Dysmenorrhea refers to the symptom of painful menstruation. It can be divided into 2 broad categories: primary (occurring in the absence of pelvic pathology) and secondary (resulting from identifiable organic diseases).
A complete history should include the following:
Clinical features of primary dysmenorrhea include the following:
The following may indicate secondary dysmenorrhea[1, 2, 3] :
A complete physical examination should be performed. A pelvic examination is crucial for excluding uterine irregularities, cul-de-sac tenderness, or suggestive nodularities and includes the following:
See Presentation for more detail.
No tests are specific to the diagnosis of primary dysmenorrhea. The following laboratory studies may be performed to identify or exclude organic causes of secondary dysmenorrhea:
If pelvic pathology is suspected, the following imaging studies may be considered:
Other more invasive studies that may be considered are as follows:
See Workup for more detail.
Pharmacotherapy is the most reliable and effective treatment for relieving dysmenorrhea. Treatment of secondary dysmenorrhea involves correction of the underlying organic cause.
NSAIDs specifically approved by the FDA for treatment of dysmenorrhea are as follows:
Other NSAIDs and analgesics that have been used include the following:
Although not approved by the FDA for treating dysmenorrhea, the following OCs are also used:
Preventive measures for outpatient management of dysmenorrhea include the following:
See Treatment and Medication for more detail.
Dysmenorrhea is defined as difficult menstrual flow or painful menstruation. It is one of the most common gynecologic complaints in young women who present to clinicians.[4] Optimal management of this symptom depends on an understanding of the underlying cause. Dysmenorrhea can be divided into 2 broad categories: primary (spasmodic) and secondary (congestive).[5]
Primary dysmenorrhea is defined as menstrual pain that is not associated with macroscopic pelvic pathology (ie, occurs in the absence of pelvic disease). It typically occurs in the first few years after menarche[6] and affects as many as 50% of postpubertal females.[7] Secondary dysmenorrhea is defined as menstrual pain resulting from anatomic or macroscopic pelvic pathology,[6, 8] as is seen in women with endometriosis or chronic pelvic inflammatory disease. It is most often observed in women aged 30-45 years.
The following risk factors are associated with more severe episodes of dysmenorrhea[9] :
Some (not all) studies have found obesity and alcohol consumption to be associated with dysmenorrhea.[10, 11, 12] Physical activity and the duration of the menstrual cycle do not appear to be associated with increased menstrual pain.[10]
Although dysmenorrhea is not life-threatening, it 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.[13]
The 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. 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. (See Presentation.)
No tests are specific to the diagnosis of primary dysmenorrhea. Studies that may be indicated to elucidate the cause of secondary dysmenorrhea include laboratory tests, abdominal or transvaginal ultrasonography, hysterosalpingography, hysteroscopy, or laparoscopy. (See Workup.)
Treatment of dysmenorrhea is aimed at providing symptomatic relief as well as inhibiting the underlying processes that cause symptoms. Grading dysmenorrhea according to the severity of pain and the degree of limitation of daily activity may help guide the treatment strategy. Medications used may include NSAIDs and opioid analgesics, as well as oral contraceptives (OCs). In addition to pain relief, mainstays of treatment include reassurance and education. Other therapies have been proposed, but most are not well studied. (See Treatment.)
Historical attitudes toward menstrual pain were often dismissive. Pain was often attributed to women’s emotional or psychological states or to misconceptions about sex and sexual behaviors. Although the etiology and pathophysiology of dysmenorrhea have not been fully elucidated, research has led to data supporting concrete physiologic explanations for dysmenorrhea, which discredit these prior dismissive theories.[13, 14, 15]
Current evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin F2α (PGF2α), a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium.[16] 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.[17] A 3-fold increase in endometrial prostaglandins occurs from the follicular phase to the luteal phase, with a further increase occurring during menstruation.[18] The increase in prostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increased myometrial tone and excessive uterine contraction.[8]
Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. Substantial amounts of leukotrienes have been demonstrated in the endometria of women with primary dysmenorrhea that does not respond to treatment with prostaglandin antagonists.[11, 19, 20, 21, 22]
The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced uterine blood flow, and pain in primary dysmenorrhea.[23, 24, 13, 25] Vasopressin’s role in the endometrium may be related to prostaglandin synthesis and release.
