• Rising oestrogen from developing ovarian follicles stimulates endometrial regeneration and proliferation
• Endometrium thickens from ~1 mm to ~3–5 mm
• Glands are straight and tubular
• Spiral arteries elongate

• Post-ovulation, the corpus luteum produces progesterone
• Progesterone transforms the proliferated endometrium into a secretory state (ready for implantation)
• Glands become tortuous and secrete glycogen-rich fluid
• Spiral arteries become maximally coiled
• Stroma becomes oedematous ("decidualisation" in preparation for implantation)

• If no implantation → corpus luteum regresses → progesterone withdrawal
• This triggers:
  1. Spiral artery vasoconstriction → ischaemia → tissue necrosis
  2. Release of prostaglandins (PGF₂α and PGE₂) from the ischaemic endometrium → promote vasoconstriction initially, then vasodilation and myometrial contractions
  3. Release of matrix metalloproteinases (MMPs) → enzymatic breakdown of extracellular matrix → detachment of functionalis
  4. Activation of fibrinolytic system — local tissue plasminogen activator (tPA) prevents clot formation within the uterine cavity (this is why menstrual blood normally does not clot; when flow is very heavy, the fibrinolytic capacity is overwhelmed → passage of clots)

Normal menstruation is a finely controlled process of tissue breakdown + haemostasis:

• Vasoconstriction of spiral arteries (initial haemostasis)
• Platelet plug formation at the torn vessel ends
• Fibrin deposition — limited, as local fibrinolysis keeps the cavity fluid
• Endometrial regeneration from the basalis begins even during menstruation, sealing off exposed vessels
• Myometrial contraction compresses intramural blood vessels

• Most common hereditary bleeding disorder ^[3]
• Population incidence ~1:100, but clinically significant ~1:20,000
• HMB occurs in 60–90% of women with vWD ^[3]
• vWF mediates platelet adhesion (GPIb to subendothelial collagen) and serves as carrier protein for factor VIII
• Deficiency → impaired platelet adhesion + ↓factor VIII → mucocutaneous bleeding pattern
• Some studies show 10–15% of women with HMB have underlying vWD ^[3]
• Types: Type 1 (quantitative ↓, AD, most common ~70%), Type 2 (qualitative defects, AD), Type 3 (severe quantitative ↓, AR, rare)

• Platelet function disorders (Bernard-Soulier syndrome, Glanzmann thrombasthenia, storage pool disorders) ^[3]
• Haemophilia carriers — female carriers of haemophilia A/B can have factor levels as low as 30–50%, enough to cause HMB
• Immune thrombocytopenia (ITP) — autoimmune platelet destruction → ↓platelet count → mucocutaneous bleeding including HMB ^[3]
• Liver disease — ↓synthesis of clotting factors + impaired oestrogen metabolism
• Chronic kidney disease — uraemic platelet dysfunction (↑NO → inhibits platelets; anaemia → altered blood rheology → ↓platelet-endothelium contact) ^[3]

When to suspect a coagulopathy (ACOG screening tool):

• HMB since menarche
• History of postpartum haemorrhage
• Surgery-related bleeding
• Bleeding associated with dental work
• ≥ 2 bruising symptoms (> 5 cm, without trauma)
• Frequent epistaxis (> 1/month)
• Family history of bleeding disorder
• Personal history of easy bleeding from minor cuts

• Localised overgrowths of endometrial glands/stroma projecting into cavity
• More commonly associated with IMB than pure HMB, but can contribute to heavy cyclical bleeding if large or multiple
• Why they bleed: aberrant vasculature with poor contractile ability + surface erosion + interference with orderly endometrial shedding
• Prevalence: found in 10–40% of women investigated for AUB

• Adenomyosis: may be a/w dysmenorrhea, commonly mid-30s to 40s ^[1]
• Ectopic endometrial glands within the myometrium → disrupts myometrial contraction → impaired vascular compression → heavy bleeding
• Also increases uterine surface area and alters local prostaglandin/MMP production
• Classical triad: HMB + dysmenorrhoea + bulky, tender uterus
• Important differential from fibroids — adenomyosis gives a uniformly enlarged, boggy, tender uterus rather than a nodular, firm one

