Case 5 Dysmenorrhoea
Description of dysmenorrhoea
Definition
Dysmenorrhoea is defined as cyclic lower abdominal pain that occurs with, or precedes, menstruation.1 Depending on the aetiology of the condition, dysmenorrhoea may be classified as either primary or secondary. Primary dysmenorrhoea is a functional disorder that has no identifiable pathological aetiology and is typically associated with ovulation. Pain caused by a demonstrable pathology to the pelvic or reproductive structures, however, is referred to as secondary dysmenorrhoea.1
Epidemiology
The prevalence of dysmenorrhoea varies across the globe, affecting between 16.8 and 81 per cent of women.2 Of the two categories of menstrual pain, primary dysmenorrhoea is the most common, contributing to around ninety per cent of dysmenorrhoeic cases.3 Primary dysmenorrhoea usually begins during adolescence or the early twenties, generally after regular ovulation is established, and usually after the first three to six menstrual cycles.4 Unlike the prevalence of secondary dysmenorrhoea, which increases with advancing age, the prevalence of primary dysmenorrhoea diminishes with age and, in some cases, following pregnancy.4
Aetiology and pathophysiology
Primary dysmenorrhoea is caused by abnormal eicosanoid production, specifically, an abnormal increase in endometrium-derived prostaglandin (PG) F2α and PGE2. These proinflammatory compounds are formed under the influence of progesterone, but can also rise following endometrial shedding, endometrial cell necrosis,4 excess omega 6 fatty acid intake, low omega 3 fatty acid consumption and/or abnormal fatty acid metabolism.3,5,6 The PGs implicated in the pathogenesis of dysmenorrhoea exhibit a wide range of effects. PGF2α, for instance, affects the gastrointestinal (GI) tract, causing nausea, vomiting and diarrhoea.4 PGF2α is also a potent smooth muscle stimulant and vasoconstrictor, which, in sufficient quantities, can cause uterine ischaemia, myometrial contractions and uterine pain.3 In contrast, PGE2 is a potent vasodilator and a possible contributor to excessive menstrual bleeding.4 While the cytokine hypothesis of dysmenorrhoea is theoretically plausible, evidence from clinical studies is mixed.7,8
As opposed to the proinflammatory state of primary dysmenorrhoea, the cause of secondary dysmenorrhoea is primarily pathological. Conditions usually associated with secondary dysmenorrhoea include endometriosis, uterine adenomycosis, leiomyomata or fibroids, pelvic adhesions, cervical stenosis, pelvic inflammatory disease, in situ intrauterine device and endometrial polyps.1,4
Other factors that may increase the severity or duration of dysmenorrhoea are anxiety, low levels of exercise, low fish consumption and cigarette smoking.1,3 Several studies also report a higher risk of dysmenorrhoea among women with high stress (i.e. occupational or perceived stress) compared to those with low stress.9,10
Clinical manifestations
Dysmenorrhoea typically presents as recurrent, spasmodic lower abdominal or suprapubic pain that is sharp or dull in quality.4 In many cases, the pain radiates to the lower back or thighs. Some women also report symptomatic improvement following the application of heat to the abdomen or by assuming the fetal position.4 In primary dysmenorrhoea symptoms usually begin 1–3 days before menses, peak 24 hours after the onset of menstruation and subside 2–3 days later. In secondary dysmenorrhoea, menstrual pain may commence long before menses begins and continue well after menstruation has ceased.1 It is not uncommon for women with either type of dysmenorrhoea to also experience concomitant nausea, vomiting, diarrhoea, constipation, headache, fatigue, irritability, nervousness, urinary frequency, dizziness, sleeplessness and depression.1,3
Clinical case
23-year-old woman with primary dysmenorrhoea
Rapport
Adopt the practitioner strategies and behaviours highlighted in Table 2.1 (chapter 2) to improve client trust, communication and rapport, as well as the accuracy and comprehensiveness of the clinical assessment.
Health history
Lifestyle history
Illicit drug use
Diet and fluid intake | |
Breakfast | White toast with butter, coffee. |
Morning tea | Coffee, banana or carrot cake. |
Lunch | Leftover dinner, sandwich with white bread, ham, tomato, lettuce and pickles. |
Afternoon tea | Coffee. |
Dinner | Chicken or beef and vegetable stirfry with white rice, penne carbonara with mushrooms, focaccia with grilled chicken or roast beef, eggplant, capsicum and lettuce. |
Fluid intake | 3–4 cups of instant coffee a day, 2–3 cups of water a day. |
Food frequency | |
Fruit | 0–1 serve daily |
Vegetables | 2–3 serves daily |
Dairy | 0–1 serve daily |
Cereals | 5–6 serves daily |
Red meat | 6–7 serves a week |
Chicken | 1–2 serves a week |
Fish | 0 serves a week |
Takeaway/fast food | twice a week |
Diagnostics
Pathology tests
Fatty acids
Plasma or red cell fatty acid analysis assesses the concentration of fatty acids within the plasma or erythrocyte, including omega 3, omega 6 and omega 9 polyunsaturated fatty acids, saturated fatty acids and trans fatty acids. Given that the fatty acid composition of plasma and erythrocytes is correlated with the dietary intake of fatty acids,11 this test can help to determine whether excess omega 6 fatty acid intake and/or low omega 3 fatty acid consumption are contributing factors in dysmenorrhoea.3,5
Hormones and eicosanoids
Several small studies have compared the plasma concentrations of oxytocin, follicle-stimulating hormone, 17β-estradiol, vasopressin, luteinising hormone, progesterone and PGF2α in healthy controls to women with primary dysmenorrhoea.7,12,13 However, findings from these studies have been inconsistent, rendering questionable the value of hormone testing in women with dysmenorrhoea.
Functional tests
A female hormone profile measures salivary levels of oestradiol, progesterone, testosterone and dehydroepiandrosterone (DHEA) over a single 28-day menstrual cycle. While saliva is a valid and reliable sample source for hormone analysis,14 the value of hormone testing in women with dysmenorrhoea is questionable as female hormones appear to play little to no role in the pathogenesis of the condition.
Diagnosis
Expected outcomes
Based on the degree of improvement reported in clinical studies that have used CAM interventions for the management of dysmenorrhoea,15–18 the following are anticipated: