AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

Dysmenorrhea is one of the most common gynecologic complaints in young women who present to clinicians (Jamieson, 1996).

The term dysmenorrhea is derived from the Greek words dys, meaning difficult/painful/abnormal, meno, meaning month, and rrhea, meaning flow. Dysmenorrhea is defined as difficult menstrual flow or painful menstruation. The optimal management of this symptom depends on an understanding of the underlying cause. Dysmenorrhea is classified as primary (spasmodic) or secondary (congestive) (Dawood, 1985).

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 menarche (Koltz, 1995) and affects up to 50% of postpubescent females (Dawood, 1988).

Secondary dysmenorrhea is defined as menstrual pain resulting from anatomic and/or macroscopic pelvic pathology (Dawood, 1990; Koltz, 1995), 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 (Harlow, 1996):

1. Earlier age at menarche
2. Long menstrual periods
3. Heavy menstrual flow
4. Smoking
5. Positive family history

Obesity and alcohol consumption were found to be associated with dysmenorrhea in some (not all) studies (Andersch, 1982; Sundell, 1990; Parazzini, 1994). Physical activity and the duration of the menstrual cycle do not appear to be associated with increased menstrual pain (Andersch, 1982).

Pathophysiology

The etiology and pathophysiology of dysmenorrhea have not been fully elucidated. Nonetheless, the following may be involved.

Primary dysmenorrhea

Growing evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin F2alpha (PGF2alpha), a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium (Willman, 1976). 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 dysmenorrheic women and correlated well with the degree of pain (Helsa, 1992; Eden, 1998). A 3-fold increase in endometrial prostaglandins occurs from the follicular phase to the luteal phase, with a further increase occurring during menstruation (Speroff, 1997; Dambro, 1998). 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 (Dawood, 1990).

Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus (Helsa, 1992). Significant amounts of leukotrienes have been demonstrated in the endometrium of women with primary dysmenorrhea that does not respond to treatment with prostaglandin antagonists (Demers, 1984; Rees, 1987; Chegini, 1988; Sundell, 1990; Nigam, 1991).

The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea (Akerlund, 1979). 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 (Smith, 1993).

Frequency

United States

Dysmenorrhea may affect more than half of menstruating women. The prevalence of dysmenorrhea can be quite variable. A survey of 113 patients in a family practice setting showed a prevalence of dysmenorrhea of 29-44% (Sobczyk, 1978). With the availability of oral contraceptives (OCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), both of which are effective in relieving symptoms of primary dysmenorrhea, the actual prevalence rate may be higher.

The peak incidence of primary dysmenorrhea occurs in late adolescence and the early 20s (Fraser, 1992). The incidence of dysmenorrhea in adolescents is reportedly as high as 92% (Andersch, 1982). The incidence falls with increasing age and with increasing parity. The prevalence and severity of dysmenorrhea in parous women were significantly lower (Andersch, 1982). 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.

In an epidemiologic study of an adolescent population (aged 12-17 y), Klein and Litt reported a prevalence of dysmenorrhea of 59.7%. 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

See US Frequency.

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 (Dawood, 1984).

Race

No data suggest that race affects the incidence of dysmenorrhea.

Sex

See Frequency.

Age

See Frequency.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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 gravity 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 (Malinak, 1980; Simpson, 1980). The history should include questions pertaining to sexual abuse because this is reportedly associated with dysmenorrhea and chronic pelvic pain (Jamieson, 1997).
• 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 dysmenorrhea (Smith, 1993; Smith, 1997):
    • 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 (Propst, 1998; Barbieri, 1999).
  • 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

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

The most important differential diagnosis of primary dysmenorrhea is secondary dysmenorrhea.

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab 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

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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 neuroectomy has been efficacious in some patients for as long as 12 months after treatment (Gurgan, 1992; Chen, 1996).

Consultations

In patients with refractory symptoms, a multidisciplinary approach may be indicated.

Diet

Both a low-fat vegetarian diet (Barnard, 2000) and fish-oil supplements (Harel, 1996) have been reported to reduce menstrual pain in some women.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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, 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.

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.

