Heavy Menstrual Bleeding (hmb)
Heavy menstrual bleeding is excessive menstrual blood loss (>80 mL per cycle) that interferes with a woman's physical, social, emotional, or material quality of life.
Heavy Menstrual Bleeding (HMB)
1. Definition
Heavy Menstrual Bleeding (HMB) — let's break the name down:
- "Menstrual" = relating to menses (Latin: month) — the cyclical shedding of the endometrium
- "Heavy" = exceeding a clinically significant threshold of blood loss
- "Bleeding" = haemorrhage from the uterine cavity
HMB is defined as excessive menstrual blood loss (MBL) that interferes with a woman's physical, social, emotional, and/or material quality of life. [1]
This is the modern NICE (2018/2024) and FIGO (2011, updated 2018) definition. It deliberately moves away from the old quantitative cut-off of > 80 mL per cycle (which was based on the alkaline haematin method and was impractical in clinical practice). The key philosophical shift is that the woman herself decides what is "heavy" — if it impacts her quality of life, it warrants investigation and treatment.
Why 80 mL historically?
The 80 mL threshold was derived from population studies showing that women losing > 80 mL/cycle were at significantly increased risk of iron deficiency anaemia (IDA). However, many women losing < 80 mL still report significant impact on quality of life, and some losing > 80 mL are asymptomatic. Hence the shift to a subjective, patient-centred definition.
| Old Term | Modern Preferred Term | Notes |
|---|---|---|
| Menorrhagia | Heavy menstrual bleeding (HMB) | "Menorrhagia" still widely used clinically but FIGO discourages it |
| Metrorrhagia | Intermenstrual bleeding (IMB) | Bleeding between periods |
| Menometrorrhagia | HMB + IMB | Heavy and irregular |
| Polymenorrhoea | Frequent menstrual bleeding | Cycle < 21 days |
| Oligomenorrhoea | Infrequent menstrual bleeding | Cycle > 35 days |
| Dysfunctional uterine bleeding (DUB) | Abnormal uterine bleeding (AUB) — ovulatory dysfunction subtype | "DUB" is outdated; replaced by the PALM-COEIN system |
FIGO now uses the umbrella term "Abnormal Uterine Bleeding" (AUB) and classifies causes using the PALM-COEIN system. HMB is one presentation pattern within AUB. [1]
To understand what is "abnormal," you must know normal:
| Parameter | Normal Range |
|---|---|
| Cycle length | 24–38 days (FIGO 2018) |
| Duration of flow | ≤ 8 days |
| Volume of blood loss | 5–80 mL per cycle (average ~30–40 mL) |
| Regularity | Variation of ≤ 7–9 days cycle-to-cycle |
2. Epidemiology
- HMB affects approximately 10–30% of women of reproductive age worldwide [2]
- In Hong Kong, it is one of the most common gynaecological complaints presenting to outpatient clinics
- Prevalence peaks in the perimenopausal period (40–50 years) — why? Because anovulatory cycles become more frequent as ovarian reserve declines, leading to unopposed oestrogen stimulation of the endometrium
- Also common at the extremes of reproductive life: shortly after menarche (immature HPO axis → anovulation) and approaching menopause
- Leading cause of iron deficiency anaemia in premenopausal women [3]
- Accounts for a significant proportion of hysterectomies — historically up to 60% of hysterectomies were performed for HMB
- Substantial economic burden: lost work days, cost of sanitary products, medical consultations
- High prevalence of uterine fibroids (leiomyomas) in Chinese women — a major structural cause of HMB
- Endometrial cancer screening awareness is increasing but cervical screening uptake is still suboptimal
- Adenomyosis is increasingly recognised with improved MRI and transvaginal ultrasound availability
3. Risk Factors
Think of these by category:
- Extremes of reproductive age (adolescence and perimenopause) — anovulatory cycles
- Uterine fibroids — especially submucosal fibroids (distort the endometrial cavity → increased surface area + impaired haemostatic mechanisms)
- Adenomyosis — ectopic endometrial glands within the myometrium → uterine enlargement, impaired contractility
- Endometrial polyps — focal overgrowths of endometrial tissue
- Pelvic inflammatory disease (PID) — chronic endometritis
- Intrauterine contraceptive device (IUCD/copper IUD) — increases menstrual blood loss by 20–50% (mechanism: local inflammatory reaction, increased prostaglandin production → vasodilation and impaired haemostasis)
- Nulliparity is sometimes cited, though parity effects are complex
- Coagulation disorders: von Willebrand disease (vWD) is present in 10–15% of women with HMB [3], inherited platelet function disorders, haemophilia carrier status
- Hypothyroidism — thyroid hormone influences endometrial physiology and coagulation factor levels
- Liver disease — impaired clotting factor synthesis and oestrogen metabolism
- Chronic kidney disease — uraemic platelet dysfunction
- Obesity — peripheral aromatisation of androgens to oestrogen in adipose tissue → relative oestrogen excess → endometrial hyperplasia
- Anticoagulant therapy (warfarin, DOACs, heparin)
- Antiplatelet agents (aspirin, clopidogrel)
- Copper IUD (as above)
- Tamoxifen — acts as partial oestrogen agonist on endometrium → polyps, hyperplasia, and rarely carcinoma
- Hormonal contraceptive issues — breakthrough bleeding with progestogen-only methods
4. Anatomy and Physiology of Normal Menstruation
Understanding HMB requires a solid grasp of uterine anatomy and the physiology of menstruation. Let me walk you through this from first principles.
