Dysmenorrhea
Dysmenorrhea
Author: Andrew S. Coco, MD, Associate Professor, Family Practice Residency, Lancaster General Hospital, Lancaster, Penn.
Peer Reviewers: Sarah L. Berga, MD, Associate Professor, Departments of Obstetrics, Gynecology, Reproductive Sciences, and Psychiatry, University of Pittsburgh, Pittsburgh, Penn; and Ellen L. Sakornbut, MD, Associate Professor and Program Director, Department of Family Medicine, University of Tennessee, Memphis, Tenn.
Editor’s Note—Many doctors still don’t consider dysmenorrhea a medical problem, and more importantly fail to ask their patients about it. It’s assumed to be a nuisance that women put up with and manage themselves with over-the-counter medications and comfort measures. Many women would not deem it a worthy topic to discuss with a physician due to a sense of embarrassment or fear of being chided. Unfortunately, surveys present a different picture: dysmenorrhea is an extremely common problem that often goes under treated and leads to a significant amount of absenteeism from work. As primary care providers, we need to become more aware of the widespread prevalence and effective treatments. We need to remember to ask our young women patients about their menstrual symptoms.
Dysmenorrhea means painful menstrual period. On a clinical basis, dysmenorrhea is divided into primary and secondary based on etiology. Secondary dysmenorrhea is due to a specific pathological condition, whereas primary dysmenorrhea is a biochemical process without any identifiable physical exam abnormalities. Because the symptoms are identical in both categories, it is extremely important to perform a pelvic exam in order to detect causes of secondary dysmenorrhea so that treatment can be tailored appropriately. The two types of dysmenorrhea can also generally be differentiated by age of onset. Since most of the causes of secondary dysmenorrhea, like uterine fibroids for example, occur in older women, it is more common in this age group. On the other hand, primary dysmenorrhea is a problem for adolescents and young women.
This article will discuss the causes of secondary dysmenorrhea and the ways to distinguish it from primary dysmenorrhea through history and a careful physical examination. But the focus will be on primary dysmenorrhea. The intent is to raise physician awareness of the high prevalence and often inadequate treatment of this problem. The treatment options including alternatives for those who don’t respond to the usual remedies will also be discussed.
Secondary Dysmenorrhea
Secondary dysmenorrhea is defined as painful menstruation secondary to an underling pathologic process, or, occasionally from an iatrogenic cause. As mentioned previously, the onset typically occurs at an older age and the symptoms can usually be associated with a specific pelvic abnormality. A history of pain during anovulatory cycles, or persisting after menses is also characteristic. The most common causes of secondary dysmenorrhea are listed in Table 1.
| Table 1. Common Etiologies of Secondary Dysmenorrhea |
| • Adenomyosis |
| • Pelvic inflammatory disease |
| • Cervical agenesis |
| • Myomas |
| • Intrauterine contraceptive devices |
| • Endometriosis |
| • Adhesions |
| • Ovarian cysts |
| • Ovarian, bowel, or bladder tumors |
| • Inflammatory bowel disease |
| • Imperforate hymen |
Distinguishing Secondary from Primary Dysmenorrhea
Secondary causes of dysmenorrhea must be excluded due to the vastly different treatment of the two conditions. Often the distinction between primary and secondary dysmenorrhea can be ascertained by obtaining a careful history and performing a physical exam. Some of the circumstances in which the diagnosis of secondary dysmenorrhea should be considered include: 1) occurrence within the first few cycles after menarche; 2) beginning after age 25-30; 3) occurring after a history of painless menstruation; 4) minimal relief with nonsteroidal anti-inflammatory medications (NSAIDs); and 5) presence of an abnormality on physical exam. For instance, it would be rare to find primary dysmenorrhea in a woman after years of relatively painless periods. Or, amenorrhea associated with dysmenorrhea during the first several cycles after menarche is characteristic of a congenital outflow obstruction like cervical agenesis.
Some secondary causes can be differentiated through inquiring about the age of menarche and menstrual cycle characteristics like regularity and timing of pain. Endometriosis is particularly difficult, yet crucial to distinguish. It can present as progressive dysmenorrhea, but in contrast to primary disease, is often accompanied by pain during intercourse. Family history is also important when considering endometriosis, as it is familial, occurring in 7% of first-degree relatives of individuals with confirmed disease vs. approximately 1% of the first-degree relatives of husbands of affected women.1,2 The importance of an early diagnosis cannot be overstated. Timely detection allows for prevention of long-term sequelae like pain and possibly, infertility.