In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea. Type C pain neurons are stimulated by the anaerobic metabolites generated by an ischemic endometrium. Women with dysmenorrhea appear to have enhanced pain sensitivity compared to women without dysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain.[15] This enhanced pain sensitivity may increase the risk of affected women to other chronic conditions (eg, fibromyalgia) as well as negatively impact their quality of life.[15]
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.
In primary dysmenorrhea, there is a highly complex interplay between hormones and mediators, basal body temperature, sleep patterns, and the central nervous system (CNS), the extent of which is not completely understood.[13]
A study by Liu et al found that patients with primary dysmenorrhea had significantly increased cortical thickness and decreased subcortical volumes.[26]
Elevated prostaglandins may also play a role in secondary dysmenorrhea, but by definition, concomitant pelvic pathology must be present. A number of factors may be involved in the pathogenesis of secondary dysmenorrhea, including the following:
Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.[1]
Risk factors for primary dysmenorrhea include the following:
Risk factors for secondary dysmenorrhea include the following :
In the following sections, the more common causes of secondary dysmenorrhea are briefly summarized.
Uterine leiomyomata are benign tumors of the uterine musculature that are a common cause of dysmenorrhea because they enlarge when stimulated by estrogen. They are up to 9 times more common in black women than in white women.[27]
In addition to pain with menses, patients may present with menorrhagia, abdominal distention, or pressure. Pelvic examination may reveal a uterine mass or irregularity. Ultrasonography is often used for determining size and location of fibroids, though computed tomography (CT) is used if ultrasonographic information is limited.[28, 29] Unless patients are symptomatic from profound anemia, these patients can be safely discharged with appropriate gynecologic follow-up. Potential complications are anemia and infertility.[30]
PID is an infection of the uterus and fallopian tubes, with or without ovarian or parametrial involvement. It is an ascending infection that develops during or immediately after menses; if chronic, it can lead to dysmenorrhea. The most common causative pathogens are Chlamydia trachomatis and Neisseria gonorrhoeae, though PID also can be caused by other organisms, such as Gardnerella vaginalis, anaerobes, and gram-negative rods.[28]
Previously, the diagnosis of PID, though primarily clinical, was based on the presence of 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 blood cells [WBCs] on vaginal smear).[28]
Data from the PEACH (Pelvic inflammatory disease Evaluation And Clinical Health) trial shows that the presence of adnexal tenderness has a sensitivity of 95.5% for histologic endometritis. The findings of this trial support empiric treatment of all women at risk for PID with adnexal tenderness and no other obvious cause.
On the basis of data from the PEACH trial, the Centers for Disease and Control and Prevention (CDC) recommends that all women who are at risk for PID and who exhibit adnexal, uterine, or pelvic tenderness on bimanual examination in the absence of any other explanation for these findings be treated empirically for PID.[31]
In addition to appropriate analgesia, patients require appropriate antibiotic coverage. The most commonly used regimen consists of ceftriaxone 250 mg IM and doxycycline 100 mg daily for 14 days.[28] Patients should be hospitalized if outpatient therapy fails, if they have intractable nausea or vomiting, if they have a complicating tubo-ovarian abscess, or if they are immunocompromised.[28] Complications include tubo-ovarian abscess and Fitz-Hugh Curtis syndrome (perihepatitis) if pus from the fallopian tubes leaks into the peritoneum.
Tubo-ovarian abscess is a loculated infection within the fallopian tubes or ovaries, usually occurring as a sequela of PID. It is often polymicrobial.
