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Dysmenorrhoea - 20 Marks

Definition

• Primary dysmenorrhoea: Menstrual pain WITHOUT any underlying pelvic pathology
• Secondary dysmenorrhoea: Painful menstruation ASSOCIATED with underlying pelvic/organic pathology

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Incidence

• Affects approximately 60% of menstruating women, making it the most common gynaecological complaint
• Leading cause of short-term school/work absenteeism in young women
• Treatment failure rate with conventional approaches is approximately 20-25%

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PRIMARY DYSMENORRHOEA

Age of Onset and Features

• Typically appears within 1-2 years of menarche, when ovulatory cycles are established
• Predominantly affects younger women but may persist into the 40s
• Associated with ovulatory cycles (anovulatory cycles are not usually painful)

Pathophysiology

1. In the late luteal phase, progesterone withdrawal triggers lysosomal membrane destabilisation and release of phospholipase A2
2. Phospholipase A2 cleaves membrane phospholipids → releases arachidonic acid
3. Arachidonic acid enters the cyclooxygenase (COX) pathway → generates prostaglandins (PGF2α, PGE2) and thromboxane A2
4. Women with primary dysmenorrhoea have upregulated COX enzyme activity and prostanoid synthase activity
5. PGF2α is the predominant prostaglandin - causes:
   • Increased uterine muscle contractions (dysrhythmic pattern)
   • Increased uterine basal tone
   • Increased active pressure
   • Decreased uterine blood flow → ischaemia → pain (similar to angina)
6. PGE2 contributes to peripheral nerve hypersensitivity, sensitising pain receptors
7. Prostaglandin concentrations are highest in the secretory endometrium vs. proliferative endometrium

This explains why NSAIDs (COX inhibitors) are the first-line treatment.

Clinical Features

• Begins a few hours before or just after onset of menstrual flow
• Lasts 48-72 hours (most severe in the first 1-2 days)
• Colicky, crampy, suprapubic - similar to labour pains
• May radiate to lumbosacral back and anterior thighs
• Relieved by abdominal massage, counterpressure, or movement (unlike peritonitic pain)

• Nausea, vomiting
• Diarrhoea
• Headache
• Fatigue
• Rarely, syncopal episodes

Signs

• Vital signs are normal
• Suprapubic tenderness on palpation
• Normal bowel sounds; no upper abdominal or rebound tenderness
• Bimanual examination: uterine tenderness during the episode; no cervical excitation tenderness, no adnexal pathology
• Pelvic organs are normal

Diagnosis

1. Detailed history: confirm cyclic nature; rule out dyspareunia, abnormal uterine bleeding, nonmidline focal pain
2. Pelvic examination: assess uterine size/shape/mobility, adnexal structures, uterosacral ligaments
3. NAAT for gonorrhoea and chlamydia; CBC, ESR if infection suspected
4. Pelvic ultrasound if symptoms do not resolve with NSAIDs
5. Laparoscopy is NOT necessary for initial diagnosis if pelvic exam and ultrasound are normal

Management

• Act by inhibiting COX enzymes → reduce prostaglandin synthesis
• Start 1-2 days before anticipated menstrual onset and continue for 2-3 days
• Should be taken regularly, not as needed
• Examples:
  • Ibuprofen 400-600 mg every 4-6 hours
  • Naproxen sodium 500 mg initially, then 250 mg 6-8 hourly
  • Mefenamic acid 500 mg initially, then 250 mg every 6 hours
• Success rate ~80%; failure → switch to another NSAID or add hormonal therapy

• Suppress ovulation → decrease endometrial proliferation → decrease prostanoid production
• Also reduce menstrual flow volume
• Effective in ~90% of cases
• Can be used continuously (no pill-free interval) to suppress menstruation entirely

• Medroxyprogesterone acetate (oral or depot injection)
• Cause endometrial atrophy → reduce prostaglandin production
• Levonorgestrel-releasing IUS (Mirena) - highly effective

• GnRH agonists (for refractory cases) - cause pseudomenopause; limited by hypoestrogenic side effects
• Transdermal patches, vaginal ring

• Heat application (heating pad to lower abdomen) - proven effective
• Regular exercise
• Low-fat vegetarian diet and omega-3 fatty acids (fish oils) - reduce PGE2-derived eicosanoids
• Vitamin B1 (thiamine) 100 mg/day - shown effective in RCT
• Magnesium supplementation - promising evidence
• Transcutaneous electrical nerve stimulation (TENS)
• Yoga, acupuncture

• Laparoscopic uterine nerve ablation (LUNA) - transection of uterosacral ligament fibres
• Presacral neurectomy - more effective but with more complications
• Reserved for cases not responding to medical therapy AND with no organic pathology

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SECONDARY DYSMENORRHOEA

Definition and Key Differences from Primary

Causes of Secondary Dysmenorrhoea (Differential Diagnosis)

1. Endometriosis - most common cause; ectopic endometrial tissue responds to hormones
2. Adenomyosis - endometrial glands within myometrium; presents with heavy, prolonged bleeding + dysmenorrhoea; "boggy, symmetrically enlarged tender uterus"
3. Uterine leiomyomata (fibroids)
4. Endometrial polyps
5. Non-hormonal IUD (copper IUD) - increases menstrual flow and prostanoid production
6. Cervical stenosis
7. Congenital anomalies causing outflow obstruction (e.g., imperforate hymen, transverse vaginal septum, bicornuate uterus)
8. Intrauterine synechiae (Asherman syndrome)
9. Pelvic congestion syndrome
10. Chronic PID / subacute salpingo-oophoritis

• Irritable bowel syndrome
• Inflammatory bowel disease (Crohn's, ulcerative colitis)
• Interstitial cystitis
• Musculoskeletal: myofascial pain, low back syndrome

Most Important Causes - Endometriosis and Adenomyosis

Endometriosis

• Presence of functional endometrial tissue outside the uterine cavity
• Common sites: ovaries (chocolate cysts), uterosacral ligaments, pouch of Douglas, rectovaginal septum
• Symptoms: cyclical pelvic pain, deep dyspareunia, infertility, dysmenorrhoea
• Signs: fixed, retroverted uterus; tender nodules on uterosacral ligaments; restricted uterine mobility; adnexal masses
• Diagnosis: Laparoscopy is gold standard (visual + histological)
• Management: NSAIDs, COCPs, progestins, GnRH agonists, danazol, surgical ablation/excision

Adenomyosis

• Endometrial glands and stroma within the myometrium
• Commonly affects multiparous women in their 40s
• Symptoms begin up to 2 weeks before menses and persist after cessation
• Signs: diffusely enlarged, soft, tender uterus (usually <14 cm); normal mobility
• Diagnosis: clinical; confirmed histologically only (at hysterectomy); TVUS has 68-86% accuracy
• Management: NSAIDs, hormonal therapy (same as endometriosis); definitive cure = hysterectomy

Management of Secondary Dysmenorrhoea

• Treat the underlying cause
• NSAIDs for symptomatic relief
• Hormonal suppression (COCPs, progestins, GnRH agonists, LNG-IUS) to reduce endometrial activity
• Surgical: laparoscopy for endometriosis; hysterectomy for adenomyosis (definitive)
• Uterine artery embolisation for adenomyosis/fibroids

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Intractable Dysmenorrhoea

• Surgical nerve interruption (LUNA, presacral neurectomy)
• Reassess for missed organic pathology (laparoscopy)
• Multidisciplinary pain management

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Summary Table

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