Dysmenorrhoea โ Primary & Secondary Causes
Structured 9-step pathway ยท Menstrual pain ยท UK GP / RCGP SCA
Progress0 / 9
The full reasoning pathway โ separate primary dysmenorrhoea (no pathology) from secondary causes such as endometriosis, escalate red flags, treat stepwise, modify factors, and safety-net.StartDecisionInvestigateActionReferStop / Admit
PresentationPainful periods
Primary (starts with menarche, no pathology) vs secondary (later onset, other symptoms). Dyspareunia, IMB, subfertility, bowel/bladder cyclical symptoms.
Step 1 ยท Safety โ secondary cause / red flagsSecondary cause / red flags?
Later onset, deep dyspareunia, cyclical bowel/bladder symptoms, subfertility, pelvic mass โ endometriosis, fibroids, PID, adenomyosis.
Gynaecology suspected endometriosis (diagnostic delay is common), structural disease, or pain refractory to first-line treatment; treat PID promptly.
Step 8 ยท self-care & modifiable factors
Step 8 ยท Self-care & modifiable factorsAdjuncts to drug therapy
Local heat, regular exercise, and TENS can ease primary dysmenorrhoea; stop smoking (linked to worse symptoms). Optimise the chosen treatment โ take NSAIDs at onset and regularly through the painful days; consider continuous/tricycling of hormonal contraception to reduce bleed frequency. Address impact on school/work and mood.
Step 9 ยท review & safety-net
Step 9 ยท Review & safety-netReview the trial; when to escalate
Review after ~3 months of NSAID ยฑ hormonal treatment; if inadequate, switch/escalate or reconsider a secondary cause. Reassess / refer if new deep dyspareunia, cyclical bowel/bladder symptoms, subfertility, a pelvic mass, or pain unresponsive to 3โ6 months of treatment โ don't keep treating presumed primary dysmenorrhoea that isn't settling. Same-day if severe pain + fever/discharge (PID) or signs of an acute abdomen.
โ ๏ธ Think endometriosis early: secondary dysmenorrhoea with dyspareunia, cyclical bowel/bladder symptoms or subfertility deserves prompt assessment โ diagnostic delay is often years.
1
Safety
Red Flags โ Exclude secondary and surgical causes first
Dysmenorrhoea is common, but secondary causes (endometriosis, PID, ectopic) must be excluded, especially with atypical or changing pain patterns.
Deep dyspareunia + progressive pain Pain worsening over time, dyspareunia, dyschezia โ Urgent Gynaecology (endometriosis)
Postcoital / intermenstrual bleeding Associated with dysmenorrhoea โ cervical/endometrial pathology โ 2WW if age >45
New onset dysmenorrhoea in older woman Secondary dysmenorrhoea after years of pain-free periods โ fibroids, adenomyosis, malignancy
Palpable pelvic mass Mass on examination โ urgent USS + gynaecology referral (fibroid, ovarian cyst, endometrioma)
Adolescent with severe disability Missing school/work every cycle โ endometriosis must be considered; early referral reduces diagnostic delay (avg 7โ8 yrs)
Endometriosis affects 1 in 10 women of reproductive age but has an average diagnostic delay of 7โ8 years in the UK (APPG on Endometriosis 2020). The key clinical signal is progressive worsening pain that does not respond to NSAIDs and is associated with deep dyspareunia, dyschezia (painful defaecation), and subfertility. PID must be considered in any sexually active woman with pelvic pain and fever โ untreated PID causes tubal infertility and ectopic pregnancy. These are the diagnoses most frequently missed in GP consultations for menstrual pain.
2
Diagnose
History โ Primary vs secondary dysmenorrhoea differentiation
Pain onset timing
Primary: starts 6โ12 months after menarche, coincides with ovulatory cycles; Secondary: later onset, often >25 yrs
Pain character
Cramping, colicky, central/suprapubic with radiation to thighs/back. Severity: use NRS 0โ10; duration (1โ3 days typical for primary)
Pain pattern change
Key question: "Has it gotten worse over time?" Progressive worsening โ secondary cause until proven otherwise
Associated symptoms
Deep dyspareunia (endometriosis); dyschezia (endo, rectovaginal); dysuria (bladder endo, PID); heavy bleeding (fibroids, adenomyosis)
Trying to conceive? Subfertility + dysmenorrhoea โ endometriosis screening priority
Contraception use
COCP, Mirena, POP โ relieves primary dysmenorrhoea; Copper IUD can worsen dysmenorrhoea
Response to NSAIDs
Good response to ibuprofen โ primary dysmenorrhoea likely. Poor/no response โ secondary cause more likely
The response to NSAIDs is a diagnostic test โ prostaglandin-mediated primary dysmenorrhoea responds well to NSAIDs (NNT 3). Failure to respond to adequate NSAIDs should prompt investigation for secondary causes. Progressive worsening is the single most important red flag โ primary dysmenorrhoea tends to be stable or improve with age/after childbirth, while secondary causes (especially endometriosis) progressively worsen. Quantifying the impact on daily function (days off work/school) helps justify onward referral and resonates with the RCGP focus on patient-centred outcomes.