Most commonly, patients present with fever and gradually worsening pelvic pain and tenderness; nausea, vomiting, and vaginal bleeding or discharge may be present as well. Examination may elicit tenderness on cervical motion and in the adnexal area. A pelvic mass may be present, though it is often difficult to palpate.[28] Tubo-ovarian abscesses can be detected on pelvic ultrasonography or abdominal CT as a complex cystic structure in the pelvis, with or without loculations.[29]
Patients are often admitted for intravenous (IV) antibiotic therapy covering Neisseria gonorrhoeae, Chlamydia, anaerobes, and gram-negative organisms. If medical therapy fails or if peritoneal signs are found on examination, surgical drainage is indicated.[28] Infertility is almost always a complication of tubo-ovarian abscess.[28] The most feared complication, however, is rupture, which can lead to septic shock and death; this is a true surgical emergency.[30]
Ovarian torsion involves twisting of the adnexal structures, which leads 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.[32]
Patients often present with severe, intermittent, colicky, unilateral pelvic or lower abdominal pain, frequently associated with nausea and vomiting. The diagnosis is often delayed because the presentation of ovarian torsion can resemble those of other disease entities, such as appendicitis or renal colic.[28, 30]
Because of these resemblances and the consequent potential for diagnostic uncertainty, CT is often performed before any other imaging modality. It is important to be familiar with the typical CT findings for torsion: ovarian enlargement exceeding 5 cm with a corkscrew appearance of the ipsilateral fallopian tube.[29] A 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.[30]
If there is a high level of suspicion for ovarian torsion, a gynecologic consultation should be obtained early. Laparoscopy is not only diagnostic but also therapeutic and potentially fertility-saving.[30] These patients are all admitted.
A hemorrhagic ovarian cyst comes from an ovarian follicle in the absence of ovulation; consequently, these cysts are exclusively found in menstruating females.
Patients often present with the 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. Signs of peritoneal irritation may be apparent as well. Although CT and ultrasonography can be used to visualize hemoperitoneum and the cyst,[29] laparoscopy is required for the definitive diagnosis.[28]
Endometriosis is the presence of endometriumlike 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 that was cyclic with menses.[28] It is important to note, however, that endometriosis can exist concomitantly with other disease processes causing dysmenorrhea; this makes the diagnosis even more difficult.[33]
The history may also include chronic pelvic pain unresponsive to antibiotics or analgesics. In addition, a good obstetric history may elicit frequent miscarriages or difficulty conceiving.[28, 33] The classic examination finding is a fixed uterus with “ash” spots (purple-blue discolorations) on the cervix, though this finding is not always present.[28]
In the future, CT may hold some promise as a diagnostic tool,[29] but at present, endometriosis can be definitively diagnosed only via laparoscopy or laparotomy. Some argue that definitive diagnosis may not even be necessary.[33] Often, endometriosis, if found, is assumed to be the cause of discomfort when it may not be. Even if endometriosis is the cause of dysmenorrhea, surgery may not be necessary if pain is controlled with hormonal therapy or analgesia.[33] The main complication of endometriosis is rupture of an endometrioma.
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; accordingly, diagnosis is difficult.
Definitive diagnosis is typically accomplished by means of transvaginal ultrasonography or magnetic resonance imaging (MRI). When the latter is used, the key finding is a thickened junctional zone (JZ line)—that is, 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.[34]
IUCDs (IUDs) may cause bladder or uterine perforation. The sooner a patient has a uterine perforation after IUCD placement, the more likely it is that she will present with peritoneal signs.[28] Patients with bladder perforation may have recurrent cystitis that is unresponsive to antibiotics. The IUCD must be removed immediately to prevent further damage to the uterine or bladder walls. Abdominal radiographs may reveal the location of an IUCD if the string is not seen in the vaginal vault. A gynecologist should be consulted early.[28]
Besides dysmenorrhea, patients with premenstrual dysphoric disorder (formerly premenstrual syndrome) may have bloating, body aches, migraine headaches, breast tenderness, and emotional complaints. The effects of these symptoms are occasionally debilitating. Aside from possible vaginal brownish discharge or bleeding, pelvic examination findings are normal. It is the emergency physician’s responsibility to ensure adequate analgesia and appropriate follow-up with a gynecologist.
