eMedicine Specialties > Emergency Medicine > Obstetrics & Gynecology
Dysmenorrhea
Updated: Dec 31, 2009
Introduction
Background
Dysmenorrhea refers to the syndrome of painful menstruation. Its prevalence is estimated at 25% of women and up to 90% of adolescents.1 No significant difference exists in prevalence or incidence between races, though the most common causes of dysmenorrhea differ by age (see History). Although it is not life-threatening, dysmenorrhea can be debilitating and psychologically taxing for many women. Some choose to self-medicate at home and never seek medical attention for their pain. Dysmenorrhea is responsible for significant absenteeism from work, and it is the most common reason for school absence among adolescents.1
Dysmenorrhea can be divided into 2 broad categories: primary and secondary. Primary dysmenorrhea occurs in the absence of pelvic pathology, whereas secondary dysmenorrhea results from identifiable organic diseases.
Pathophysiology
Historical attitudes toward menstrual pain were often dismissive. Pain was often attributed to women's emotional or psychological states and misconceptions about sex and sexual behaviors. Research has now established concrete physiologic explanations for dysmenorrhea, which discredit these prior theories.1,2
Primary dysmenorrhea usually begins within the first 6 months after menarche once a regular ovulatory cycle has been established. During menstruation, sloughing endometrial cells release prostaglandins, which cause uterine ischemia through myometrial contraction and vasoconstriction. Elevated levels of prostaglandins have been measured in the menstrual fluid of women with severe dysmenorrhea. These levels are especially high during the first 2 days of menstruation. Vasopressin may also play a similar role.1,3
Secondary dysmenorrhea may present at any time after menarche, but it most commonly arises when a woman is in her 20s or 30s, after years of normal, relatively painless cycles. Elevated prostaglandins may also play a role in secondary dysmenorrhea, but, by definition, concomitant pelvic pathology must also be present. Common causes include endometriosis, leiomyomata (fibroids), adenomyosis, pelvic inflammatory disease, and intrauterine device (IUD) use.
Note that, though the hormonal link to dysmenorrhea may partially explain its pathophysiology, hormones do not explain the total story. There is a very complex interplay between these hormones, basal body temperature, sleep patterns, and the central nervous system, the extent of which is not completely understood.1
Frequency
United States
Its prevalence is estimated at 25% of women and up to 90% of adolescents.1
Mortality/Morbidity
Dysmenorrhea itself is not life threatening, but it can have a profoundly negative impact on a woman's day-to-day life. In addition to missing work or school, she may be unable to participate in sports or other activities, compounding the emotional distress brought on by the pain.
Race
No significant difference exists in prevalence or incidence between races.
Age
The most common causes of dysmenorrhea differ by age (see History).
Clinical
History
Primary dysmenorrhea may be distinguished from secondary dysmenorrhea by means of a thorough history. Pertinent information includes not only character and onset of pain but also history of similar pain, associated symptoms (eg, dyspareunia), age at menarche, abnormal vaginal bleeding or discharge, obstetric and contraceptive history, and HIV status.4 A family history should be sought for bleeding diatheses or sickle cell disease. Some differentiating factors of primary and secondary dysmenorrhea are listed below:
- Primary dysmenorrhea
- Onset within 6 months after menarche
- Lower abdominal/pelvic pain begins with onset of menses and lasts 8-72 hours
- Low back pain
- Medial/anterior thigh pain
- Headache
- Diarrhea
- Nausea/vomiting
- Secondary dysmenorrhea
- Onset in 20s or 30s, after relatively painless menstrual cycles in the past
- Infertility
- Heavy menstrual flow or irregular bleeding
- Dyspareunia
- Vaginal discharge
- Pain may not be relieved by nonsteroidal anti-inflammatory drugs (NSAIDs)
Physical
A complete physical examination should be performed. For younger adolescents who have never been sexually active, a careful abdominal examination is appropriate. In older adolescents or those known to be sexually active, a pelvic examination is crucial. This examination includes inspection of the external genitalia for rashes, swelling, or discoloration; the vaginal vault for discharge, blood, or foreign bodies; the cervix for the above, plus any masses or signs of infection; and a bimanual examination to assess cervical motion tenderness, uterine or adnexal tenderness, or any masses in the pelvis.4 Pelvic ultrasonography should be considered in women who are suspected of having secondary dysmenorrhea. Attention should also be paid to the abdominal examination and back/flank examinations to rule out pelvic pain as a presentation of gastrointestinal (GI) and upper genitourinary (GU) pathology, respectively.
