Dysmenorrhea, defined as painful menstruation, is the most common gynecologic condition affecting women. Reported prevalence varies widely, ranging from 17% to as high as 90%. Some women experience relatively minimal pain, whereas others are significantly limited in their ability to function during their menses. Of all menstrual-related symptoms, lower abdominal and back pain are the symptoms most strongly associated with absences from or decreased efficacy at work and school. Up to 15% of women with dysmenorrhea experience symptoms of sufficient severity to cause absenteeism from work, school, and other activities. Flexibility in hours or the ability to work from home may mitigate this problem, but, even for those women who do not miss work or school for menstrual-related symptoms, the reduced focus and productivity associated with those symptoms negatively affect performance. An estimated 600 million hours or $2 billion annually is lost in the United States secondary to missed work or reduced functional abilities due to menstrual pain and associated symptomatology.5 Lack of access to menstrual hygiene products may also contribute to absenteeism and reduced efficacy at work or school. However, the role of access to needed resources has not been explicitly explored in available literature on the effect of menstruation on performance. Future research to distinguish between absences based on menstrual symptoms and absences based on unmet product needs would further help to guide policy. Dysmenorrhea is often underreported and undertreated, and adequate management of dysmenorrhea will improve overall quality of life as well as alleviate financial and academic burdens for many women.
Dysmenorrhea is classified as primary or secondary based on whether or not an underlying etiology is identified.8 Primary dysmenorrhea is pain with menses for which there is no underlying abnormality, whereas secondary dysmenorrhea is pain associated with conditions such as endometriosis, pelvic inflammatory disease, leiomyomas, and interstitial cystitis. Treatment of secondary dysmenorrhea focuses on the causative pelvic pathology or medical condition. Primary dysmenorrhea accounts for the majority of painful menses in ovulatory women. This review will focus on the pathophysiology and treatment options for primary dysmenorrhea.
DIAGNOSIS
Primary dysmenorrhea presents at the onset of ovulatory cycles, which is usually within 6–12 months of menarche but can be as long as 2 years after menarche in some adolescents. Its prevalence decreases with increasing age in a large percentage of sufferers. Patients describe pain that is crampy and of fluctuating intensity, with the onset of pain shortly before or at the onset of bleeding and lasting up to 72 hours. The pain is located in the suprapubic region and can radiate to the upper thigh or back or both. Pain intensity usually peaks at 24–36 hours from the onset of menses, and the duration is rarely longer than a few days.1 Additional symptoms include nausea, vomiting, bloating, and diarrhea. Risk factors for dysmenorrhea, which is typically identified as primary rather than secondary in adult study participants based on history, normal examination findings, and absence of other known causes for menstrual pain, include the following: age younger than 30 years, body mass index (BMI, calculated as weight in kilograms divided by height in meters squared) less than 20, smoking, menarche at younger than 12 years, longer menstrual cycles or duration of bleeding, irregular or heavy menstrual flow, a history of sexual assault, and a family history of dysmenorrhea. The prevalence of moderate to severe primary dysmenorrhea generally decreases as women age, and childbirth is associated with a reduction in the prevalence and severity of primary dysmenorrhea. Improvements are not seen in women who experienced pregnancies that ended in miscarriage or abortion.
A physical examination revealing a normal-sized, mobile, nontender uterus and the absence of mucopurulent discharge, uterosacral nodularity, or an adnexal mass is consistent with primary dysmenorrhea. A pelvic examination is not necessary to initiate treatment in an adolescent with a classic history of primary dysmenorrhea. As such, initial treatment is amenable to telehealth platforms and does not need to be delayed if a face-to-face visit is inconvenient for the patient or otherwise impossible to arrange (eg, during periods of reduced office hours related to contagion-containment strategies). An atypical presentation, abnormal physical examination findings, or lack of improvement with medical therapy should prompt evaluation for causes of secondary amenorrhea. A pelvic examination and radiologic testing, such as abdominal or transvaginal ultrasound scan, should be performed for a patient whose symptoms do not respond to empiric therapy. Surgical evaluation may be warranted based on the findings or clinical suspicion.
PATHOPHYSIOLOGY
Primary dysmenorrhea appears to be the result of increased proteinoid secretion by way of the cyclooxygenase pathway.3 The proteinoid class include prostaglandins (PGs), thromboxane's, and prostacyclin's. Ovulatory progesterone levels stabilize cellular lysosomes, but, at the end of the luteal phase when progesterone levels decline, lysosomes break down and release phospholipase A2 This explains why the pain of dysmenorrhea begins with ovulatory cycles and not with anovulatory early menses. This enzyme starts the cyclooxygenase pathway with resultant proteinoid production. Prostaglandins are a group of lipid compounds that are involved in multiple physiologic and pathologic conditions in the body. There are nine classes of PGs, but PGF2? and PGE are the major culprits involved with primary dysmenorrhea.3 Not only does PGF2? cause uterine contractions that restrict blood flow, but it is also directly involved in arcuate vessel constriction. Both mechanisms of action produce hypoxia that leads to the accumulation of anaerobic metabolites that stimulate pain receptors. Prostaglandin also lowers the threshold for pain perception by sensitizing these same nerve receptors. Prostaglandin E2 has dual mechanisms of action depending on receptor interaction, causing either myometrial contraction or relaxation and uterine vessel constriction or dilation.7 The peak hours of menstrual pain correlate with the highest levels of PGs. Accompanying gastrointestinal symptoms are also a recognized consequence of PGs.