Dysmenorrhea may affect more than 50% of menstruating women, and its reported prevalence has been highly variable (eg, 45-95%[15] ). A survey of 113 patients in a family practice setting showed a prevalence of 29-44%,[35] but figures as high as 90% in women aged 18-45 years have been reported.[4] The use of oral contraceptives (OCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), both of which are effective in ameliorating symptoms of primary dysmenorrhea, may hinder accurate assessment of prevalence.
Primary dysmenorrhea peaks in late adolescence and the early 20s.[36] The incidence falls with increasing age and with increasing parity. In many studies,[10, 37, 38] though not all,[4] the reported prevalence and severity of dysmenorrhea in parous women are substantially lower. An epidemiologic study found no significant differences in prevalence and severity of dysmenorrhea between nulligravid women and those in whom pregnancy had been terminated by either spontaneous or induced abortion.[10]
In an epidemiologic study of an adolescent population (age range, 12-17 years), Klein and Litt reported that dysmenorrhea had a prevalence of 59.7%.[39] 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 were (12.3%), even after socioeconomic status was adjusted for.
The prevalence of dysmenorrhea worldwide is similar to that in the United States. Reported prevalences have ranged from 15.8% to 89.5%, with higher rates reported in adolescent populations.[40, 41, 42, 10, 43, 37, 44, 45]
A study of 408 young Italian women found that the prevalence of dysmenorrhea was 84.1% when only menstrual pain was considered, 55.2% when menstrual pain was associated with a need for medication, 31.9% when menstrual pain was associated with absenteeism, and 25.3% when menstrual pain was associated with both a need for medication and absenteeism.[46]
In a longitudinal population study of 9,067 Australian women, researchers found that those who began smoking by age 13 had the greatest risk of developing chronic dysmenorrhea. Overall, approximately 60% of the women reported experiencing dysmenorrhea symptoms at some time during the study period.[47, 48]
The prevalence of period pain was higher among current smokers (29%) than nonsmokers (23%). Compared with never-smokers, ex-smokers had a 33% increased risk of chronic symptoms (odds ratio, 1.33; 95% confidence interval, 1.05 - 1.68), while current smokers had a 41% increased risk (odds ratio, 1.41; 95% CI, 1.17 - 1.70). After adjustment for socioeconomic status, lifestyle, and reproductive factors, women who began smoking before or by age 13 had a 59% increased risk (odds ratio, 1.59; 95% CI, 1.18 – 2.15), those who began at ages 14-15 had a 50% increased risk (1.50; 95% CI 1.18 to 1.90), and those who began at age 16 or older had a 26% increased risk (1.26; 95% CI 1.03 to 1.55).[47, 48]
In a cross-sectional study of 311 female Iranian undergraduate students (aged 18-27 y), the prevalence of primary dysmenorrhea was 89.1%.[49] Factors that were significantly associated with higher dysmenorrhea pain intensity included younger age as well as familial factors (eg, low maternal formal education, family history of dysmenorrhea), social factors (living at home), and menstruation factors (eg, higher menstrual bleeding severity and shorter menstrual intervals).[49]
The most common causes of dysmenorrhea differ by age. The prevalence of this condition is estimated to be 25% among adult women and as high as 90% among adolescents.
No data suggest that race affects the incidence of dysmenorrhea.
With the use of NSAIDs, the prognosis for primary dysmenorrhea is excellent. The prognosis for secondary dysmenorrhea varies, depending on the underlying disease process. If a diagnosis of secondary dysmenorrhea is missed, the underlying pathology may lead to increased morbidity, including difficulty conceiving.[33]
Although dysmenorrhea itself is not life-threatening, it can have a profound negative impact on a woman’s day-to-day life. Besides missing work or school, she may be unable to participate in sports or other activities and thus experience additional emotional distress. Some 10% of dysmenorrheal women have severe pain that can be incapacitating. Dysmenorrhea is a public health problem associated with substantial economic loss related to work absences (an estimated 600 million work hours and 2 billion dollars in the United States).[50]
A cross sectional study that included 897 adolescent girls reported that those in the dysmenorrhea group had significantly higher depression, aggression, insomnia, daytime sleepiness and sleep apnea scores compared to the control and the premenstrual syndrome groups.[51]
The 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 assess the degree of disruption to school, work, and social activities.