- Primary dysmenorrhea
- May have lower abdominal tenderness
- May have uterine tenderness or normal pelvic examination findings
- Cervical stenosis may contribute to retrograde flow.
- Secondary dysmenorrhea
- Palpable uterine mass or masses
- Cervical motion tenderness
- Adnexal tenderness or palpable mass or masses
- Vaginal or cervical discharge
- Visible vaginal pathology (mucosal tears, masses, prolapse)
- Normal abdominal and pelvic examinations do not rule out pathology. Ultrasonography or other imaging modalities may be warranted if suspicion of secondary dysmenorrhea is high.
Causes
Risk factors for dysmenorrhea
- Primary dysmenorrhea
- Early age at menarche (<12 y)
- Nulliparity
- Heavy or prolonged menstrual flow
- Smoking
- Positive family history
- Obesity
- Secondary dysmenorrhea
- Leiomyomata (fibroids)
- Pelvic inflammatory disease
- Tubo-ovarian abscess
- Ovarian torsion
- Ovarian cysts
- Endometriosis
- Adenomyosis
- Intrauterine device
Causes of secondary dysmenorrhea
This section provides brief synopses on the more common causes of secondary dysmenorrhea.
Uterine leiomyoma
Uterine leiomyoma are benign tumors of the uterine musculature. They are up to 9 times more common in black women than white women.5 It is a common cause of dysmenorrhea as they enlarge when stimulated by estrogen. In addition to pain with menses, patients may also present with menorrhagia, abdominal distension, or pressure. Pelvic examination may reveal a uterine mass or irregularity. Ultrasonography is often used for determining size and location of fibroids, though CT scan is used if ultrasound information is limited.4,6 Unless patients are symptomatic from profound anemia, these patients can be safely discharged with appropriate gynecologic follow up. Potential complications are anemia and infertility.7
Pelvic inflammatory disease
Pelvic inflammatory disease (PID) is an infection of the uterus, fallopian tubes, with or without ovarian or parametrial involvement. It is an ascending infection that develops during or immediately after menses, and if chronic, can lead to dysmenorrhea. The most common infectious organisms are Chlamydia trachomatis and Neisseria gonorrhoeae, although it can be caused by other organisms, such as Gardnerella vaginalis, anaerobes, and gram-negative rods.4
Previously, the diagnosis, while primarily clinical, was based on having 3 major criteria (abdominal pain, adnexal pain, and cervical motion tenderness), and 1 minor criterion (fever, vaginal discharge, leukocytosis, positive cervical cultures, gram-negative stain, intracellular diplococci, or white cells on vaginal smear).4
More recent data from the Pelvic Inflammatory Disease Evaluation and Clinical Health (PEACH) trial shows that the presence of adnexal tenderness has a sensitivity of 95.5% for histologic endometritis. This trial supports the empiric treatment of all women at risk for pelvic inflammatory disease with adnexal tenderness and no other obvious cause. Based on data from the PEACH trial, the Centers for Disease and Control and Prevention (CDC) recommends that all women at risk for pelvic inflammatory disease and who exhibit adnexal, uterine, or pelvic tenderness on bimanual examination, and no other explanation for these findings, be treated empirically for pelvic inflammatory disease.8
In addition to appropriate analgesia (see Treatment below) patients need to be treated with appropriate antibiotic coverage; the most commonly used regimen is ceftriaxone 250 mg IM and doxycycline 100 mg per day for 14 days.4 Patients should be hospitalized if they outpatient therapy fails, if they have intractable nausea or vomiting, if they have a complicating tubo-ovarian abscess, or if they are immunocompromised.4 Complications include tubo-ovarian abscess and Fitz-Hugh Curtis syndrome (perihepatitis) if pus from the fallopian tubes leaks into the peritoneum.
