rash occurs
Mefenamic acid (Ponstel)
Inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in decrease of prostaglandin synthesis. Higher incidence of diarrhea compared to other NSAIDS.
Dosing
Adult
500 mg PO initially, followed by 250 mg q6h for 2-3 d; not to exceed 1 g/d
Pediatric
Not established
Interactions
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effects of antihypertensives; may decrease diuretic effects of loop and thiazide diuretics; may increase PT when taking anticoagulants (instruct patients to watch for signs/symptoms of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Contraindications
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding; history of asthma, urticaria, or allergic-type reactions to aspirin or other NSAIDS; treatment of perioperative pain in setting of coronary artery bypass graft surgery
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Diarrhea may occur (reduce dose or discontinue use); caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during concomitant anticoagulant/antiplatelet therapy; discontinue if a rash occurs
Contraceptives
Dysmenorrhea can be prevented altogether in some patients by use of OCs, although these agents are not approved by the FDA for this indication. OCs may be an appropriate treatment choice in patients who do not wish to conceive. The combination OCs suppress the hypothalamic-pituitary-ovarian axis and thereby inhibit ovulation and prevent prostaglandin production in the late luteal phase. This generally significantly reduces the amount of menstrual flow and effectively alleviates primary dysmenorrhea in most patients. Use of OCs in a manner that reduces the number of menstrual cycles (by extending the use of active pills and avoiding the pill-free week or with extended-cycle formulations) may be beneficial for some patients.51,52
Combination OCs, the levonorgestrel intrauterine device, and depot medroxyprogesterone acetate provide effective pain relief and are associated with a reduced menstrual flow. The use of NSAIDs in combination with an OC may be necessary, especially during the first few cycles after initiation of the OC. The dose of ethinyl estradiol should generally be less than 50 mcg. A monophasic OC containing 30 mcg of ethinyl estradiol is a reasonable choice. To date, studies comparing the efficacy of various OC formulations in the management of dysmenorrhea have not been performed.
Medroxyprogesterone acetate (DMPA; DepoProvera)
Inhibits secretion of gonadotropins, thereby inhibiting ovulation and decreasing thickness of endometrium.
Dosing
Adult
IM formulation: 150 mcg IM q3mo
Subcutaneous suspension (104 mg/0.65 mL): 1 injection q3mo
Pediatric
Not established
Interactions
Aminoglutethimide (not currently available in the US) may significantly decrease serum concentrations
Contraindications
Documented hypersensitivity; undiagnosed vaginal bleeding; known or suspected malignancy of breast; active thrombophlebitis or current or past history of thromboembolic disorders or cerebral vascular disease; significant liver disease
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
May cause a significant decrease in bone mineral density that may not be reversible, this risk is increased with increasing duration of use, not generally recommended for use longer than 2 years; caution in hepatic impairment, glucose intolerance, depression, or ocular disorders; may cause fluid retention; may cause menstrual irregularities and amenorrhea; weight gain observed
Levonorgestrel-releasing intrauterine device (Mirena)
Inhibits secretion of gonadotropins, thereby inhibiting ovulation and decreasing thickness of endometrium.
Dosing
Adult
52 mg levonorgestrel, inserted intrauterine; removed after 5 years
Pediatric
Not established
Interactions
Not established
Contraindications
Documented hypersensitivity; undiagnosed vaginal bleeding; known or suspected malignancy of breast; acute liver disease or liver tumor (benign or malignant); known or suspected uterine or cervical neoplasia or unresolved abnormal Pap smear; untreated acute cervicitis or vaginitis, including bacterial vaginosis or other lower genital tract infections until infection is controlled; genital actinomycosis; history of ectopic pregnancy or condition that would predispose to ectopic pregnancy; congenital or acquired uterine anomaly including fibroids if they distort the uterine cavity; acute pelvic inflammatory disease (PID) or a history of PID unless there has been a subsequent intrauterine pregnancy; postpartum endometritis or infected abortion in the past 3 months; conditions associated with increased susceptibility to infections with micro-organisms (eg, leukemia, AIDS, and IV drug abuse); woman or her partner has multiple sexual partners
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
May cause menstrual irregularities and amenorrhea; may cause PID, embedment in the myometrium, perforation of uterus, or ovarian cyst
Ethinyl estradiol and gonane progestin (norgestimate, norgestrel, levonorgestrel, or desogestrel) (Ortho-Cyclen, Ovral, Lo-Ovral, Alesse, Levlen, Levlite, Nordette, Desogen, Ortho-Cept)
Reduces secretion of LH and FSH from pituitary by decreasing amount of gonadotropin-releasing hormones.