Consider gravidity and parity status, previous pelvic infections, dyspareunia, infertility, and pelvic injuries or surgical or other procedures.
In addition, assess symptoms such as nausea, vomiting, bloating, diarrhea, and fatigue, which may be observed in patients with dysmenorrhea.
Consider the patient’s sexual history, including the choice of contraceptive methods. If oral contraceptives (OCs) have been used, establish their effect (if any) on relieving or exacerbating the condition. Moreover, discuss the use of other agents that affect dysmenorrhea pain.
A family history should be sought for bleeding diatheses or sickle cell disease. Such a history may be helpful in differentiating endometriosis from primary dysmenorrhea.[52]
The history should include questions pertaining to sexual abuse because this is reportedly associated with dysmenorrhea and chronic pelvic pain.[53]
In summary, a complete history should include the following[28] :
Primary dysmenorrhea should be distinguished from secondary dysmenorrhea on the basis of clinical features. Clinical features of primary dysmenorrhea include the following:
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.
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[1, 2] :
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 for excluding uterine irregularities, cul-de-sac tenderness, or suggestive nodularities. This examination includes the following[28] :
Women with primary dysmenorrhea usually have normal findings on pelvic examination. Lower abdominal or uterine tenderness may be present. Cervical stenosis may contribute to retrograde flow.
Women with secondary dysmenorrhea may have pelvic pathology, though normal findings do not exclude the condition. Women with endometriosis who present with secondary dysmenorrhea have physical findings about 40% of the time.[54, 55] A palpable uterine mass may be present. Cervical motion tenderness may be noted. There may be adnexal tenderness or a palpable mass. Vaginal or cervical discharge may be seen. Visible vaginal pathology (eg, mucosal tears, masses, or prolapse) may be visible.
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) pathology and upper genitourinary (GU) pathology, respectively.
No tests are specific to the diagnosis of primary dysmenorrhea. The diagnosis is made on the basis of clinical findings.
Laboratory studies may be indicated to elucidate the cause of secondary dysmenorrhea. Noninvasive studies may include abdominal and transvaginal ultrasonography. Other more invasive studies, including hysterosalpingography, may be required. Further investigation might include hysteroscopy or laparoscopy; the latter is usually indicated when initial interventions fail to relieve symptoms.
The following laboratory studies may be performed to identify or exclude organic causes of secondary dysmenorrhea:
Although these tests can be useful adjuncts in the workup of dysmenorrhea, they also may be misleading at times. For instance, the CBC may show a normal white blood cell (WBC) count in as many as 56% of patients with PID. On the other hand, the WBC count can be elevated as a consequence of physiologic stress.
In a patient with associated vaginal bleeding, the hematocrit may be normal even when the patient has obvious hypovolemia on examination (eg, positive orthostasis or tachycardia), especially if hemorrhage started within minutes to hours of presentation.[28] Moreover, the EIA and DNA probe tests for gonorrhea and chlamydia have varying sensitivities, ranging from 86% to 93%.[28]
Accordingly, for diagnosing dysmenorrhea and its underlying cause, laboratory testing should be understood to play an ancillary rather than a primary role and should not be allowed to replace a sound clinical basis for the diagnosis.
In cases of well-established primary dysmenorrhea, imaging studies are of little value. However, if pelvic pathology is suspected, abdominal and transvaginal ultrasonography are inexpensive and effective modalities.