The uterus is a hollow, thick-walled muscular organ:
- Endometrium (inner mucosal layer):
- Functionalis — the superficial 2/3 that is shed during menstruation. It is the hormonally responsive layer.
- Basalis — the deep 1/3 that is NOT shed; it serves as the regenerative reservoir for the functionalis after menstruation.
- Myometrium (muscular layer): three layers of smooth muscle — critical for:
- Uterine contractions during menstruation (helps expel menstrual debris and compress blood vessels)
- Postpartum haemostasis ("living ligature" concept)
- Serosa/Perimetrium (outermost layer)
- Uterine arteries (branches of internal iliac arteries) → arcuate arteries (run circumferentially in the outer myometrium) → radial arteries (penetrate inward through the myometrium) → branch into:
- Straight arteries (arteriolae rectae) — supply the basalis (do NOT undergo cyclical changes)
- Spiral arteries (arteriolae spirales) — supply the functionalis and are THE key players in menstruation
The spiral arteries are unique:
- They are exquisitely responsive to ovarian hormones (oestrogen and progesterone)
- During the secretory phase, they become increasingly coiled under the influence of progesterone
- When progesterone is withdrawn (corpus luteum regression), spiral arteries undergo intense vasoconstriction → tissue ischaemia → necrosis of the functionalis → shedding = menstruation
4.3 The Menstrual Cycle — Endometrial Perspective
- 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:
- Spiral artery vasoconstriction → ischaemia → tissue necrosis
- Release of prostaglandins (PGF₂α and PGE₂) from the ischaemic endometrium → promote vasoconstriction initially, then vasodilation and myometrial contractions
- Release of matrix metalloproteinases (MMPs) → enzymatic breakdown of extracellular matrix → detachment of functionalis
- 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
Key Concept: Why Does HMB Occur?
HMB results from disruption of any of these haemostatic mechanisms:
- Increased endometrial surface area (e.g., fibroids, polyps)
- Impaired myometrial contraction (e.g., adenomyosis, fibroids distorting myometrium)
- Abnormal endometrial haemostasis (e.g., increased local fibrinolysis, altered prostaglandin ratios — ↑PGE₂:PGF₂α ratio → more vasodilation)
- Abnormal hormone-driven endometrial growth (e.g., anovulation → unopposed oestrogen → thick, fragile endometrium that sheds irregularly)
- Systemic coagulopathy (e.g., vWD, anticoagulant use)
5. Aetiology (with Pathophysiology)
This is THE classification system for causes of AUB in reproductive-age women. It is both an acronym and a mnemonic.
The PALM-COEIN system divides causes into Structural (PALM) and Non-structural (COEIN). [1]
| Letter | Category | Structural? |
|---|---|---|
| P | Polyp | Structural |
| A | Adenomyosis | Structural |
| L | Leiomyoma (fibroid) | Structural |
| M | Malignancy & hyperplasia | Structural |
| C | Coagulopathy | Non-structural |
| O | Ovulatory dysfunction | Non-structural |
| E | Endometrial | Non-structural |
| I | Iatrogenic | Non-structural |
| N | Not yet classified | Non-structural |
Let's go through each one systematically.
Definition: Localised overgrowths of endometrial glands and stroma, forming a polypoid mass projecting into the uterine cavity.
Pathophysiology:
- Polyps are oestrogen-sensitive — they arise from monoclonal proliferation of endometrial stromal cells
- They increase the endometrial surface area → more tissue to bleed from
- They have aberrant vasculature (thick-walled vessels with poor contractile ability) → impaired local haemostasis
- Large polyps may undergo surface erosion and ulceration → irregular bleeding/spotting
- Polyps may interfere with normal endometrial shedding — acting as a physical "plug" that prevents complete shedding, leading to prolonged/irregular bleeding
Epidemiology:
- Found in 10–40% of women with AUB
- Prevalence increases with age, peaking in the 5th decade
- Risk factors: obesity, tamoxifen use, oestrogen exposure, hypertension
Clinical pattern: Often causes intermenstrual bleeding (IMB) or postmenstrual spotting rather than classically heavy cyclical bleeding, but can contribute to HMB.
Definition: Presence of endometrial glands and stroma within the myometrium (at least 2.5 mm deep from the endomyometrial junction, or > one low-power field).