Tubo-ovarian abscess
Tubo-ovarian abscess is a loculated infection within the fallopian tubes and/or ovaries, and is usually sequela of pelvic inflammatory disease. It is often polymicrobial. Patients present most commonly with fever and gradually worsening pelvic pain and tenderness, although nausea, vomiting, and vaginal bleeding or discharge may be present as well. Examination may elicit tenderness upon cervical motion and in the adnexal area. Pelvic mass may be present, although this is often difficult to palpate.4 Tubo-ovarian abscesses can be detected on pelvic sonogram or abdominal CT scan as a complex cystic structure in the pelvis, with or without loculations.6
Patients are often admitted for intravenous antibiotics that cover Neisseria gonorrhoeae, Chlamydia, anaerobes, and gram-negative organisms. If medical therapy fails or if peritoneal signs are found on examination, then surgical drainage is indicated.4 Infertility is almost always a complication of tubo-ovarian abscess.4 The most feared complication is rupture, which can lead to septic shock and death; it is a true surgical emergency if this occurs.7
Ovarian torsion
Ovarian torsion involves twisting of the adnexal structures, leading to ischemia and ultimately necrosis if the process is not reversed in time. In a nonpregnant woman, it is almost always caused by an abnormality in the ovary such as a cyst or a tumor. Torsion can occur in pregnancy without a requisite adnexal abnormality, and, in one large series, 20% of the patients found to have torsion were pregnant.9
Patients often present with severe, intermittent, colicky, unilateral pelvic or lower abdominal pain, associated with nausea and vomiting. The diagnosis is often delayed because it can resemble other disease entities, such as appendicitis or renal colic.4,7 Because of these differential diagnoses, CT scan is often performed before any other imaging modality. It is important to be familiar with the CT findings for torsion6 : an ovarian enlargement of >5 cm with a corkscrew appearance of the ipsilateral fallopian tube.6 Sonogram will usually show a large ovarian mass or cyst, but ultrasonographic evidence of torsion is difficult to obtain because the appearance changes depending on the length of time elapsed.7
If suspicion for ovarian torsion is high, gynecologic consultation should be obtained early because laparoscopy is not only diagnostic but also therapeutic and potentially fertility-saving.7 These patients are all admitted.
Ovarian cyst rupture/hemorrhage
A hemorrhagic ovarian cyst comes from an ovarian follicle in the absence of ovulation; thus, they are exclusively found in menstruating females. They often present with acute onset of pelvic or abdominal pain, along with nausea and vomiting. Examination may reveal an adnexal mass, but almost all patients with ruptured ovarian cysts have some level of adnexal tenderness. Patients may have signs of peritoneal irritation as well. Although CT scan and ultrasonography can be used to visualize hemoperitoneum and the cyst,6 laparoscopy is needed for the definitive diagnosis.4
Endometriosis
Endometriosis is the presence of endometrial-like tissue found outside of the uterus, most commonly in the ovaries. Women often present with dyspareunia and pelvic and back pain. Although endometriosis is a diagnosis of exclusion, patients may give a history of dysmenorrhea in the past that is cyclic with menses.4 However, it is important to note that this disease can exist concomitantly with other disease processes causing dysmenorrhea, making the diagnosis even more difficult.10 The history may also include chronic pelvic pain unresponsive to antibiotics or analgesics. A good obstetric history may also elicit frequent miscarriages or difficulty conceiving.4,10 The classic examination finding is a fixed uterus with “ash” spots (purple-blue discolorations) on the cervix, though this if not always present.4
Although CT scanning may hold some promise as a diagnostic tool in the future,6 laparoscopy or laparotomy are still the only means by which endometriosis can be definitively diagnosed. There is controversy as to whether definitive diagnosis is even necessary.10 Many times, the assumption is that the endometriosis, if found, is the cause of patient discomfort when it may not be. Conversely, if endometriosis is the cause of dysmenorrhea, surgery may not be necessary if pain is controlled with hormonal therapy, analgesia, or both.10 The main complication of endometriosis is rupture of an endometrioma.
Adenomyosis
Adenomyosis is defined as an invasion of myometrium by uterine adrenal glands. It is a rare disease and can resemble uterine leiomyomas and endometrial carcinoma in its presentation; thus, it is difficult to diagnosis. Definitive diagnosis is by transvaginal ultrasonography or MRI. When the latter is used, one is looking for a thickened junctional zone (JZ line), or the border between myometrium and endometrium. One paper showed that adenomyosis should be in the differential diagnosis when a patient is treated for presumptive endometriosis and has chronic persistent pain.11
Intrauterine device
Intrauterine devices (IUDs) may cause bladder or uterine perforation. The sooner a patient has a uterine rupture from the time of IUD placement, the more likely they can present with peritoneal signs.4 Patients with bladder perforation may have recurrent cystitis unresponsive to antibiotics. It is very important to remove the IUD immediately to prevent further damage to the uterine or bladder walls. Abdominal radiographs may reveal the location of an IUD if the string is not seen in the vaginal vault. A gynecologist should be consulted early.4
Premenstrual dysmorphic disorder (formerly premenstrual syndrome)
In addition to dysmenorrhea, patients may also have bloating, body aches, migraine headaches, breast tenderness, and emotional complaints. The effects of these symptoms in rare instances can be debilitating. Besides possible vaginal brownish discharge or bleeding, the pelvic examination findings will be normal. It is the emergency physician's responsibility to ensure adequate analgesia and appropriate follow up with a gynecologist. See Premenstrual Dysphoric Disorder for additional information.
