Dysmenorrhoea

❍ At a glance

• Dysmenorrhoea affects 45-90% of menstruating women¹ and is frequently normalised and undertreated. Primary dysmenorrhoea is prostaglandin-mediated with no structural cause; secondary dysmenorrhoea arises from an underlying condition. The two must be distinguished: primary dysmenorrhoea is a diagnosis of exclusion, not a default label.
• The average delay between onset of endometriosis symptoms and diagnosis is 6-10 years internationally.³ Suspect secondary dysmenorrhoea when pain is worsening, onset is later in reproductive life, there is dyspareunia, dyschezia, or subfertility, or when standard treatment provides incomplete relief.
• NSAIDs are first-line for primary dysmenorrhoea and work best when started the day before expected onset - not after pain is established. Around 80% of women respond.²
• A normal pelvic ultrasound does not exclude endometriosis. Peritoneal and superficial implants are below the resolution of standard USS. Referral should not be delayed by a negative ultrasound result.

❍ Presentation and investigation

Primary dysmenorrhoea typically begins in adolescence within one to two years of menarche as ovulatory cycles become established. Pain starts hours before or at the onset of menstruation, peaks in the first one to two days, and resolves by day two or three. It is cramping, suprapubic or lower abdominal, and may radiate to the lower back and anterior thighs. Associated features include nausea, diarrhoea, headache, and fatigue. Pelvic examination is normal. Primary dysmenorrhoea is a clinical diagnosis in an adolescent with characteristic features and no secondary red flags; investigation is not required initially.

Secondary dysmenorrhoea should be suspected when onset is later in reproductive life; pain is worsening progressively; pain begins well before menstruation or persists after it; there is dyspareunia, dyschezia (painful defecation during menstruation), dysuria, or subfertility; pelvic examination is abnormal; or empirical treatment provides incomplete relief. The most common causes are endometriosis, adenomyosis, uterine fibroids, and sequelae of pelvic inflammatory disease.

Where secondary dysmenorrhoea is suspected: pelvic examination (uterosacral nodularity, fixed retroverted uterus, or adnexal tenderness suggest endometriosis; tender boggy uterus suggests adenomyosis); TVS to assess for fibroids, endometriomas, and other structural pathology. A normal ultrasound does not exclude endometriosis - diagnostic laparoscopy remains the gold standard. STI screen where PID is possible. FBC and ferritin if associated heavy bleeding.

❍ Management

NSAIDs are the most effective first-line treatment, reducing prostaglandin synthesis.² Mefenamic acid (500 mg three times daily) and naproxen (500 mg twice daily) are commonly used; start the day before expected onset or at first signs of bleeding for maximum effect. Around 80% of women with primary dysmenorrhoea respond.

Hormonal therapy: the COCP reduces endometrial prostaglandin production and suppresses ovulation. Continuous COCP cycling (no pill-free week) provides better control in women with severe dysmenorrhoea. The LNG-IUS (Mirena) is highly effective where heavy bleeding coexists. The progestogen-only pill and etonogestrel implant are alternatives for women in whom oestrogen is contraindicated.

Where secondary dysmenorrhoea is suspected: empirical hormonal suppression (COCP, POP, or LNG-IUS) is appropriate while awaiting specialist review - it provides meaningful symptom relief without significantly delaying diagnosis. Referral should still proceed; hormonal treatment does not exclude endometriosis. Heat application and TENS have modest evidence as adjuncts.

❍ Referral criteria

Refer to gynaecology for: suspected endometriosis or adenomyosis; dysmenorrhoea with dyspareunia, dyschezia, or subfertility; inadequate response to NSAIDs and two cycles of hormonal therapy; abnormal pelvic examination; or progressive worsening of symptoms. Referral should not be delayed by a negative pelvic ultrasound - normal USS does not exclude endometriosis, and the average diagnostic delay of 6-10 years³ reflects exactly this pattern of repeated reassurance without timely investigation.