Breaking down the word: "adeno" = gland, "myo" = muscle, "-osis" = condition → a condition of glands within muscle.
Pathophysiology — why does adenomyosis cause HMB?
- Uterine enlargement → increased endometrial surface area
- Impaired myometrial contractility — islands of ectopic endometrial tissue within the myometrium disrupt the orderly contraction of smooth muscle fibres → cannot compress intramural blood vessels effectively → prolonged/heavy bleeding
- Altered local haemostatic environment — ectopic endometrial tissue produces increased local prostaglandins, MMPs, and angiogenic factors
- Increased vascularity — angiogenesis around ectopic foci
- Dysmenorrhoea is very characteristic — because the ectopic tissue within the myometrium undergoes cyclical swelling under hormonal influence, causing pain
Epidemiology:
- Historically diagnosed only on hysterectomy specimens (prevalence 20–35%)
- With improved imaging (MRI, high-resolution TVUSS), increasingly diagnosed non-invasively
- More common in women aged 40–50, multiparous women, and those with prior uterine surgery (C-section, curettage)
Definition: Benign monoclonal neoplasms of uterine smooth muscle cells (myocytes), surrounded by a pseudocapsule of compressed myometrium.
Breaking down the word: "leio" = smooth, "myo" = muscle, "-oma" = tumour → tumour of smooth muscle.
Epidemiology:
- Most common pelvic tumour in women [1]
- Lifetime incidence: up to 70–80% by age 50 (higher in Black/African women)
- In Hong Kong/Chinese populations: very common, frequently encountered in O&G clinics
- Risk factors: early menarche, nulliparity, obesity, family history, Black ethnicity
- Protective: combined oral contraceptive pill (COCP), smoking (anti-oestrogenic effect)
Pathophysiology — why do fibroids cause HMB?
The key is location, not just size:
FIGO Leiomyoma Sub-classification System [1]:
| Type | Location | Description |
|---|---|---|
| 0 | Submucosal - pedunculated intracavitary | Entirely within cavity on a stalk |
| 1 | Submucosal | ≥ 50% intracavitary |
| 2 | Submucosal | < 50% intracavitary (≥ 50% intramural) |
| 3 | Intramural | Contacts endometrium; 100% intramural |
| 4 | Intramural | Does not contact endometrium |
| 5 | Subserosal | ≥ 50% intramural |
| 6 | Subserosal | < 50% intramural |
| 7 | Subserosal - pedunculated | Entirely subserosal on a stalk |
| 8 | Other | Cervical, parasitic, broad ligament |
Submucosal fibroids (Types 0, 1, 2) are the most likely to cause HMB. Even a small submucosal fibroid can cause significant HMB, while a large subserosal fibroid may cause no bleeding at all.
Mechanisms by which fibroids cause HMB:
- Increased endometrial surface area — submucosal fibroids distort and expand the cavity
- Impaired myometrial contractility — intramural fibroids interfere with the "living ligature" mechanism
- Venous ectasia — fibroids compress venous drainage → congestion of the overlying endometrium → fragile, engorged vessels that bleed easily
- Altered local vasoactive mediators — endometrium overlying fibroids has increased VEGF, altered prostaglandin ratios (↑PGE₂, ↓PGF₂α), and increased fibrinolytic activity
- Ulceration of overlying endometrium in submucosal fibroids → direct bleeding source
Endometrial hyperplasia and endometrial carcinoma must ALWAYS be considered in the differential, especially in:
- Women > 40 years with HMB [1]
- Perimenopausal/postmenopausal women
- Women with risk factors for unopposed oestrogen exposure: obesity, PCOS, tamoxifen, nulliparity, late menopause, oestrogen-only HRT
Pathophysiology:
- Chronic unopposed oestrogen stimulation → endometrial proliferation without progesterone-induced differentiation → endometrial hyperplasia (with or without atypia)
- Hyperplasia without atypia: ~1–3% progression to carcinoma over 20 years
- Atypical hyperplasia: ~25–30% progression to endometrial carcinoma [1]
- Endometrial carcinoma: abnormal neovascularisation, friable tissue → HMB or IMB or postmenopausal bleeding (PMB)
Classification of endometrial hyperplasia (WHO 2014/2020):
- Hyperplasia without atypia — low risk of progression
- Atypical hyperplasia / Endometrioid Intraepithelial Neoplasia (EIN) — high risk of progression; often coexists with or harbours early carcinoma
Other malignancies to consider:
- Cervical carcinoma (typically presents with IMB, postcoital bleeding)
- Uterine sarcoma (rare; leiomyosarcoma)
- Gestational trophoblastic disease
Red Flags for Malignancy in HMB
Always exclude malignancy in:
- Age > 40 with new-onset HMB
- Any postmenopausal bleeding
- HMB not responding to medical treatment
- Irregular, non-cyclical bleeding pattern
- Risk factors: obesity, PCOS, tamoxifen, family history (Lynch syndrome)
5.5 C — Coagulopathy (AUB-C)
Definition: Systemic disorders of haemostasis that manifest as HMB.