Drug Category: 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. Because they are used for short periods in otherwise healthy young women, they are generally well tolerated and free of serious toxicity. 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 (Zhang, 1998). 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.

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. 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 (Morrison, 1999).

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.

Drug Name	Ibuprofen (Advil, Motrin, Nuprin)
Description	DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Adult Dose	400 mg PO q4-6h; not to exceed 3.2 g/d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
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 hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Drug Name	Diclofenac (Cataflam, Voltaren)
Description	Inhibits prostaglandin synthesis by decreasing activity of enzyme cyclooxygenase, which in turn decreases formation of prostaglandin precursors.
Adult Dose	50 mg PO tid; not to exceed 150 mg/d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
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 hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Category D in third trimester of pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; low WBC counts occur rarely and usually return to normal in ongoing therapy; discontinuation of therapy may be necessary if persistent leukopenia, granulocytopenia, or thrombocytopenia

Drug Name	Ketoprofen (Orudis, Oruvail, Actron)
Description	For relief of mild to moderate pain and inflammation. Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Doses greater than 75 mg do not increase therapeutic effects. Administer high doses with caution and closely observe patient for response.
Adult Dose	25-50 mg PO q6-8h prn; not to exceed 300 mg/d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
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 hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Drug Name	Meclofenamate sodium
Description	Decreases activity of cyclooxygenase, which results in decreased formation of prostaglandin precursors.
Adult Dose	100 mg PO tid for up to 6 d; not to exceed 300 mg/d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; active GI bleeding; ulcer disease
Interactions	Aspirin decreases effects; decreases effects of diuretics; increases toxicity of warfarin and methotrexate
Pregnancy	B - Usually safe but benefits must outweigh the risks.
Precautions	Category D in third trimester of pregnancy; diarrhea may occur (reduce dose or discontinue use)

Drug Name	Mefenamic acid (Ponstel)
Description	Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Adult Dose	500 mg PO initially, followed by 250 mg q6h for 2-3 d; not to exceed 1 g/d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
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 hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Category D in third trimester of pregnancy; may have adverse effects in fetus; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy

Drug Category: Oral 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) may be beneficial for some patients.

Combination OCs 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.

Drug Name	Ethinyl estradiol and norethindrone (Ortho-Novum, Ovcon 50, Ortho-Novum 7/7/7)
Description	Reduces secretion of LH and FSH from pituitary by decreasing amount of gonadotropin-releasing hormones.
Adult Dose	Schedule 1 (Sunday starter): Begin dose on first Sunday after onset of menstruation; start that Sunday if menstrual period starts on Sunday 21-tab package: 1 tab qd for 21 d followed by 7 d off medication; new course begins on eighth d after taking last tab 28-tab package: 1 tab qd without interruption Schedule 2 (Day 1 starter): Start dose on day 1 of menstrual cycle21-tab package: 1 tab qd for 21 d followed by 7 d off medication; begin new course on day 8 after taking last tab Continue dosing cycle if 1 period missed; pregnancy test required if 2 periods missed
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; endometrial and hepatic cancer; thromboembolic disorders; undiagnosed vaginal bleeding; smokers >35 y; cardiovascular disease
Interactions	Phenobarbital, phenytoin, paramethadione, carbamazepine, troglitazone, rifampicin, and griseofulvin induce enzymes that levels of contraceptive steroids; oral anticoagulants may increase thromboembolic potential
Pregnancy	X - Contraindicated in pregnancy
Precautions	Caution in patients diagnosed with hepatic impairment, migraine, seizure disorders, cerebrovascular disorders, breast cancer, or thromboembolic disease

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal 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.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Nahrain Alzubaidi, MD to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