Dosing
Adult
1 tab/d PO for 21 d followed by 7 d off medication (or taking inactive tab); begin new course on day 8 after taking last active tab
Schedule 1 (Sunday starter): Begin dose on first Sunday after onset of menstruation; start that Sunday if menstrual period starts on Sunday
Schedule 2 (Day 1 starter): Start dose on day 1 of menstrual cycle
Perform pregnancy test if menstrual period is missed
Pediatric
Not established
Interactions
Phenobarbital, phenytoin, primidone, carbamazepine, oxcarbazepine, barbiturates, ethosuximide, felbamate, topiramate, rifampin, rifabutin, griseofulvin, modafinil, and St. John's wort induce enzymes that decrease concentrations of contraceptive steroids; broad-spectrum antibiotics may decrease effectiveness
Contraindications
Documented hypersensitivity; endometrial or other estrogen-dependent cancers; hepatic cancer or active liver disease; thromboembolic disorders; undiagnosed vaginal bleeding; smokers >35 y; cardiovascular or cerebrovascular disease; headaches with focal neurological symptoms; pregnancy
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Caution in patients diagnosed with hepatic impairment, migraine, or seizure disorders
Ethinyl estradiol and estrane progestin (norethindrone or ethynodiol acetate) (Ortho-Novum, Ovcon 50, Ortho-Novum 7/7/7, Brevicon, LoEstrin, Modicon, Tri-Norinyl, Demulen, Zovia)
Reduces secretion of LH and FSH from pituitary by decreasing amount of gonadotropin-releasing hormones.
Dosing
Adult
1 tab/d for 21 d followed by 7 d off medication (or taking inactive tab); begin new course on day 8 after taking last active tab
Schedule 1 (Sunday starter): Begin dose on first Sunday after onset of menstruation; start that Sunday if menstrual period starts on Sunday
Schedule 2 (Day 1 starter): Start dose on day 1 of menstrual cycle
Perform pregnancy test if menstrual period is missed
Pediatric
Not established
Interactions
Phenobarbital, phenytoin, primidone, carbamazepine, oxcarbazepine, barbiturates, ethosuximide, felbamate, topiramate, rifampin, rifabutin, griseofulvin, modafinil, and St. John's wort induce enzymes that decrease concentrations of contraceptive steroids; broad-spectrum antibiotics may decrease effectiveness
Contraindications
Documented hypersensitivity; endometrial or other estrogen-dependent cancers; hepatic cancer or active liver disease; thromboembolic disorders; undiagnosed vaginal bleeding; smokers >35 y; cardiovascular or cerebrovascular disease; headaches with focal neurological symptoms; pregnancy
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Caution in patients diagnosed with hepatic impairment, migraine, or seizure disorders
Ethinyl estradiol and drospirenone (Yasmin, YAZ)
Reduces secretion of LH and FSH from pituitary by decreasing amount of gonadotropin-releasing hormones.
Dosing
Adult
24-tab package (YAZ): 1 tab per d for 24 d followed by 4 d off medication (or taking inactive tab); begin new course on d 5 after taking last active tab
28-tab package (Yasmin): 1 tab per d for 21 d followed by 7 d off medication (or taking inactive tab); begin new course on d 8 after taking last active tab
Schedule 1 (Sunday starter): Begin dose on first Sunday after onset of menstruation; start that Sunday if menstrual period starts on Sunday
Schedule 2 (Day 1 starter): Start dose on d 1 of menstrual cycle
Perform pregnancy test if menstrual period is missed
Pediatric
Not established
Interactions
Phenobarbital, phenytoin, primidone, carbamazepine, oxcarbazepine, barbiturates, ethosuximide, felbamate, topiramate, rifampin, rifabutin, griseofulvin, modafinil, and St. John's wort induce enzymes that decrease concentrations of contraceptive steroids; broad-spectrum antibiotics may decrease effectiveness; increased risk of hyperkalemia with other hyperkalemic drugs (ACE inhibitors, angiotensin-II receptor blockers, aldosterone antagonists, potassium-sparing diuretics, NSAIDs, heparin)
Contraindications
Documented hypersensitivity; endometrial or other estrogen-dependent cancers; hepatic cancer or active liver disease; thromboembolic disorders; undiagnosed vaginal bleeding; smokers >35 y; cardiovascular or cerebrovascular disease; headaches with focal neurological symptoms; pregnancy; renal insufficiency, adrenal insufficiency, or any other conditions that predisposes to hyperkalemia
Precautions
Pregnancy
X - Contraindicated; benefit does not outweigh risk
Precautions
Caution in patients diagnosed with hepatic impairment, migraine, or seizure disorders
Follow-up
Patient Education
For excellent patient education resources, visit eMedicine's Pregnancy and Reproduction Center and Women's Health Center. Also, see eMedicine's patient education articles Birth Control Overview, Birth Control FAQs, Menstrual Pain, Ovarian Cysts and Mittelschmerz.