The premenstrual syndrome (PMS), although not a cause of secondary dysmenorrhea, can often be confused with it. A distinction is often possible based on history. The pain of PMS is usually restricted to the breasts and abdominal symptoms tend to be bloating rather than lower abdominal cramping. PMS symptoms generally begin before the onset of menses and resolve early on in the cycle. Psychological aspects are much more important in PMS than in primary dysmenorrhea. There are some investigators who have found that dysmenorrhea is more common in women with PMS, suggesting that cyclic ovarian function and its attendant hormonal excursions trigger more severe reactions in vulnerable phenotypes.
Sexual history comes into play when pelvic inflammatory disease (PID) or ectopic pregnancy is present. A past history of PID, sexually transmitted diseases, multiple sexual partners or unprotected sex places women at increased risk for these conditions.
Physical examination, however, is the key to detecting secondary causes. For example, a pelvic exam will reveal the presence of an imperforate hymen and a speculum exam may detect a pedunculated myoma protruding from the external os. A bimanual exam may reveal an irregularly enlarged uterus characteristic of uterine myomas. Pelvic inflammatory disease is associated with tender adnexa and cervical motion tenderness. Endometriosis is suggested by a fixed uterus or uterosacral nodularity; an ovarian neoplasm by an adnexal mass. When the diagnosis is still in doubt after a pelvic examination, transvaginal sonography or hysteroscopy can be used to confirm or clarify physical exam findings.
Primary Dysmenorrhea
Primary dysmenorrhea is a common problem in young women. It is defined as crampy, low midline abdominal pain occurring at the onset of menstruation in the absence of any identifiable pelvic disease. Disturbingly, many doctors don’t consider primary dysmenorrhea a medical problem, and more importantly, fail to ask their patients about it. Since nonsteroidal anti-inflammatory drugs (NSAIDs) are available over the counter, it is assumed that women are treating themselves adequately. Unfortunately, patients may not be knowledgable about the effective use of available over-the-counter medicine.
Epidemiology
Primary dysmenorrhea is the single most common gynecologic problem in menstruating women. Many women fail to report it in medical interviews, even when daily activities are hampered; instead it’s endured as a normal part of life. Reported prevalence rates are as high as 90%.3 A recent study of college students, based on one-year diaries, found 72% of periods were painful, especially during the first day of menses, and 60% of the women reported at least one episode of severe pain.4 In a convenience sample of 289 public high school students in Canada, 98% of the women reported use of non-pharmacological methods (heat, etc.) to manage menstrual discomfort.5
The problem of absenteeism from school or work has been under-appreciated. In the Harlow study on college women, 42% of women reported absenteeism from work or diminished activity, although only a small percentage of women missed work or school for a given menstrual cycle.4 Other longitudinal studies show rates of absenteeism ranging from 34% to 50%.6,7 Another study estimates that dysmenorrhea accounted for 600 million lost work hours and 2 billion dollars in lost productivity annually.8
Several risk factors have been found to be associated with more severe episodes: earlier age at menarche, long menstrual periods, smoking, obesity, and alcohol consumption.4 Other studies have failed to find an association with obesity and alcohol, and so controversy remains.6,7,9 Another report, involving 1147 urban adolescents, found that attempting to lose weight was also significantly associated with increased menstrual pain.10 Most studies show a decreased prevalence and improved symptomatology with physical activity. There is some reliable data to substantiate the widely held view that menstrual pain diminishes after childbearing. In a well-done longitudinal study, there was a decreased prevalence and severity of dysmenorrhea after parity.7 Nulliparas had no changes in menstrual characteristics. Sundell and colleagues were unwilling to conclude that this was due to childbearing alone, but the results were suggestive and significant. This epidemiological information provides us with more information for patient education efforts. Perhaps, the potential for decreasing painful periods will provide sufficient motivation for some women to adopt healthy lifestyle changes, such as smoking cessation and gradual weight reduction.
Pathophysiology
The pathophysiology of primary dysmenorrhea, although not precisely understood, can be explained by the action of uterine prostaglandins, particularly PGF2. Ovulation, or a pattern of hormone exposure mimicking that of an ovulatory cycle, is necessary to produce prostaglandins. The prostaglandin theory of dysmenorrhea relates the variations in PGF2 levels during the menstrual cycle with the symptoms of dysmenorrhea. PGF2 levels are low during the follicular phase. A gradual decrease of progesterone during the luteal phase triggers endometrial sloughing. As endometrial cells disintegrate, PGF2 is released and menstruation begins. PGF2 causes myometrial contractions, as well as ischemia. Convincing clinical evidence backs up this theory. Women with higher PGF2 levels have more severe symptoms; levels peak at day 2 of menses, which correlates with the timing of the worst symptoms. Further, numerous studies have demonstrated the effectiveness of NSAIDs, which are known to inhibit PGF2.11
Clinical Presentation
Primary dysmenorrhea presents during adolescence, typically within three years of menarche.12 Symptoms tend to occur more than six months after the start of menarche when ovulatory cycles are well established. Pain is manifested as intermittent spasms centered in the suprapubic area. Radiation to the low back or legs is possible. Associated symptoms of nausea, vomiting, diarrhea, fatigue, fever, headache, or lightheadedness are not uncommon. Cramping develops quickly, usually within hours of the start of menstruation, and peaks within the first day or two of the cycle. Symptoms resolve before the end of the cycle.