• Akerlund M. Pathophysiology of dysmenorrhea. Acta Obstet Gynecol Scand Suppl. 1979;87:27-32. [Medline].
• Akerlund M, Stromberg P, Forsling ML. Primary dysmenorrhoea and vasopressin. Br J Obstet Gynaecol. Jun 1979;86(6):484-7. [Medline].
• Andersch B, Milsom I. An epidemiologic study of young women with dysmenorrhea. Am J Obstet Gynecol. Nov 15 1982;144(6):655-60. [Medline].
• Barbieri RL, Propst AM. Physical examination findings in women with endometriosis: uterosacral ligament abnormalities, lateral cervical displacement and cervical stenosis. J Gynecol Tech. 1999;135:102.
• Barnard ND, Scialli AR, Hurlock D, Bertron P. Diet and sex-hormone binding globulin, dysmenorrhea, and premenstrual symptoms. Obstet Gynecol. Feb 2000;95(2):245-50. [Medline].
• Chegini N, Rao CV. The presence of leukotriene C4- and prostacyclin-binding sites in nonpregnant human uterine tissue. J Clin Endocrinol Metab. Jan 1988;66(1):76-87. [Medline].
• Chen FP, Chang SD, Chu KK, Soong YK. Comparison of laparoscopic presacral neurectomy and laparoscopic uterine nerve ablation for primary dysmenorrhea. J Reprod Med. Jul 1996;41(7):463-6. [Medline].
• Dawood MY. Dysmenorrhea. J Reprod Med. Mar 1985;30(3):154-67. [Medline].
• Dawood MY. Dysmenorrhea. Clin Obstet Gynecol. Sep 1983;26(3):719-27. [Medline].
• Dawood MY. Ibuprofen and dysmenorrhea. Am J Med. Jul 13 1984;77(1A):87-94. [Medline].
• Dawood MY. Dysmenorrhea. Clin Obstet Gynecol. Mar 1990;33(1):168-78. [Medline].
• Dawood MY. Overall approach to the management of dysmenorrhea. In: Dawood MY, ed. Dysmenorrhea. Baltimore: Williams & Wilkins;1981:261-79.
• Dawood MY. Nonsteroidal anti-inflammatory drugs and changing attitudes toward dysmenorrhea. Am J Med. May 20 1988;84(5A):23-9. [Medline].
• Demers LM, Hahn DW, McGuire JL. Newer concepts in dysmenorrhea research: leukotrienes and calcium channel blockers. In: Dawood MY, McGuire JL, Demers LM, eds. Premenstrual Syndrome and Dysmenorrhea. London: Pitman;1984:205-13.
• Dingfelder JR. Primary dysmenorrhea treatment with prostaglandin inhibitors: a review. Am J Obstet Gynecol. Aug 15 1981;140(8):874-9. [Medline].
• Eden JA. Dysmenorrhea and premenstrual syndrome. In: NF Hacker, JG Moore, eds. Essentials of Obstetrics and Gynecology. 3rd ed. Philadelphia: WB Saunders;1998:386-92.
• Fraser IS. Prostaglandins, prostaglandin inhibitors and their roles in gynaecological disorders. Baillieres Clin Obstet Gynaecol. Dec 1992;6(4):829-57. [Medline].
• Gurgan T, Urman B, Aksu T, et al. Laparoscopic CO2 laser uterine nerve ablation for treatment of drug resistant primary dysmenorrhea. Fertil Steril. Aug 1992;58(2):422-4. [Medline].
• Harel Z, Biro FM, Kottenhahn RK, Rosenthal SL. Supplementation with omega-3 polyunsaturated fatty acids in the management of dysmenorrhea in adolescents. Am J Obstet Gynecol. Apr 1996;174(4):1335-8. [Medline].
• Harlow SD, Park M. A longitudinal study of risk factors for the occurrence, duration and severity of menstrual cramps in a cohort of college women. Br J Obstet Gynaecol. Nov 1996;103(11):1134-42. [Medline].
• Israel SL. Dysmennorhea as an abnormal manifestation of the menstrual cycle. In: Diagnosis and Treatment of Menstrual Disorders and Sterility. 5th ed. Hagerstown Md: Harper & Row;1967:132.
• Jamieson DJ, Steege JF. The prevalence of dysmenorrhea, dyspareunia, pelvic pain, and irritable bowel syndrome in primary care practices. Obstet Gynecol. Jan 1996;87(1):55-8. [Medline].