• Uterine fibroid: commonest structural cause ^[1]
• Usually due to submucosal (or intramural) leiomyomas ^[1]
• May be a/w pressure symptoms ^[1] — urinary frequency, constipation, pelvic heaviness
• Key point: location determines bleeding — submucosal (FIGO types 0–2) > intramural (types 3–4) > subserosal (types 5–7) in likelihood of causing HMB
• An enormous subserosal fibroid may cause zero bleeding, while a 1 cm submucosal fibroid can cause flooding

• Endometrium: polyp, hyperplasia, CA endometrium ^[1]
• Endometrial hyperplasia (with or without atypia) → overgrown, friable endometrium with abnormal vasculature
• Endometrial carcinoma → neovascularisation, tissue necrosis, friable surface → bleeding (often irregular or postmenopausal, but can present as HMB in premenopausal women)
• Cervical carcinoma: more typically IMB/PCB, but advanced disease can cause heavy irregular bleeding
• Must be considered in any woman > 40 with new-onset HMB or AUB not responding to treatment

• Uterine AVM ^[1] — arteriovenous malformation with high-flow shunting → can cause torrential bleeding; rare but important; often iatrogenic (post-curettage, post-C/S)
• C/S scar defect (isthmocele) ^[1] — a niche in the uterine scar traps blood → post-menstrual spotting/prolonged bleeding; increasingly recognised with rising C/S rates

• Coagulopathy: other bleeding symptoms, RFs, FHx ^[1]
• Especially if HMB since menarche (not likely if mid-reproductive age) ^[1]
• von Willebrand disease (vWD) is the most common inherited bleeding disorder — HMB occurs in 60–90% of women with vWD; 10–15% of women with HMB have vWD ^[4]
• Other coagulopathies: ITP, platelet function disorders, haemophilia carrier status, factor deficiencies ^[3]
• Acquired: anticoagulant/antiplatelet drugs, liver disease (↓clotting factor synthesis), renal disease (uraemic platelet dysfunction — ↑NO → inhibit platelet) ^[3]
• Approach: pattern of bleeding — platelet type (mucocutaneous: petechiae/purpura, epistaxis, menorrhagia) vs coagulation type (deep-seated: haemarthrosis, muscle haematoma, ICH) ^[3][5]

• Anovulation: e.g. start and end of reproductive life, PCOS ^[1]
• The old term "dysfunctional uterine bleeding (DUB)" encompasses this ^[1]
• In anovulatory DUB, there is disruption in HPO axis leading to chronic endometrial lining stimulation by estrogen, and is more common in extreme of reproductive ages ^[1]
• In ovulatory DUB, hormonal axis is normal but there is hemostatic and vasoconstrictive dysfunction in the endometrial lining ^[1]
• Causes: PCOS (most common in reproductive age), hypothalamic amenorrhoea, hyperprolactinaemia, thyroid disease, perimenopause, post-menarche
• Bleeding pattern: irregular, unpredictable, and often prolonged — this is a key distinguisher from structural causes

• Imbalance in local hemostasis factors (AUB-E): not a/w structural cause ^[1]
• Occur when ↑fibrinolytic, vasodilatory factors (e.g. prostaglandin, tPA) with ↓pro-thrombotic, vasoconstrictory factors (e.g. progesterone) ^[1]
• A diagnosis of exclusion — the endometrium's own haemostatic mechanisms are dysfunctional
• This is the pathophysiological rationale for why tranexamic acid (antifibrinolytic) works for HMB — it counteracts ↑tPA

• Copper IUCD due to foreign body reaction ^[1]
• Anticoagulants (warfarin, DOACs, heparin) and antiplatelets (aspirin, clopidogrel, NSAIDs)
• Hormonal contraceptives: unscheduled breakthrough bleeding from contraceptives ^[1]
• Tamoxifen: partial oestrogen agonist on endometrium → polyps, hyperplasia
• SSRIs: impair platelet serotonin uptake → ↓aggregation