Miscellaneous
Medicolegal Pitfalls
- Failure to make a diagnosis: Careful evaluation of pain is important in order to avoid delay in the diagnosis of potentially life-threatening disorders such as ectopic pregnancy or pelvic neoplasm.
- Complications of diagnostic procedures: Invasive procedures should be performed only if clinically indicated. If complications develop following poorly indicated procedures, the medicolegal risk is significant.
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Keywords
primary dysmenorrhea, secondary dysmenorrhea, painful menstruation, painful menses, spasmodic dysmenorrhea, congestive dysmenorrhea, endometriosis, pelvic inflammatory disease, PID, ovarian cysts, ovarian tumors, cervical stenosis, cervical occlusion, adenomyosis, fibroids, uterine polyps, intrauterine adhesions, congenital malformations, bicornuate uterus, subseptate uterus, intrauterine contraceptive devices, IUCDs, intrauterine devices, IUDs, transverse vaginal septum, pelvic congestion syndrome, Allen-Masters syndrome
Contributor Information and Disclosures
Author
Karim Anton Calis, PharmD, MPH, FASHP, FCCP, Professor, Medical College of Virginia, Virginia Commonwealth University, Clinical Professor, University of Maryland; Clinical Specialist, Endocrinology and Women's Health, Director, Drug Information Service, Mark O Hatfield Clinical Research Center, National Institutes of Health
Karim Anton Calis, PharmD, MPH, FASHP, FCCP is a member of the following medical societies: American College of Clinical Pharmacy, American Society of Health-System Pharmacists, and Endocrine Society
Disclosure: Nothing to disclose.
Coauthor(s)
Vaishali Popat, MD, MPH, Medical Officer, Food and Drug Administration
Vaishali Popat, MD, MPH is a member of the following medical societies: American Association of Clinical Endocrinologists and Endocrine Society
Disclosure: Nothing to disclose.
Devra K Dang, PharmD, BCPS, CDE, Assistant Clinical Professor, University of Connecticut School of Pharmacy, Clinical Faculty, Burgdorf Health Center
Disclosure: Nothing to disclose.
Sophia N Kalantaridou, MD, Assistant Professor, Department of Obstetrics and Gynecology, University of Ioannina Medical School, Greece
Disclosure: Nothing to disclose.
Medical Editor
Anthony Charles Sciscione, DO, Director, Division of Maternal-Fetal Medicine, Professor, Department of Obstetrics and Gynecology, Drexel University College of Medicine
Anthony Charles Sciscione, DO is a member of the following medical societies: American College of Obstetricians and Gynecologists and American Medical Association
Disclosure: Nothing to disclose.
Pharmacy Editor
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Managing Editor
A David Barnes, MD, PhD, MPH, FACOG, Consulting Staff, Department of Obstetrics and Gynecology, Mammoth Hospital, Mammoth Lakes, California, Pioneer Valley Hospital, Salt Lake City, Utah, Warren General Hospital, Warren, Pennsylvania and Mountain West Hospital, Tooele, Utah
A David Barnes, MD, PhD, MPH, FACOG is a member of the following medical societies: American College of Forensic Examiners, American College of Obstetricians and Gynecologists, American Medical Association, Association of Military Surgeons of the US, and Utah Medical Association
Disclosure: Nothing to disclose.
CME Editor
Frederick B Gaupp, MD, Consulting Staff, Department of Family Practice, Hancock Medical Center
Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians
Disclosure: Nothing to disclose.
Chief Editor
Michel E Rivlin, MD, Professor, Coordinator of Quality Assurance/Quality Improvement, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.