This is a frequently underdiagnosed cause. Studies suggest that 10–20% of women presenting with HMB have an underlying bleeding disorder [3].
Key conditions:
- 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
Definition: HMB occurring in the context of disordered ovulation (anovulation or oligo-ovulation).
This is the modern replacement for the old term "dysfunctional uterine bleeding (DUB)".
Pathophysiology — this is critical to understand:
- In a normal ovulatory cycle, oestrogen drives proliferation and then progesterone from the corpus luteum stabilises and organises the endometrium, producing a synchronised, orderly shedding
- In anovulation: no corpus luteum → no progesterone → unopposed oestrogen
- Result:
- Endometrium keeps proliferating under oestrogen → becomes thick, fragile, and disorganised
- Without progesterone-induced organisation, the endometrium has unstable vasculature and inadequate structural support
- Eventually, the endometrium outgrows its blood supply or random areas undergo focal breakdown → irregular, unpredictable, and often heavy bleeding
- The bleeding is often prolonged because there is no coordinated progesterone withdrawal to produce a synchronised shed
Causes of anovulation (focus on Hong Kong):
- PCOS — most common cause in reproductive-age women; hyperandrogenism + oligo-anovulation + polycystic ovarian morphology
- Hypothalamic-pituitary dysfunction: stress, excessive exercise, eating disorders, hyperprolactinaemia
- Thyroid disorders: hypothyroidism (→ ↑TRH → ↑prolactin → anovulation; also altered coagulation factor levels), hyperthyroidism
- Perimenopause: declining ovarian reserve → irregular folliculogenesis → anovulatory cycles
- Adolescence: immature HPO axis → anovulation in first 2–3 years post-menarche
Clinical pattern: Irregular timing and flow — distinguishes it from structural causes which tend to cause regular but heavy cycles.
Definition: HMB occurring in the context of a primary disorder of the endometrial haemostatic mechanisms, in the absence of structural or systemic causes.
This is essentially a diagnosis of exclusion — the endometrium itself has disordered local regulation of haemostasis.
Pathophysiology:
- Increased local fibrinolysis (↑tissue plasminogen activator, tPA) → clots that form at spiral artery stumps are prematurely dissolved
- Altered prostaglandin ratio: ↑PGE₂ (vasodilator) and ↓PGF₂α (vasoconstrictor) → net vasodilation → increased blood loss
- Increased production of matrix metalloproteinases (MMPs) → excessive tissue breakdown
- Deficient endothelin-1 (potent vasoconstrictor) production
- Reduced endometrial repair mechanisms
This is why tranexamic acid (an antifibrinolytic) is so effective for HMB — it counteracts the increased local fibrinolysis.
Definition: HMB caused by medical interventions.
Key causes:
- Copper IUD — increases menstrual blood loss by 20–50% through local inflammatory reaction → ↑prostaglandin production → vasodilation + impaired haemostasis
- Anticoagulants: warfarin, DOACs (rivaroxaban, apixaban, dabigatran), heparin
- Antiplatelet agents: aspirin, clopidogrel
- Hormonal breakthrough bleeding: progestogen-only contraceptives, DMPA (depot medroxyprogesterone acetate), subdermal implants, hormonal IUS during the first 3–6 months
- Tamoxifen: partial oestrogen agonist on endometrium → polyps, hyperplasia
- SSRIs: may affect platelet function (platelets take up serotonin via SERT; SSRIs block this → impaired platelet aggregation)
- Corticosteroids: affect vascular integrity
- Chemotherapy: bone marrow suppression → thrombocytopenia
Conditions that don't fit neatly into the above categories:
- Chronic endometritis (e.g., from PID — particularly Chlamydia trachomatis)
- Arteriovenous malformations (AVMs) of the uterus
- Isthmocele (caesarean section scar defect) — pooling of blood in the niche → post-menstrual spotting
- Myometrial hypertrophy
- Rare conditions
6. Classification
6.1 FIGO PALM-COEIN (as above)
| Pattern | Description | Common Causes |
|---|---|---|
| Heavy cyclical (regular) | Heavy but predictable periods | Fibroids, adenomyosis, coagulopathy, endometrial causes |
| Heavy irregular | Unpredictable heavy bleeding | Ovulatory dysfunction, polyps, malignancy |
| Intermenstrual | Between periods | Polyps, cervical pathology, hormonal contraception |
| Postcoital | After intercourse | Cervical ectropion, cervical polyp, cervical carcinoma, cervicitis |
| Postmenopausal | After 12 months amenorrhoea | Endometrial carcinoma until proven otherwise |
| Age Group | Most Common Causes |
|---|---|