• Chronic endometritis (e.g., PID)
• Endometriosis ^[1] — although classically causes dysmenorrhoea, it can contribute to HMB
• Myometrial hypertrophy
• Rare conditions

• Always exclude pregnancy in any woman of reproductive age with abnormal vaginal bleeding
• Early pregnancy: miscarriage (threatened, inevitable, incomplete, complete), ectopic pregnancy, molar pregnancy ^[1]
• Late pregnancy: bloody show (normal), placenta praevia, placental abruption ^[1]
• Mechanism: disruption of the pregnancy-endometrial interface or abnormal trophoblastic tissue

• Thyroid disease: most commonly a/w oligo-amenorrhoea ^[1] — but can also cause HMB
• Hypothyroidism → ↑TRH → ↑prolactin → anovulation → HMB; also affects coagulation factors and endometrial oestrogen/progesterone receptor expression
• Hyperthyroidism → can cause oligomenorrhoea or light periods (though relationship is variable)

• Hyperprolactinemia ^[1] — prolactin excess → suppresses GnRH pulsatility → anovulation → irregular and/or heavy bleeding
• Causes: prolactinoma, drugs (antipsychotics, metoclopramide), hypothyroidism, stalk effect

• Why: To exclude pregnancy → must be done (or document no unprotected sex) before EA ^[1]
• Rationale from first principles: any reproductive-age woman with abnormal vaginal bleeding could be pregnant. Threatened miscarriage, incomplete miscarriage, ectopic pregnancy, and gestational trophoblastic disease all present with vaginal bleeding. Performing endometrial sampling on a pregnant patient would be harmful.
• Interpretation: positive → redirect to pregnancy-related workup; negative → proceed with HMB investigation

• CBC: Hb, platelets ^[1]
• Why: to assess the consequence of HMB (anaemia) and screen for haematological causes
• Key findings and interpretation:

• Why: provides morphological information that CBC numbers alone cannot
• Key findings:
  • Pencil cells, anisopoikilocytosis ^[6] → iron deficiency
  • Target cells → thalassaemia trait (co-existing with IDA common in Hong Kong Chinese population)
  • Schistocytes → consider DIC, TTP (rare but serious)
  • Rule out platelet clumping (EDTA-induced pseudothrombocytopenia) ^[3]

This is the first-line imaging modality for structural assessment.

Pelvic US when suspect structural pathology ^[1]

• Suspicious of fibroids: uterus palpable abdominally, Hx/PE suggestive of pelvic mass, examination inconclusive or difficult ^[1]
• Suspicious of adenomyosis: TVUS for significant dysmenorrhoea, bulky tender uterus on PE ^[1]
• Transvaginal for small fibroid (< 12w) ^[1]
• Trans-abdominal for large fibroids (> 12w) ^[1]

Two approaches:

Key findings and interpretation:

Endometrial thickness assessment ^[1]:

• Post-menopausal women: endometrial thickness ≤ 4 mm → NPV 99.4–100% for endometrial carcinoma ^[1]
• At 4 mm cut-off: sensitivity 96%, specificity 53% ^[1]
• At 5 mm cut-off: sensitivity 96%, specificity 61% ^[1]
• Pre-menopausal women: endometrial thickness varies with the menstrual cycle (thinnest during menstruation ~1–4 mm, thickest in late secretory phase ~8–16 mm), so a single measurement is less useful

MRI: for complex OTs, planning for UAE or suspicious for sarcoma ^[1]