Ultrasonography is relatively noninvasive, can easily be performed in the emergency department (ED), and reveals most relevant pelvic pathology. For instance, endometriosis may appear as a complex mass with a speckled appearance.[28] Pelvic ultrasonography is indicated for evaluating situations such as ectopic pregnancy, ovarian cysts, fibroids, and intrauterine contraceptive devices (IUCDs). It is highly sensitive for detecting pelvic masses.
Hysterosalpingography is used to exclude endometrial polyps, leiomyomas, and congenital abnormalities of the uterus. Intravenous pyelography is indicated if uterine malformation is confirmed as a cause or contributing factor for the dysmenorrhea.
Although computed tomography (CT) is not routinely ordered in the ED for patients with dysmenorrhea, it does have some utility, particularly in identifying ovarian torsion.[28, 30, 29] Magnetic resonance imaging (MRI) also is not routinely ordered in the ED but has some ability to detect adenomyosis and submucous myomas that might otherwise be missed by other imaging modalities.[28]
On occasion, other more invasive studies, including laparoscopy, hysteroscopy, and dilatation and curettage (D&C), 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 D&C may be indicated to evaluate intrauterine pathology found on imaging. An endometrial biopsy may be indicated if endometritis is considered likely.
Many women never seek medical attention for dysmenorrhea. Self-medication with analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) and direct application of heat are common effective strategies.
When a patient is seen in the emergency department (ED), evaluation should begin with the ABCs (A irway, B reathing, C irculation) and should consider serious diagnoses such as hemorrhagic shock and sepsis.
A patient whose history and clinical presentation clearly suggest primary dysmenorrhea may be treated symptomatically and provided with appropriate follow-up. A patient whose presentation is less clear or whose vital signs or physical findings are abnormal deserves a more thorough workup, including full laboratory studies, pelvic ultrasonography, and potentially an obstetrics/gynecology consultation.
Treatment of dysmenorrhea is aimed at providing symptomatic relief as well as inhibiting the underlying processes that cause symptoms. Grading dysmenorrhea according to the severity of pain and the degree of limitation of daily activity may help guide the treatment strategy. Medications used may include NSAIDs and opioid analgesics, as well as oral contraceptives (OCs). In addition to pain relief, mainstays of treatment include reassurance and education. Other therapies have been proposed, but most are not well studied.
In patients with refractory symptoms, a multidisciplinary approach may be indicated. Patients with pelvic pain do not routinely need consultation with a gynecologist in the ED, though they should be directed to follow up on an outpatient basis. Exceptions include certain infectious entities (eg, abscesses), as well as endometriosis.
Patients with both primary and secondary dysmenorrhea should be provided with appropriate gynecologic follow-up. If they do not have regular medical care, an appointment with a primary medical doctor is also indicated.
Treatment of primary dysmenorrhea is directed at providing relief from the cramping pelvic pain and associated symptoms (eg, headache, nausea, vomiting, flushing, and 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 by using agents that inhibit prostaglandin synthesis and possess 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. Lack of response to NSAIDs and OCs (or a combination thereof) may increase the likelihood of a secondary cause for dysmenorrhea.
Treatment of secondary dysmenorrhea involves correction of the underlying organic cause. Specific measures (medical or surgical) may be required to treat pelvic pathologic conditions (eg, endometriosis) and to ameliorate the associated dysmenorrhea. Periodic use of analgesic agents as adjunctive therapy may be beneficial.
NSAIDs are the most common treatment for both primary and secondary dysmenorrhea. They decrease menstrual pain by decreasing intrauterine pressure and lowering prostaglandin F2α (PGF2α) levels in menstrual fluid.[56, 57, 58] NSAIDs that inhibit type I prostaglandin synthetase and suppress production of cyclic endoperoxides (eg, fenamates, cyclooxygenase [COX]-2–selective agents, propionic acids, and indole acetic acids) alleviate symptoms by decreasing endometrial and menstrual fluid prostaglandin concentrations.
If taken early enough and in sufficient quantity, NSAIDs are extremely successful in alleviating menstrual pain. 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, or 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.