| Adolescent (< 20) | Anovulation (immature HPO axis), coagulopathy (esp. vWD), pregnancy complications |
| Reproductive age (20–40) | Fibroids, polyps, adenomyosis, hormonal contraception, pregnancy-related |
| Perimenopausal (40–menopause) | Anovulation, fibroids, polyps, endometrial hyperplasia/malignancy |
| Postmenopausal | Endometrial atrophy, endometrial carcinoma, polyps, HRT-related |
7. Clinical Features
7.1 Symptoms
| Symptom | Pathophysiological Basis |
|---|---|
| Prolonged menstrual bleeding (> 8 days) | Delayed endometrial repair; anovulatory cycles produce disorganised endometrium that sheds irregularly |
| Passage of clots | Normal menstrual blood does not clot due to local fibrinolysis (tPA); when blood loss exceeds fibrinolytic capacity, clots form → indicates heavy flow |
| Flooding (soaking through protection) | Flow rate exceeds absorption capacity; suggests significant volume loss |
| Need to use double protection (pad + tampon simultaneously) | Suggestive of HMB; frequently used as a clinical marker |
| Menstrual "accidents" (staining clothing/bedsheets) | Unpredictable heavy flow overwhelms protection |
| Restriction of daily activities due to periods | Direct criterion in the modern definition of HMB |
| Symptom | What It Suggests | Pathophysiological Basis |
|---|---|---|
| Dysmenorrhoea (painful periods) | Adenomyosis, fibroids, endometriosis | Adenomyosis: ectopic endometrial tissue within myometrium swells cyclically → pain; Fibroids: distortion + ischaemia; Prostaglandin excess → myometrial hypercontractility |
| Intermenstrual bleeding | Polyps, cervical pathology, malignancy | Polyps: surface erosion; Malignancy: friable neovascularisation |
| Postcoital bleeding | Cervical pathology (ectropion, polyp, carcinoma, cervicitis) | Fragile cervical epithelium/vessels disrupted by trauma |
| Pelvic pressure/heaviness | Large fibroids, adenomyosis | Mass effect of enlarged uterus on pelvic floor |
| Urinary frequency | Anterior uterine fibroid | Fibroid compresses bladder anteriorly |
| Constipation | Posterior fibroid | Fibroid compresses rectum |
| Abdominal distension | Large fibroids | Physical enlargement of uterus |
| Dyspareunia (deep) | Adenomyosis, endometriosis, fibroids | Tender, enlarged, or fixed uterus |
| Irregular cycle | Ovulatory dysfunction (PCOS, perimenopause) | Anovulation → no regular progesterone withdrawal |
| Galactorrhoea | Hyperprolactinaemia | Prolactin excess → anovulation + stimulates breast secretion |
| Hirsutism, acne | PCOS | Hyperandrogenism |
| Easy bruising, epistaxis, bleeding gums | Coagulopathy (vWD, ITP, platelet disorders) | Systemic haemostatic defect → mucocutaneous bleeding pattern |
| Weight gain, cold intolerance, constipation | Hypothyroidism | Thyroid hormone deficiency affects endometrial physiology and coagulation |
| Hot flushes, night sweats | Perimenopause | Declining oestrogen → vasomotor instability |
| Symptom | Pathophysiological Basis |
|---|---|
| Fatigue, weakness, exercise intolerance | Iron deficiency anaemia from chronic blood loss → ↓haemoglobin → ↓oxygen-carrying capacity |
| Breathlessness on exertion | Compensatory ↑cardiac output in anaemia fails to meet oxygen demands during activity |
| Palpitations | Hyperdynamic circulation (↑stroke volume, ↑heart rate) to compensate for anaemia |
| Pica / pagophagia (craving ice) | Iron deficiency — mechanism not fully understood but specific to IDA |
| Dizziness, lightheadedness | Reduced cerebral oxygenation in severe anaemia |
| Reduced quality of life, anxiety, depression | Direct impact of heavy bleeding on daily functioning, social embarrassment |
| Subfertility | Submucosal fibroids distorting cavity, anovulation, endometrial polyps |
7.2 Signs
| Sign | Pathophysiological Basis |
|---|---|
| Pallor (conjunctival, palmar crease, nail bed) | Iron deficiency anaemia → ↓haemoglobin → ↓red colour of blood → pale mucous membranes |
| Koilonychia (spoon-shaped nails) | Severe iron deficiency → impaired nail matrix keratinisation |
| Glossitis (smooth, red tongue) | Iron deficiency → atrophy of tongue papillae (rapidly dividing cells sensitive to iron deficiency) |
| Angular cheilitis (cracks at mouth corners) | Iron deficiency → epithelial thinning and secondary infection |
| Tachycardia | Compensatory response to anaemia — ↑heart rate to maintain cardiac output |
| Flow murmur (systolic ejection murmur) | Hyperdynamic, low-viscosity blood flow across normal valves in anaemia |
| Peripheral oedema (severe cases) | High-output cardiac failure in severe/prolonged anaemia |