Diagnosis
The diagnosis of primary dysmenorrhea is clinical, based on a focused history and focused physical exam. The history is the typical crampy pain during menstruation and the physical exam findings are normal. The bimanual pelvic exam is the focus of the physical assessment. Findings are usually negative except for midline pain during menstruation. As mentioned previously, the intent of the examination is to rule out secondary causes. Given the usual history and a normal pelvic exam, further diagnostic evaluation is unnecessary. Indeed, it is often preferable to confirm the diagnosis via a therapeutic trial of NSAIDs rather than pursue any diagnostic studies. A failure to respond to NSAIDs should raise doubts about the diagnosis.
Treatment
The most effective treatment for primary dysmenorrhea is NSAIDs. Success rates range from about 80-85%.11 Numerous studies over the last 15 years have demonstrated the efficacy of these familiar drugs. Oral contraceptives (OCs) comprise another effective and well-studied choice, especially when birth control is desirable. A small minority of patients do not respond to these two options. The alternative treatments are numerous, ranging from laproscopic surgery to acupuncture, with much less evidence to support their use. Laparoscopy is used to determine the presence or absence of endometriosis. If found, laparoscopic fulgaration of endometriosis often reduces pain and improves fecundity.
NSAIDs
The first option for most women is one of the NSAIDs. In fact, some claim that these well known drugs have revolutionized the therapeutic approach to dysmenorrhea.11 As mentioned in the pathophysiology section, NSAIDs control pain through the inhibition of the production and release of prostaglandins of the E and F series. Since prostaglandins are responsible for uterine contractions, it follows that their administration would alleviate dysmenorrheic symptoms. There are many choices available and practically all have been shown effective. A systematic review of minor analgesics in primary dysmenorrhea concluded that naproxen, ibuprofen, mefenamic acid, and aspirin were all effective, but that ibuprofen had the most favorable risk-benefit ratio.13 Perhaps, it should be the first choice for most women. Table 2 lists NSAIDs with their doses. Response is rapid with these agents, often within 30-60 minutes. Because responses may vary among individuals, a trial with a different agent is prudent before assuming failure. Also, it is important to keep in mind that it may take up to two cycles before a complete response is realized. Some contraindications to inquire about include aspirin allergy, dyspepsia, and inflammatory bowel disease. NSAIDs should be taken prophylactically when possible (i.e., with the onset of bleeding/spotting or even before [in those with predictable cycles]).
| Table 2. NSAIDs Doses for Primary Dysmenorrhea | |||
| Generic name | Brand name | Dosage (mg) | Interval (h) |
| Ibuprofen | Motrin, Advil, Nuprin | 400-800 | 6 |
| Naproxen | Naprosyn | 250-375 | 6-8 |
| Naproxen sodium | Anaprox, Aleve | 220-550* | 6-12 |
| Ketoprofen | Orudis | 50-75 | 6-8 |
| Flurbiprofen | Ansaid | 50 | 6 |
| Oxaprozin | Daypro | 600 | 24 |
| Aspirin | Generic | 650 | 4 |
| Celecoxib | Celebrex | 100-200 | 12 |
| Indomethacin | Indocin | 25-50 | 6-8 |
| Diclofenac potassium | Cataflam | 50 | 8 |
| Rofecoxib | Vioxx | 25-50 | 24 |
| Salsalate | Salflex | 500-1000 | 8 |
| Etodolac | Lodine | 200-400 | 8-12 |
| Choline magnesium | Trisalate | 1000 | 8 |
| Mefenamic acid | Ponstel | 250 | 6 |
| Piroxicam | Feldene | 20 | 24 |
| Nabumetome | Relafen | 1000-2000 | 24 |
| * Starting dose 550 mg followed by 275 mg every 6-8 h or 550 mg every 12 h. | |||
| Starting dose 500 mg followed by 250 mg every 8 h. | |||
Unfortunately, many adolescents are not using NSAIDs in effective doses despite their widespread availability in over-the-counter preparations.14 In one report, 25% of teenagers used suboptimal doses of medications, and 43% took them too infrequently.14 Primary care providers would do well to expand their history taking to include details about over-the-counter drug dosing regimens when encountering a young female with primary dysmenorrhea.