• When: second-line imaging when USS is inconclusive, when surgical planning requires precise mapping (e.g., multiple fibroids, laparoscopic myomectomy planning), when differentiating adenomyosis from fibroids, or when uterine sarcoma is suspected
• Advantages: superior soft tissue contrast; best for adenomyosis diagnosis (junctional zone thickening > 12 mm is diagnostic); precise fibroid mapping
• Key findings:
  • Fibroids: well-circumscribed, low T2 signal masses (dense smooth muscle)
  • Adenomyosis: junctional zone thickening > 12 mm, T2 low-signal thickening with bright T2 foci (ectopic glands)
  • Sarcoma: irregular margins, high T2 signal, necrosis, rapid growth, no calcification (contrast fibroids which have regular margins, low T2 signal, may calcify)

• Saline instilled into the uterine cavity during TVUS → outlines intracavitary lesions
• Alternative but NOT available in HK ^[1]
• Excellent for differentiating submucosal fibroids from polyps and for assessing degree of intracavitary protrusion

Endometrial aspirate/sampling (EA): a simple out-patient procedure ^[1]

What it is: a thin suction curette (e.g., Pipelle device) is passed through the cervical os into the uterine cavity to aspirate a sample of endometrial tissue for histopathological examination.

Indications ^[1]:

• Presence of RFs for endometrial pathology: e.g., obesity, PCOS, on tamoxifen, failed treatment ^[1]
• Age ≥ 40y with persistent IMB or irregular bleeding ^[1]
• Age ≥ 45y with regular heavy period ^[1]
• Abnormal Pap smear: AGC-endometrial (1st line), other AGC (with colposcopy), benign endometrial cells (if ≥ 45y + symptomatic or post-menopausal) ^[1]
• Monitoring in previous endometrial pathology or surveillance in high-risk (e.g., HNPCC/Lynch syndrome) ^[1]

Procedure ^[1]:

• To be done during speculum exam
• Insertion of endometrial suction curette to aspirate endometrial tissue
• Send for histopathology
• Can be completed in ~5 minutes without anaesthesia
• Must exclude pregnancy before EA ^[1]

Interpretation of histopathology:

Limitations:

• "Blind" procedure — may miss focal lesions (polyps, small submucosal fibroids)
• Sensitivity for endometrial cancer is ~90–99% (high but not perfect)
• Insufficient sample rate ~5–15%

Hysteroscopy ± endometrial biopsy: diagnostic and therapeutic ^[1]

What it is: direct visualisation of the uterine cavity using a small-calibre endoscope (typically 3 mm for diagnostic, 5–9 mm for operative) passed through the cervix.

Indications — superior to EA but limited availability ^[1]:

• Suspected endometrial polyp or submucosal fibroids ^[1]
• Irregular bleeding while on hormonal therapy for > 3 months ^[1]
• Endometrial aspirate failed or inconclusive ^[1]
• Diagnostic hysteroscopy: to aid planning and assess suitability for definitive hysteroscopic myomectomy (> 50% protrusion into cavity) ^[1]

Advantages over EA:

• Direct visualisation → can identify focal lesions (polyps, submucosal fibroids) that EA misses
• Targeted biopsy at suspicious endometrial sites ^[1]
• Therapeutic: removal of lesion, e.g., polyp ^[1], or submucosal fibroid resection

Setting ^[1]:

• Under GA or LA (out-patient procedure)

Key findings:

Tranexamic acid: oral Transamin 1g TDS up to 4 days, max 4g daily ^[1]

Name breakdown: "trans" = across, "examic" = from tranexamic acid, a synthetic lysine analogue. Think of it as blocking ("trans-locking") the fibrinolytic system.

Mechanism of Action (from first principles):

• During menstruation, the endometrium produces tissue plasminogen activator (tPA), which converts plasminogen → plasmin → dissolves fibrin clots
• In HMB, there is ↑fibrinolytic, vasodilatory factors (e.g., prostaglandin, tPA) ^[1] → clots at spiral artery stumps are prematurely dissolved → bleeding continues
• Tranexamic acid is a lysine analogue that binds to the lysine-binding sites on plasminogen → blocks plasminogen from binding to fibrin → inhibits fibrinolysis → clots are preserved → reduced blood loss
• It does NOT cause systemic hypercoagulability at therapeutic doses — it works locally at the site of clot formation