More on Dysmenorrhea |
Overview: Dysmenorrhea |
| Differential Diagnoses & Workup: Dysmenorrhea |
| Treatment & Medication: Dysmenorrhea |
| Follow-up: Dysmenorrhea |
| References |
| Next Page » |
References
Durain D. Primary dysmenorrhea: assessment and management update. J Midwifery Womens Health. Nov-Dec 2004;49(6):520-8. [Medline].
Proctor ML, Murphy PA, Pattison HM, Suckling J, Farquhar CM. Behavioural interventions for primary and secondary dysmenorrhoea. Cochrane Database Syst Rev. Jul 18 2007;CD002248. [Medline].
French L. Dysmenorrhea. Am Fam Physician. Jan 15 2005;71(2):285-91. [Medline].
Baines PA, Allen GM. Pelvic pain and menstrual related illnesses. Emerg Med Clin North Am. Aug 2001;19(3):763-80. [Medline].
Proctor M, Farquhar C. Diagnosis and management of dysmenorrhoea. BMJ. May 13 2006;332(7550):1134-8. [Medline].
Kalish GM, Patel MD, Gunn ML, Dubinsky TJ. Computed tomographic and magnetic resonance features of gynecologic abnormalities in women presenting with acute or chronic abdominal pain. Ultrasound Q. Sep 2007;23(3):167-75. [Medline].
Kamaya A, Shin L, Chen B, Desser TS. Emergency gynecologic imaging. Semin Ultrasound CT MR. Oct 2008;29(5):353-68. [Medline].
Walker CK, Wiesenfeld HC. Antibiotic therapy for acute pelvic inflammatory disease: the 2006 Centers for Disease Control and Prevention sexually transmitted diseases treatment guidelines. Clin Infect Dis. Apr 1 2007;44 Suppl 3:S111-22. [Medline].
Houry D, Abbott JT. Ovarian torsion: a fifteen-year review. Ann Emerg Med. Aug 2001;38(2):156-9. [Medline].
Levy BS, Apgar BS, Surrey ES, Wysocki S. Diagnosis and management: chronic pelvic pain and endometriosis. OBG Management. 2007/03;supp:S3-S13.
Parker JD, Leondires M, Sinaii N, Premkumar A, Nieman LK, Stratton P. Persistence of dysmenorrhea and nonmenstrual pain after optimal endometriosis surgery may indicate adenomyosis. Fertil Steril. Sep 2006;86(3):711-5. [Medline].
Wong CL, Farquhar C, Roberts H, Proctor M. Oral contraceptive pill as treatment for primary dysmenorrhoea. Cochrane Database Syst Rev. Apr 15 2009;CD002120. [Medline].
Ziaei S, Zakeri M, Kazemnejad A. A randomised controlled trial of vitamin E in the treatment of primary dysmenorrhoea. BJOG. Apr 2005;112(4):466-9. [Medline].
Latthe P, Mignini L, Gray R, Hills R, Khan K. Factors predisposing women to chronic pelvic pain: systematic review. BMJ. Apr 1 2006;332(7544):749-55. [Medline].
[Best Evidence] Witt CM, Reinhold T, Brinkhaus B, Roll S, Jena S, Willich SN. Acupuncture in patients with dysmenorrhea: a randomized study on clinical effectiveness and cost-effectiveness in usual care. Am J Obstet Gynecol. Feb 2008;198(2):166.e1-8. [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].
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].
Further Reading
Keywords
dysmenorrhea, dysmenorrhea symptoms, dysmenorrhea causes, dysmenorrhea treatment, primary dysmenorrhea, secondary dysmenorrhea, menstrual pain, painful periods, menorrhalgia, pelvic pain, menstrual cramps, endometriosis, uterine fibroids, uterine adenomyosis, chronic pelvic inflammatory disease, leiomyomata, adenomyosis, endometrial polyps
Overview: Dysmenorrhea