Whereas some NSAIDs (especially the fenamates) have been touted as being particularly effective for dysmenorrhea, scientific data to support such claims are sparse and generally weak.[59] Moreover, well-designed prospective comparative studies have not been performed. The NSAIDs specifically approved by the US Food and Drug Administration (FDA) for treatment of dysmenorrhea are as follows:
Aspirin may not be as effective as these NSAIDs, and acetaminophen may be a useful adjunct for alleviating only mild menstrual cramping pain.[59, 60]
NSAIDs that achieve peak serum concentrations within 30-60 minutes and have a faster onset of action (eg, ibuprofen, naproxen, and meclofenamate) may be preferred. However, individual patient response varies, and patients may need to try several agents before finding one that works. Some NSAIDs (eg, indomethacin) should be avoided, because they have a higher incidence of adverse effects.
COX-2 specific inhibitors have also proven effective in relieving menstrual pain. Their selectivity reduces the GI symptoms caused by inhibition of the COX-1 receptor. Despite some preliminary data suggesting efficacy in patients with primary dysmenorrhea, COX-2 inhibitors have not been demonstrably superior to conventional NSAIDs.[61]
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.[62]
In an emergency setting, patients who do not respond to NSAIDs may require treatment with narcotics for pain control. Patients whose symptoms are not relieved by NSAIDs are very likely to have an underlying pelvic condition (eg, endometriosis).
In a study comparing montelukast, a leukotriene-receptor antagonist, with placebo in patients with dysmenorrhea, montelukast was effective in reducing pain.[63] Clinicians may consider this agent as an alternative to hormonal therapy or in lieu of NSAIDs.
Simple analgesics, such as aspirin and acetaminophen, may also be useful, especially when NSAIDs are contraindicated.
OCs, which block monthly ovulation and may decrease menstrual flow, may also relieve symptoms. An update of a Cochrane review showed some evidence of symptomatic benefit in patients with primary dysmenorrhea, though no specific preparation showed superiority over any other.[64] In some patients, OCs can prevent dysmenorrhea altogether, even though these agents are not approved by the FDA for this indication.
OCs may be an appropriate choice for patients who do not wish to conceive. Combination OCs suppress the hypothalamic-pituitary-ovarian axis, thereby inhibiting ovulation and preventing prostaglandin production in the late luteal phase. This generally reduces the amount of menstrual flow and alleviates primary dysmenorrhea in most patients. Use of OCs in a manner that reduces the number of menstrual cycles may be beneficial for some patients.[65, 66]
Combination OCs, the levonorgestrel intrauterine device, and depot medroxyprogesterone acetate[67] provide effective pain relief and are associated with reduced menstrual flow. It may be necessary to add an NSAID to the OC, especially during the first few cycles after initiation of the OC. The ethinyl estradiol dose should generally be less than 50 µg; a monophasic OC containing 30 µg is a reasonable choice. To date, studies comparing the efficacy of various OC formulations in the management of dysmenorrhea have not been performed.
In a study of women with primary dysmenorrhea, Petraglia et al found that estradiol valerate plus dienogest and ethinyl estradiol plus levonorgestrel were comparably effective in relieving dysmenorrheic pain. Each of the treatments was taken orally by over 200 women daily for three 28-day cycles, with the number of days of pain and the degree of pain being evaluated. Based on the patients’ self-assessments, the investigators determined that pain was reduced by both treatments by approximately the same number of days (by 4.6 days for estradiol valerate plus dienogest, by 4.2 days for ethinyl estradiol plus levonorgestrel).[68]
Other therapies for dysmenorrhea have been proposed, but most are not well studied. A low-fat vegetarian diet[69, 27] [70] pyridoxine, magnesium, and vitamin E are examples.[25, 71]
In addition, acupuncture,[72, 73, 74, 75, 76] acupressure,[77, 75] aromatherapy,[87] various herbal medicines and dietary supplements,[78, 79] transdermal nitroglycerin, calcium-channel blockers, beta-adrenergic agonists, antileukotrienes, transcutaneous electrical nerve stimulation (TENS) units, and massage therapy and isometric exercise[80] have been suggested for therapeutic use in this setting. Topical application of continuous low-level heat may be beneficial for some patients.[81, 82] Interruption of nerve pathways has been performed, but data are limited.[83, 84, 85]
Various measures have been used to manage dysmenorrhea in the outpatient setting, including the following:
A Cochrane review of 5 randomized controlled trials showed that certain behavioral interventions may be effective at treating primary and secondary dysmenorrhea.[14]
Treatment of primary dysmenorrhea is directed at providing relief from the cramping pelvic pain and associated symptoms that typically accompany or immediately precede the onset of menstrual flow. To date, pharmacotherapy has been the most reliable and effective treatment for relieving dysmenorrhea. Nonsteroidal anti-inflammatory drugs (NSAIDs) and combination oral contraceptives (OCs) are the most commonly used therapeutic modalities for the management of primary dysmenorrhea.