3
Diagnose
Classification โ Primary vs secondary, and identify underlying cause
Primary dysmenorrhoea
No structural pathology. Caused by prostaglandin-mediated myometrial hypercontractility โ uterine ischaemia. Onset within 2 yrs of menarche. Responds to NSAIDs/COCP.
Uterine leiomyomas. Menorrhagia + cramping. Submucous fibroids most symptomatic. Diagnosed on USS.
Ovarian cysts / endometrioma
Ovarian endometrioma ('chocolate cyst'). Adnexal mass on examination or USS. Deep dyspareunia.
Iatrogenic
Copper IUD โ prostaglandin-mediated worsening. Consider IUD removal if refractory dysmenorrhoea after IUD insertion.
Primary dysmenorrhoea affects up to 90% of adolescent women โ it is the leading cause of recurrent school absenteeism. The critical distinction is whether this is primary (functional, prostaglandin-driven, responsive to treatment) or secondary (structural, requiring investigation and often specialist intervention). Endometriosis is frequently dismissed as "bad periods" โ the RCGP curriculum and NICE NG73 emphasise the importance of early referral to reduce the diagnostic delay that leads to infertility, chronic pain, and reduced quality of life.
4
Diagnose
Examination โ Targeted pelvic and abdominal assessment
Abdominal examination
Suprapubic tenderness, uterine/adnexal masses, rebound (peritonism if acute)
Cervical appearance (erosion, polyp, discharge), IUD threads visible; take STI swabs if PID suspected
Recto-vaginal exam
If deep endometriosis suspected: nodularity in pouch of Douglas, uterosacral ligament thickening โ highly specific for deep endo
BMI and general
Low BMI โ primary dysmenorrhoea more likely; obesity + heavy periods โ adenomyosis/fibroids
Pelvic examination can be deferred in young adolescents who are not sexually active โ clinical history is usually sufficient to diagnose primary dysmenorrhoea and initiate treatment. However, in sexually active women or those with suspected secondary causes, examination is mandatory. Recto-vaginal examination (for nodularity in the pouch of Douglas) has a sensitivity of 60โ70% for deep endometriosis โ it can significantly accelerate referral and laparoscopic diagnosis. Cervical excitation is pathognomonic for PID and requires same-day antibiotics.
5
Diagnose
Investigations โ Targeted and proportionate
Always
ฮฒHCG โ exclude pregnancy; STI screen (chlamydia/gonorrhoea NAAT) if PID suspected or sexually active with risk factors
If secondary cause suspected
TVUSS โ first-line imaging for fibroids, adenomyosis, endometrioma, ovarian cysts. FBC if heavy bleeding.
Not recommended for endometriosis diagnosis in primary care โ poor specificity. Elevated in fibroids, adenomyosis, malignancy, pregnancy. Avoid.
MRI pelvis
If TVUSS inconclusive; suspected deep infiltrating endometriosis; adenomyosis โ specialist-requested, not primary care
Primary dysmenorrhoea
No investigation needed if: adolescent, cyclical, relieves with NSAIDs, no examination findings, no secondary cause features
NICE NG73 (Endometriosis) explicitly states that a normal ultrasound does NOT exclude endometriosis โ peritoneal deposits are invisible on USS. This is a key RCGP exam point. TVUSS is useful for identifying endometriomas, adenomyosis, and fibroids, but a normal scan does not reassure against endometriosis. CA-125 is frequently ordered but has no role in diagnosing endometriosis in primary care โ it causes unnecessary anxiety and false positives. Laparoscopy remains the gold standard diagnostic tool for endometriosis.
6
Refer
Referral Criteria โ Gynaecology and specialist pathways
Primary dysmenorrhoea with adequate NSAID/COCP response โ primary care treatment; review at 3 months
NICE NG73 states that GPs should refer women with suspected endometriosis to a specialist without waiting for trial of treatment if symptoms are severe. The historical practice of prescribing multiple treatments before referral contributes to the 7โ8 year diagnostic delay. In the RCGP SCA, failing to consider endometriosis in a young woman with progressive dysmenorrhoea and dyspareunia is a significant consultation weakness. Chronic pelvic pain with central sensitisation benefits from multidisciplinary pain management, not escalating analgesics.
Step 1NSAIDs โ start 1โ2 days before period Ibuprofen 400โ600 mg TDS with food (NNT 3); or Naproxen 500 mg BD. Take regularly, not PRN โ prostaglandin blockade requires regular dosing. If NSAID-intolerant: paracetamol 1g QDS (less effective but safe).