| Obesity | Risk factor for HMB (peripheral aromatisation → oestrogen excess); also associated with PCOS |
| Hirsutism, acne | Hyperandrogenism → consider PCOS |
| Bruising, petechiae, purpura | Coagulopathy — platelet-type bleeding pattern |
| Thyroid enlargement | Thyroid disease contributing to HMB |
| Sign | Pathophysiological Basis |
|---|---|
| Palpable pelvic/abdominal mass arising from pelvis | Large fibroid uterus (if > 12-week size, palpable abdominally) |
| Mass does not go below pubic symphysis ("can't get below it") | Arises from pelvis — classical for uterine or ovarian mass |
| Firm, irregular mass | Fibroids — multiple, firm, well-defined nodules |
| Tender suprapubic area | Adenomyosis, endometritis, PID |
| Sign | Pathophysiological Basis |
|---|---|
| Uniformly enlarged, "boggy", globular, tender uterus | Adenomyosis — diffuse infiltration of myometrium with ectopic endometrial tissue → symmetrical uterine enlargement with tenderness |
| Irregularly enlarged, firm, non-tender uterus | Fibroids — asymmetric nodular enlargement |
| Cervical polyp visible on speculum | Endocervical polyp prolapsing through os |
| Cervical mass/lesion | Cervical carcinoma, cervical ectropion |
| Cervical excitation tenderness | PID → peritoneal inflammation → pain on cervical motion |
| Adnexal mass/tenderness | Ovarian pathology, tubo-ovarian abscess (PID) |
| Blood in the vaginal fornices | Active uterine bleeding |
| Uterine enlargement not explained by fibroids | Adenomyosis, pregnancy (always exclude!) |
ALWAYS Exclude Pregnancy
In ANY woman of reproductive age presenting with abnormal vaginal bleeding, pregnancy MUST be excluded first. This means:
- Urine or serum β-hCG
- Consider ectopic pregnancy, threatened/incomplete miscarriage, gestational trophoblastic disease Even if the patient says she cannot be pregnant — test anyway.
Pictorial Blood Assessment Chart (PBAC)
A semi-objective tool where women record the number and degree of soaking of pads/tampons and passage of clots:
- Score ≥ 100 correlates with MBL > 80 mL (sensitivity ~80%, specificity ~80%)
- Useful for clinical trials and monitoring treatment response
- Not routinely used in practice but worth knowing
A structured approach:
- Menstrual history: age of menarche, cycle regularity, duration of flow, volume (pads/day, clots, flooding, double protection), LMP
- Associated symptoms: dysmenorrhoea, IMB, postcoital bleeding, pelvic pain/pressure, urinary/bowel symptoms
- Reproductive history: parity, pregnancies, desire for future fertility (crucial for management planning)
- Contraceptive history: current and past methods, especially IUD
- Smear history: last cervical screening, any abnormal results
- Systemic bleeding history: easy bruising, epistaxis, bleeding after dental work, family history of bleeding disorders
- Medical history: thyroid disease, liver/renal disease, PCOS, obesity
- Drug history: anticoagulants, antiplatelets, hormonal therapy, SSRIs
- Family history: fibroids, endometrial/ovarian/breast cancer, bleeding disorders
- Social history: impact on quality of life, work, relationships, sexual function
- Red flags: postmenopausal bleeding, intermenstrual bleeding > 40 years, weight loss, suspicious cervical appearance
High Yield Summary
Definition: HMB = excessive menstrual blood loss that interferes with physical, social, emotional, and/or material quality of life (NICE/FIGO — patient-centred, subjective definition). Old quantitative threshold was > 80 mL/cycle.
Normal menstruation: Cycle 24–38 days, flow ≤ 8 days, volume 5–80 mL. Controlled by spiral artery vasoconstriction, prostaglandin balance, local fibrinolysis, myometrial contraction, and endometrial regeneration.
PALM-COEIN Classification: Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia (structural) | Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified (non-structural).
Key pathophysiology of HMB: ↑endometrial surface area (fibroids, polyps), impaired myometrial contraction (adenomyosis, fibroids), altered local haemostasis (↑fibrinolysis, ↑PGE₂, ↓PGF₂α), unopposed oestrogen (anovulation → thick fragile endometrium), systemic coagulopathy (vWD in 10–15% of HMB).
Submucosal fibroids (FIGO types 0–2) are the fibroids most likely to cause HMB — location matters more than size.
vWD is present in 10–15% of women with HMB — screen if HMB since menarche + mucocutaneous bleeding symptoms.
Always exclude pregnancy in reproductive-age women and malignancy in women > 40 or with risk factors.
Adenomyosis: "boggy", globularly enlarged, tender uterus on examination. Fibroids: irregularly enlarged, firm, non-tender uterus.