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.
Clinical Context: Naproxen is available in both prescription and nonprescription doses. It inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis. The daily cost is approximately $3.00, compared with $0.14 for generic ibuprofen.
Clinical Context: Ibuprofen is available in both prescription and nonprescription doses. It inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis. If not contraindicated, it is the drug of choice for treatment of mild to moderate pain.
Clinical Context: Diclofenac is one of a series of phenylacetic acids that have demonstrated anti-inflammatory and analgesic properties in pharmacologic studies. It inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis.
Because diclofenac can cause hepatotoxicity, liver enzymes should be monitored in the first 8 weeks of treatment. Diclofenac is rapidly absorbed; metabolism occurs in the liver via demethylation, deacetylation, and glucuronide conjugation. The delayed-release, enteric-coated form is diclofenac sodium, and the immediate-release form is diclofenac potassium. Diclofenac carries a relatively low risk of bleeding gastrointestinal (GI) ulcers.
Clinical Context: Ketoprofen inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis. Smaller initial dosages are particularly indicated in the elderly and in those with renal or liver dysfunction. Doses higher than 75 mg do not improve therapeutic response and may be associated with a higher incidence of adverse effects.
Clinical Context: Meclofenamate inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis. Compared with other NSAIDs, it is associated with a higher incidence of diarrhea.
Clinical Context: Mefenamic acid inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis. Compared with other NSAIDs, it is associated with a higher incidence of diarrhea.
NSAIDs are highly effective in treating dysmenorrhea, especially when they are started before the onset of menses and continued through day 2. They are readily available, relatively inexpensive, and have a low side effect profile when used cautiously and in those who have no contraindications. 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.
Clinical Context: Hydrocodone plus acetaminophen is a drug combination indicated for moderate to severe pain.
Clinical Context: Medroxyprogesterone inhibits secretion of gonadotropins, thereby inhibiting ovulation and decreasing the thickness of the endometrium.
Clinical Context: The levonorgestrel-releasing intrauterine device inhibits secretion of gonadotropins, thereby inhibiting ovulation and decreasing the thickness of the endometrium.
Clinical Context: This drug combination reduces secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary by decreasing the amount of gonadotropin-releasing hormones.
Clinical Context: This drug combination reduces secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary by decreasing the amount of gonadotropin-releasing hormones.
Clinical Context: This drug combination reduces secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary by decreasing the amount of gonadotropin-releasing hormones.
Clinical Context: This drug combination reduces secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary by decreasing the amount of gonadotropin-releasing hormones.
Clinical Context: This drug combination reduces secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary by decreasing the amount of gonadotropin-releasing hormones.
Clinical Context: Reduces secretion of LH and FSH from pituitary by decreasing amount of gonadotropin-releasing hormones.
In some patients, OCs can prevent dysmenorrhea altogether, though 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. Use of OCs in a manner that reduces the number of menstrual cycles may be beneficial for some patients. Combination OCs, the levonorgestrel intrauterine device, and depot medroxyprogesterone acetate provide effective pain relief and are associated with a reduced menstrual flow.