Efficacy: reduces menstrual blood loss by ~40–50%

Dosing: 1g TDS (three times daily) during menstruation only (up to 4 days, max 4g/day) ^[1]

Advantages:

• Non-hormonal → no hormonal side effects, does not affect fertility
• Taken only during menses (not continuously)
• Can be combined with hormonal treatments or NSAIDs

Contraindications:

• Active thromboembolic disease (DVT, PE, stroke)
• History of convulsions (rare risk of seizure at high doses)
• Subarachnoid haemorrhage (risk of cerebral vasospasm)
• Severe renal impairment (dose adjustment needed — renally excreted)

Side effects: GI (nausea, diarrhoea, abdominal pain) — generally well tolerated

± Mefenamic acid: oral Ponstan 250–500 mg TDS ^[1] Note: do NOT appear to ↓blood loss in fibroids but can ↓painful menses ^[1]

Mechanism of Action:

• NSAIDs inhibit cyclooxygenase (COX) enzymes → ↓prostaglandin synthesis
• In normal endometrium, HMB is associated with ↑PGE₂ (vasodilator) relative to PGF₂α (vasoconstrictor)
• By reducing overall prostaglandin production, NSAIDs:
  • ↓PGE₂ → ↓vasodilation → ↓blood loss
  • ↓PGF₂α too, but net effect is reduced blood loss (~20–30% reduction)
  • Also ↓myometrial contractions mediated by prostaglandins → ↓dysmenorrhoea

Dosing: Mefenamic acid (Ponstan) 250–500 mg TDS during menstruation

Efficacy: ~20–30% reduction in MBL — less effective than tranexamic acid or hormonal treatments

Key limitations: Does NOT appear to reduce blood loss in fibroid-related HMB ^[1] — why? Because fibroid-related HMB is primarily structural (increased surface area, venous ectasia, impaired myometrial contraction) rather than prostaglandin-mediated

Advantages:

• Also treats dysmenorrhoea (dual benefit in HMB + pain)
• Non-hormonal
• Can be combined with tranexamic acid

Contraindications:

• Active peptic ulcer disease
• Renal impairment
• Aspirin-sensitive asthma
• Pregnancy (especially 3rd trimester — risk of premature closure of ductus arteriosus)
• Known hypersensitivity

Combined OC pills: 1st line treatment unless C/I ^[1] Combined OC pills (COCP): 1st line unless C/I ^[1]

Mechanism of Action (from first principles):

• The COCP contains synthetic oestrogen (ethinylestradiol) + progestogen (e.g., levonorgestrel, desogestrel, drospirenone)
• MoA: provide exogenous ovarian hormones → suppress HPG axis → provide manual control over menstrual cycles ^[1]
• Suppresses endogenous FSH/LH → prevents follicular development and ovulation
• Creates a thin, stable, decidualised endometrium → less tissue to shed → lighter withdrawal bleed
• The progestogen component provides progesterone-like effects: stromal decidualisation, ↓endometrial proliferation, ↓local tPA and PGE₂

Efficacy: a/w 30% reduction in average monthly blood loss ^[1]

Forms ^[1]:

• Cyclic (monthly withdrawal bleed)
• Extended (one bleed every 3 months)
• Continuous (no scheduled breaks)
• Unscheduled breakthrough bleeding may be more common in extended/continuous regimen ^[1]

Advantages ^[1]:

• Make bleeding more regular, lighter (i.e., cycle + flow control)
• ↓Dysmenorrhoea
• Effective contraceptive
• ↓Ovarian cyst, benign breast lesions, PID, ovarian/endometrial CA

Side effects ^[1]:

• Minor: N/V, dizziness, breast tenderness, fluid retention, weight gain
• Breakthrough bleeding
• CVS risk: ↑risk of MI, stroke, thromboembolism
• Minimal ↑risk in breast and cervical CA

Contraindications ^[1]:

• Full breastfeeding: oestrogen affects milk production
• Thromboembolic risk: Hx of VTE, major surgery, prolonged immobilisation, first 21 days postpartum
• Age > 35 and smoking (> 15 cigarettes/day) — ↑risk of arterial events
• History of oestrogen-dependent cancer (breast cancer)
• Uncontrolled hypertension
• Migraine with aura (↑stroke risk)
• Active liver disease
• The UK MEC (Medical Eligibility Criteria) categorises these as Category 3 (relative) or 4 (absolute) contraindications

Levonorgestrel-releasing IUCD: alternative to COC pills ^[1] Mirena IUCD if fibroids < 3 cm with no cavity distortion ^[1]

Name breakdown: "Levonorgestrel" = a synthetic progestogen; "Intrauterine System" = device placed inside the uterus

Mechanism of Action:

• Releases levonorgestrel 20 μg/day locally into the uterine cavity
• Creates a profoundly decidualised, atrophic endometrium — very thin, with few glands and minimal vascularity
• ↓Local oestrogen receptor expression → endometrium becomes insensitive to circulating oestrogen
• ↓Local prostaglandin production and fibrinolytic activity
• Does NOT reliably suppress ovulation (only ~50% of cycles are anovulatory) — its action is primarily local

Efficacy: reduces MBL by ~90–95% — the most effective medical treatment for HMB. Comparable to endometrial ablation and approaches hysterectomy in satisfaction rates.

Duration: licensed for 5 years (8 years for contraception in some formulations, but 5 years for HMB indication)

Advantages:

• Highest efficacy of all medical treatments
• Long-acting (set and forget for 5 years)
• Effective contraception simultaneously
• Can be used in women with contraindications to oestrogen
• Reduces dysmenorrhoea
• Reduces risk of endometrial hyperplasia (can be used therapeutically for hyperplasia without atypia)

Limitations/Side effects:

• Initial irregular bleeding/spotting for first 3–6 months (counsel patients — this improves)
• Hormonal side effects (less systemic than COCP as action is mainly local): breast tenderness, mood changes, acne
• Functional ovarian cysts (~10%)
• Expulsion risk (~5%)

Contraindications:

• Fibroids > 3 cm or with cavity distortion ^[1] — the device may not sit properly, higher expulsion risk, and large submucosal fibroids physically prevent insertion
• Active PID or cervicitis (insert after treatment)
• Unexplained uterine bleeding (must exclude malignancy first)
• Cervical or endometrial cancer
• Pregnancy

Mirena if fibroids < 3 cm with no cavity distortion ^[1] — this is a practical and commonly tested point

High-dose progestogen: when C/I to COC pills ^[1] Cyclical oral progestogens: e.g., Primolut N (norethisterone) 5 mg TDS on day 5–26 of each cycle ^[1]

Mechanism of Action:

• Provides exogenous progesterone → opposes endometrial proliferation → creates a decidualised, stable endometrium
• Withdrawal of progestogen at end of each treatment period → orderly, synchronised shedding → lighter, more predictable bleed
• Also suppresses HPG axis at higher doses → anovulation

Dosing: Norethisterone (Primolut N) 5 mg TDS, days 5–26 of each cycle ^[1]

• Note: short-course luteal-phase-only progestogens (days 15–26) are LESS effective than long-course (days 5–26)

Efficacy: ~80–87% reduction in MBL with long-course regimen

Indications: When COCP is contraindicated (e.g., VTE risk) or LNG-IUS is not suitable

Side effects: bloating, breast tenderness, mood changes, acne, weight gain, irregular bleeding

Contraindications: Active liver disease, history of liver tumours, pregnancy, undiagnosed vaginal bleeding

Important note: At high doses, norethisterone is partially converted to ethinylestradiol in the liver → retains some oestrogenic (and therefore thrombogenic) activity → not entirely "oestrogen-free" at doses > 5 mg/day