Oral Contraceptives
When birth control is desired, oral contraceptives become the first choice for primary dysmenorrhea for most patients. However, because daily administration is necessary, they are too cumbersome as a first line choice when compared with the highly effective NSAIDs. OCs, in contrast to NSAIDs, alleviate menstrual pain through suppression of ovulation. All OCs are effective. Although numerous reports in the literature have compared different preparations including triphasics vs. monophasics, or one type of progesterone component vs. another, results mostly reflect similar efficacy in controlling menstrual pain.15 However, oral contraceptives containing gestodene were more effective than those containing desogestrel in a prospective European trial involving 479 women followed for one year.16 All comparisons of OCs with placebos have demonstrated superiority. It is not uncommon for three menstrual cycles to transpire before menstrual pain is significantly diminished, therefore, the addition of an NSAID to the initial treatment regimen is prudent to cover for breakthrough pain. Many adolescents are unaware of this pain relieving aspect of OC.17 In a prospective study of 308 inner-city teens, those with severe symptoms that responded to OC were much more likely to take them consistently.17 Counseling young women about this benefit of pain relief from cramping could assist them in complying with a daily medication. Long-acting progestational agents like Norplant and DepoProvera can also alleviate menstrual pain. Their mechanism of action differs from OCs—they work through a reduction in endometrial, and consequently, prostaglandin volume. Their treatment in primary dysmenorrhea is probably underused. Refractory cases often respond to a continuous combination of NSAIDs and OCs, as their actions are complementary. Some contraindications to consider when prescribing OCs are cardiovascular conditions, cerebrovascular disease, hepatic problems, a history of venous thrombosis, pregnancy, and familial thrombophilias.
Alternatives
Some women with primary dysmenorrhea, unfortunately, do not obtain adequate relief of their menstrual symptoms with NSAIDs or OCs. Another small percentage of women is unable to use these first-line choices due to contraindications. Numerous alternative treatments have been explored to meet the needs of this subset. Table 3 lists some alternative options and references to support their use. The trials involving the listed alternatives are generally of small sample size and long-term follow-up is lacking. They do seem to be effective in the short-term, however, and are certainly worthy of consideration in the right circumstances. Non-responding women should be encouraged to try any safe option. A 1993 survey showed that Americans were using alternative therapies at a high rate and usually not informing their physicians of the fact.32 Concern over being criticized by their medical provider could be a factor in this lack of divulgence.
| Table 3. Alternative Therapies for Primary Dysmenorrhea |
| • Tens unit17-21 |
| • Low fat vegetarian diet22 |
| • Laproscopic presacral neuronectomy23,24 |
| • Accupuncture25 |
| • Omega-3 Fatty Acids26,27 |
| • Transdermal Nitroglycerine28 |
| • Thiamine29 |
| • Magnesium Supplements30 |
| Adapted from: Coco AS. Primary dysmenorrhea. Am Fam Physician 1999;60(2):489-496. |
Nonresponders
Women who do not respond to NSAIDs or hormonal birth control pose a dilemma.
Secondary diagnoses especially endometriosis, need to be considered, but the timing and extent of the work-up to look for other causes can be problematic. For instance, an important study on the natural history of endometriosis found that the majority of women suffer for many years before endometriosis is detected with mean delay in diagnosis being about 12 years after the onset of pain symptoms.33 Data on the natural history of primary dysmenorrhea, however, is lacking and the difficulty arises in how to identify those whom eventually become diagnosed with endometriosis. Since the diagnosis of endometriosis still requires a laparoscopic evaluation, it is not surprising that parents might be reluctant to have their teenage daughters undergo an invasive procedure for menstrual cramping when the odds of discovering a pathologic condition are unknown. Nonetheless, given the small percentage of women with primary dysmenorrhea that fail to respond to the usual treatments, serious consideration must be given to a gynecological referral to look for secondary causes when these non-responders are encountered clinically.
Summary
Dysmenorrhea represents a common symptom in gynecological patients of primary care providers. Distinguishing between primary dysmenorrhea, which occurs in young women, and secondary causes, which are due to other disease states, is mandatory. Differentiation can usually be made based on the history and physical exam. Many physicians still don’t think of primary dysmenorrhea as a medical condition and infrequently ask their patients about it. Despite the widespread availability of beneficial over-the-counter medications, surveys indicate a high rate of absent or inadequate treatment. Absenteeism from work due to severe cramping pain is not uncommon. Nonsteroidal anti-inflammatory drugs and oral contraceptives remain as highly effective first-line treatments, with a host of less well-studied alternatives for the small subset of non-responders.
References
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