Active Recall - HMB: Definition, Epidemiology, Aetiology, Pathophysiology, Clinical Features
[1] Lecture slides: Adrian Lui Gynecology Notes.pdf; Block C - O&G Theme Case 2.docx.pdf [2] Senior notes: Maksim Medicine Notes.pdf (p170 — myeloproliferative neoplasms/erythrocytosis, for systemic causes context) [3] Senior notes: Ryan Ho Haemtology.pdf (p17, p113–114, p117, p122–128, p137–138 — iron deficiency anaemia, bleeding disorders approach, vWD, haemophilia, DIC)
Differential Diagnosis of Heavy Menstrual Bleeding (HMB)
The approach to the differential diagnosis of HMB requires you to think systematically. The key question at the bedside is: Is this heavy menstrual bleeding arising from a structural uterine cause, a non-structural/functional cause, or something that is not actually uterine at all?
Let me walk you through this logically, the way you would think on a clinical attachment.
Before diving into differential diagnoses for HMB, you must first establish that the bleeding is genuinely from the uterus. This seems obvious but is a surprisingly common pitfall.
Is the bleeding from uterus? [1]
- Heavy bleeding usually from uterus [1]
- Staining, spotting, light bleeding may be from any genital tract site [1]
- Brown implies old blood from light bleeding/spotting from anywhere from upper vagina to uterus [1]
- Red can be from any genital tract sources [1]
- Non-genital?: any urinary/bowel symptoms? Only seen upon wiping/when going to toilet? [1]
Think about it: a woman says she is "bleeding heavily." Where could it come from?
- Uterine — most likely in true HMB
- Cervical — cervicitis, polyp, ectropion, carcinoma (usually postcoital or intermenstrual, not classically heavy cyclical)
- Vaginal — atrophic vaginitis, lacerations, vaginitis, carcinoma
- Vulvar — skin lesions, carcinoma (usually visible)
- Non-genital — urinary (haematuria mistaken for vaginal bleeding), rectal (haemorrhoids, rectal bleeding)
A speculum examination resolves most of this ambiguity by directly visualising the cervix and vaginal walls.
This is the most powerful discriminator at the history-taking stage.
Pattern of bleeding? [1]
Important to distinguish between heavy regular bleeding (i.e. menorrhagia) and irregular or intermenstrual bleeding because they have different d/dx [1]
| Bleeding Pattern | What It Implies | Why |
|---|---|---|
| Heavy but regular (cyclical) | Structural uterine cause or endometrial haemostatic defect | Fibroids/adenomyosis → consistent anatomical distortion causes heavy bleeding with each normal cycle; endometrial causes → local haemostatic imbalance present every cycle |
| Heavy and irregular | Ovulatory dysfunction, polyps, hyperplasia, malignancy | Anovulation → no predictable progesterone withdrawal → random, disorganised shedding; polyps/malignancy → friable tissue bleeds unpredictably |
| Intermenstrual (IMB) | Surface lesions of genital tract | Polyps, endometrial hyperplasia/carcinoma, cervical lesions → friable or abnormal tissue bleeds between periods |
| Postcoital (PCB) | Cervical pathology primarily | Mechanical trauma during intercourse disrupts fragile cervical tissue (ectropion, polyp, carcinoma, cervicitis) |
| Postmenopausal (PMB) | Malignancy until proven otherwise | Atrophic endometrium should not bleed; neoplastic tissue has abnormal vasculature |
Step 3: The Differential Diagnoses — Organised by the PALM-COEIN System
Let me present this as a comprehensive differential with the reasoning for each.
A. Structural Causes (PALM) — "Something You Can See or Image"
- 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
B. Non-Structural Causes (COEIN) — "Nothing Visible on Imaging"
- 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
These are important to exclude:
| Source | Differential | Key Distinguishing Feature |
|---|---|---|
| Cervical | Cervicitis, cervical ectropion, cervical polyp, CA cervix [1] | Usually IMB or PCB; visible on speculum |
| Vaginal | Atrophic vaginitis, lacerations, vaginitis, vaginal ulcers, CA vagina [1] | Visible on speculum; postmenopausal women (atrophic) |
| Vulvar | Vulval skin tags, sebaceous cysts, condyloma, CA vulva [1] | Visible on inspection |
| Pregnancy-related | Early: miscarriage, ectopic pregnancy, molar pregnancy [1]; Late: bloody show, placenta previa, placental abruption [1] | Always exclude with β-hCG! |
| PID | Fever, vaginal discharge: indicate PID [1] | Cervical excitation tenderness, adnexal tenderness, systemic symptoms |
| Non-genital | Haematuria, rectal bleeding | History of urinary/bowel symptoms; bleeding only with micturition/defecation |
D. The "Don't Forget" List — Special Situations
- 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
| Category | Differential | Typical Bleeding Pattern | Key Clues |