• Jamieson DJ, Steege JF. The association of sexual abuse with pelvic pain complaints in a primary care population. Am J Obstet Gynecol. Dec 1997;177(6):1408-12. [Medline].
• Klein JR, Litt IF. Epidemiology of adolescent dysmenorrhea. Pediatrics. Nov 1981;68(5):661-4. [Medline].
• Koltz MM. Dysmenorrhea, endometriosis and pelvic pain. In: Lemeke DP, Pattison J, Marshall LA, Cowley DS, eds. Primary Care of Women. Norwalk Conn: Appleton & Lange;1992:420-32.
• Lancet authors. Primary dysmenorrhoea. Lancet. Apr 12 1980;1(8172):800-1. [Medline].
• Lumsden MA. Dysmenorrhea. In: Baird DT, Michie EA, eds. Mechanism of Menstrual Bleeding. New York: Raven Press;1985:196-210.
• Milsom I, Andersch B. Effect of various oral contraceptive combinations on dysmenorrhea. Gynecol Obstet Invest. 1984;17(6):284-92. [Medline].
• Milsom I, Andersch B. Effect of ibuprofen, naproxen sodium and paracetamol on intrauterine pressure and menstrual pain in dysmenorrhoea. Br J Obstet Gynaecol. Nov 1984;91(11):1129-35. [Medline].
• Morrison BW, Daniels SE, Kotey P, et al. Rofecoxib, a specific cyclooxygenase-2 inhibitor, in primary dysmenorrhea: a randomized controlled trial. Obstet Gynecol. Oct 1999;94(4):504-8. [Medline].
• Nigam S, Benedetto C, Zonca M, et al. Increased concentrations of eicosanoids and platelet-activating factor in menstrual blood from women with primary dysmenorrhea. Eicosanoids. 1991;4(3):137-41. [Medline].
• Parazzini F, Tozzi L, Mezzopane R, et al. Cigarette smoking, alcohol consumption, and risk of primary dysmenorrhea. Epidemiology. Jul 1994;5(4):469-72. [Medline].
• Propst AM, Storti K, Barbieri RL. Lateral cervical displacement is associated with endometriosis. Fertil Steril. Sep 1998;70(3):568-70. [Medline].
• Rosenwaks Z, Seegar-Jones G. Menstrual pain: its origin and pathogenesis. J Reprod Med. Oct 1980;25(4 Suppl):207-12. [Medline].
• Simpson JL, Elias S, Malinak LR, Buttram VC Jr. Heritable aspects of endometriosis. I. Genetic studies. Am J Obstet Gynecol. Jun 1 1980;137(3):327-31. [Medline].
• Smith RP. Cyclic pelvic pain and dysmenorrhea. Obstet Gynecol Clin North Am. Dec 1993;20(4):753-64. [Medline].
• Smith RP. Gynecology in Primary Care. Baltimore: Williams & Wilkins;1997:389-404.
• Sobczyk R, Braunstein ML, Solberg L, Schuman SH. A case control survey and dysmenorrhea in a family practice population: a proposed disability index. J Fam Pract. Aug 1978;7(2):285-90. [Medline].
• Sundell G, Milsom I, Andersch B. Factors influencing the prevalence and severity of dysmenorrhoea in young women. Br J Obstet Gynaecol. Jul 1990;97(7):588-94. [Medline].
• Svennerud S. Dysmenorrhea and absenteeism. Acta Obstet Gynecol Scand. 1959;38(suppl 2):1.
• Willman EA, Collins WP, Clayton SG. Studies in the involvement of prostaglandins in uterine symptomatology and pathology. Br J Obstet Gynaecol. May 1976;83(5):337-41. [Medline].
• Ylikorkala O, Dawood MY. New concepts in dysmenorrhea. Am J Obstet Gynecol. Apr 1 1978;130(7):833-47. [Medline].
• Ylikorkala O, Kauppila A, Puolakka J. Naproxen suppositories in primary dysmenorrhoea. Lancet. Feb 3 1979;1(8110):278. [Medline].
• Zhang WY, Li Wan Po A. Efficacy of minor analgesics in primary dysmenorrhoea: a systematic review. Br J Obstet Gynaecol. Jul 1998;105(7):780-9. [Medline].

Article Last Updated: Jun 13, 2006