• Depot medroxyprogesterone acetate (DMPA / Depot Provera): 150 mg IM every 12 weeks
• Suppresses HPG axis → anovulation; causes endometrial atrophy
• Effective at reducing HMB but return of fertility can be delayed (up to 12–18 months after last injection)
• Side effects: irregular bleeding initially (then amenorrhoea in ~50% by 1 year), weight gain, ↓bone mineral density with prolonged use (reversible)
• Used in adenomyosis management ^[1]

GnRH agonists or antagonists: usually for pre-operative ↓size before hysteroscopic resection ^[1]

Name breakdown: GnRH = gonadotrophin-releasing hormone; "agonist" = initially stimulates, then desensitises

Mechanism of Action:

• GnRH agonists (e.g., leuprolide, goserelin, triptorelin) → initially cause a "flare" effect (↑FSH/LH) → then downregulate GnRH receptors on the anterior pituitary → profound ↓FSH/LH → medical menopause
• ↓Oestrogen → endometrial atrophy, ↓fibroid size (by ~30–50%), amenorrhoea
• GnRH antagonists (e.g., elagolix, relugolix, linzagolix) → immediately suppress FSH/LH without flare

MoA: desensitisation → medically induce menopause → ↓size of fibroid, ↓menstrual-related symptoms ^[1]

Efficacy: very effective at inducing amenorrhoea and ↓fibroid volume

Limitations ^[1]:

• Rapid relapse following discontinuation
• Significant climacteric symptoms with menopause-related side effects (e.g., bone density)
• Therefore NOT for long-term use ^[1] — typically limited to 3–6 months
• Can be extended with "add-back" HRT (low-dose oestrogen + progestogen) to mitigate menopausal symptoms and bone loss

Side effects ^[1]: Irregular bleeding, URTI symptoms, hot flushes, vaginal dryness, ↓bone mineral density, mood changes

Indications: primarily pre-operative — to shrink fibroids before surgery (myomectomy or hysterectomy), improve haemoglobin pre-operatively, or bridge to menopause

Progesterone receptor modulators: e.g., ulipristal acetate, mifepristone ^[1] MoA: modulate progestogen receptor in myoma tissues → ↓size of fibroids ^[1] S/E: risk of endometrial changes (mimic endometrial hyperplasia but ?long-term consequences), liver toxicity (in ulipristal) ^[1] NOT available for use in HK ^[1]

Note: Ulipristal acetate (Esmya) was widely used in Europe but was restricted in 2020 due to rare but serious liver injury. It has been largely withdrawn. Not available in HK ^[1].

• Removal of endometrial polyps under direct visualisation
• Diagnostic and therapeutic in one procedure
• Polyp can be observed (1/4 chance to spontaneously resolve if < 1 cm) ^[1]

Diagnostic hysteroscopy: to aid planning and assess suitability for definitive hysteroscopic myomectomy (> 50% protrusion into cavity) ^[1]

• Indicated for submucosal fibroids (FIGO types 0, 1, and selected type 2) with > 50% intracavitary protrusion
• Resectoscope inserted transcervically → fibroid shaved using electrocautery loop
• Preserves fertility
• Pre-operative GnRH agonist may be used to shrink fibroid and ↓endometrial thickness → easier resection

• Principle: destruction of the endometrium (functionalis AND basalis) → ↓or eliminates menstrual bleeding
• Methods: thermal balloon (Thermachoice), radiofrequency (NovaSure), microwave, rollerball, resectoscope
• Efficacy: ~80–90% have significant reduction in bleeding; ~30–40% achieve amenorrhoea
• Indications:
  • HMB refractory to medical treatment
  • Completed childbearing — pregnancy after ablation is dangerous (↑risk of placenta accreta, uterine rupture)
  • Uterine cavity not significantly distorted (normal cavity or small intramural fibroids)
• Contraindications:
  • Desire for future fertility
  • Suspected or confirmed endometrial malignancy
  • Active PID
  • Previous classical caesarean section or myomectomy with uterine cavity entry (thinned myometrium → perforation risk)
  • Large cavity (> 12 cm) — reduces efficacy
• Post-procedure contraception: required because ablation is NOT a reliable contraceptive