Step 2Combined Oral Contraceptive Pill (if contraception acceptable) Monophasic COCP (e.g. Microgynon 30, Rigevidon). Can be used continuously (tricycling) to avoid withdrawal bleeds. Significantly reduces primary dysmenorrhoea severity. Also 1st-line for endometriosis symptom management.
Step 2 altLevonorgestrel IUS (Mirena) Reduces menstrual pain and flow. Effective for primary dysmenorrhoea and endometriosis. Licensed for menorrhagia + dysmenorrhoea. Consider if COCP contraindicated or not preferred.
Step 3Progestogen-only / GnRH analogues (specialist-led) Norethisterone 5 mg TDS (day 5โ26) or continuous. GnRH analogues (Zoladex, Prostap) โ add-back HRT essential; specialist prescribing only for endometriosis.
PID TreatmentDoxycycline 100 mg BD ร 14 days + Metronidazole 400 mg BD ร 14 days + single-dose Ceftriaxone 500 mg IM (BASHH 2023) โ same-day initiation, swabs before antibiotics, GUM follow-up.
NSAIDs work by inhibiting cyclo-oxygenase (COX), reducing prostaglandin synthesis โ the direct cause of uterine cramping in primary dysmenorrhoea. Starting 1โ2 days before expected pain onset is 30% more effective than starting at pain onset. The COCP works by suppressing ovulation (eliminating the prostaglandin surge) and thinning the endometrium โ NNT approximately 5 for significant pain reduction. Levonorgestrel IUS reduces menstrual flow by 90% and significantly reduces prostaglandin-mediated pain. GnRH analogues (medical oophorectomy) are highly effective for endometriosis but cause menopausal side effects and bone loss โ never used without add-back HRT and specialist supervision.
8
Lifestyle
Non-Pharmacological โ Evidence-based adjuncts
Heat therapy Topical heat (heat pad, hot water bottle) to abdomen. RCT evidence shows equivalent effect to ibuprofen for primary dysmenorrhoea. Use continuously during pain.
TENS High-frequency TENS over abdomen. Cochrane review: effective for primary dysmenorrhoea. Available OTC. Can be used alongside NSAIDs.
Exercise Regular aerobic exercise reduces prostaglandin synthesis and endorphin release reduces pain perception. 150 min/week reduces severity by ~30%.
Omega-3 supplementation Fish oil 1โ2g/day. Anti-prostaglandin effect via arachidonic acid displacement. RCT evidence for reduction in dysmenorrhoea severity.
Dietary changes Low-fat vegetarian diet reduces oestrogen levels and pain in endometriosis. Reduce red meat. Increase fibre and vegetables.
Psychological support Chronic pain with functional impact โ CBT referral. Pain catastrophising worsens outcomes. IAPT referral available in primary care.
Pain diary Track pain severity (NRS), timing, functional impact. Informs treatment decisions and referral letters. Useful for RCGP SCA consultations.
Heat therapy is genuinely as effective as NSAIDs in RCTs for primary dysmenorrhoea (Cochrane 2014) โ it is underutilised and without side effects. TENS is available over-the-counter and is effective, particularly for women who cannot tolerate NSAIDs. Omega-3 supplementation has a modest but statistically significant effect via competitive inhibition of arachidonic acid (a prostaglandin precursor). Psychological interventions (CBT) have strong evidence for chronic pelvic pain โ pain catastrophising and central sensitisation are modifiable targets. These measures should be presented as genuine treatment options, not afterthoughts.
Acute severe pelvic pain + fever + haemodynamic compromise; suspected ectopic; signs of peritonitis
Same-day GP
Pain not responding to regular NSAIDs; new fever or vaginal discharge during treatment; difficulty passing urine
Refer if
Progressive worsening despite treatment; deep dyspareunia develops; subfertility; new pelvic mass on re-examination
NICE NG73 (Endometriosis 2017) states that if empirical treatment (COCP or progestogens) does not control symptoms within 3โ6 months, refer to a specialist โ do not continue empirical treatment indefinitely. The 7โ8 year diagnostic delay in endometriosis is partly attributable to repeated empirical treatments without referral. Functional outcome tracking (days absent from work/school) is more patient-centred than pain scores alone and forms a compelling basis for specialist referral. Safety-netting instructions for ectopic pregnancy are mandatory given the overlap with dysmenorrhoea symptoms.
Educational use only. Pathway based on: NICE NG73 (Endometriosis 2017), BASHH PID Guidelines (2023), NICE CKS Dysmenorrhoea (2023), RCOG Endometriosis Guideline (2023), Cochrane Reviews on NSAIDs and TENS for dysmenorrhoea. Always adapt to individual patient context.