|---|---|---|---|
| Structural | Fibroid (submucosal) | Heavy, regular | Irregular/enlarged firm uterus, pressure symptoms |
| Adenomyosis | Heavy, regular + dysmenorrhoea | Boggy tender uterus, age 30s–40s | |
| Endometrial polyp | IMB ± HMB | Post-menstrual spotting | |
| Endometrial hyperplasia/CA | Irregular, heavy, or PMB | Age > 40, obesity, PCOS, tamoxifen | |
| Uterine AVM | Torrential, unpredictable | Post-procedure, Doppler shows high-flow | |
| C/S scar defect | Post-menstrual spotting | Previous C/S history | |
| Non-structural | Ovulatory dysfunction | Irregular, unpredictable | Extremes of reproductive life, PCOS |
| Coagulopathy (vWD, ITP) | Heavy since menarche | Other mucocutaneous bleeding, FHx | |
| Endometrial haemostatic defect | Heavy, regular (no structural cause) | Diagnosis of exclusion | |
| Iatrogenic (Cu IUD, anticoagulants) | Related to intervention timing | Drug/device history | |
| Thyroid disease | Variable | Other thyroid symptoms | |
| Cervical | Cervicitis, polyp, ectropion, CA | PCB, IMB | Speculum findings |
| Vaginal | Atrophic vaginitis, lacerations | Spotting, light bleeding | Visible on speculum |
| Pregnancy | Miscarriage, ectopic, molar | Irregular, ± pain | Positive β-hCG |
| Non-genital | Haematuria, rectal bleeding | Not menstrual pattern | Urinary/bowel symptoms |
This is a practical bedside trick — the most likely diagnoses shift with age:
| Age | Most Likely Differentials | Why |
|---|---|---|
| Adolescent (< 20) | Anovulation (immature HPO axis), coagulopathy (esp. vWD), pregnancy | HPO axis takes 2–3 years to mature post-menarche → anovulatory cycles common; vWD often first manifests at menarche; always exclude pregnancy |
| Early reproductive (20–35) | Pregnancy complications, polyps, PID/endometritis, iatrogenic (Cu IUD, hormonal), endometriosis, ovulatory dysfunction (PCOS) | Active reproductive period → pregnancy always considered; PCOS peaks; Cu IUD commonly inserted |
| Late reproductive (35–45) | Fibroids, adenomyosis, polyps, ovulatory dysfunction (early perimenopause), endometrial hyperplasia | Fibroids grow under oestrogen influence and accumulate with age; adenomyosis typically presents in 30s–40s; anovulatory cycles begin |
| Perimenopausal (45–menopause) | Anovulation, fibroids, polyps, endometrial hyperplasia/malignancy | Ovarian reserve declines → frequent anovulation → unopposed oestrogen; must exclude malignancy |
| Postmenopausal | Endometrial carcinoma, atrophic endometritis/vaginitis, polyps, HRT-related | Any PMB = cancer until proven otherwise |
Distinguishing Key Differentials — Clinical Reasoning
These two are the most commonly confused because both cause HMB and a bulky uterus:
| Feature | Fibroids | Adenomyosis |
|---|---|---|
| Uterine contour | Irregular, nodular | Uniformly enlarged, globular |
| Consistency | Firm, hard | Boggy, soft |
| Tenderness | Usually non-tender | Tender, especially perimenstrually |
| Dysmenorrhoea | Can occur but not typical | Very characteristic |
| Age | Any reproductive age (peak 30–50) | Mid-30s to 40s |
| Imaging | Discrete, well-circumscribed masses on USS | Heterogeneous myometrium, junctional zone thickening on MRI |
| Feature | Ovulatory Dysfunction | Structural (Fibroids/Adenomyosis) |
|---|---|---|
| Cycle regularity | Irregular — variable intervals | Regular — predictable cycle length |
| Volume per cycle | Variable — can be very heavy or very light | Consistently heavy |
| Age | Extremes of reproductive life, PCOS | Peak reproductive to perimenopausal |
| Examination | Normal uterus | Enlarged uterus |
| Response to progesterone | Excellent — organises the endometrium | Partial at best |
| Feature | Coagulopathy | Endometrial (AUB-E) |
|---|---|---|
| Onset | Since menarche | Acquired, any age |
| Other bleeding | Easy bruising, epistaxis, gum bleeding, postpartum, post-surgical | No systemic bleeding |
| Family history | Often positive (vWD = AD) | Negative |
| Clotting tests | Abnormal (↑aPTT in vWD; ↓platelets in ITP) | Normal |
| Response to tranexamic acid | Partial | Good |
Coagulopathy Screening — When to Think About It
The ACOG screening criteria suggest screening for coagulopathy if:
- HMB since menarche
- Postpartum haemorrhage
- Surgery-related bleeding
- Bleeding with dental work
- ≥ 2 bruising symptoms (> 5 cm without trauma)
- Frequent epistaxis (> 1/month)
- Family history of bleeding disorder
Standard evaluation: CBC ± PBS for platelet count and morphology, clotting profile including PT and aPTT (± TT). Additional: platelet function tests and vWF function assay for positive bleeding history with negative initial testing; specific clotting factor assays and mixing tests if suspecting haemophilia. [3][5]
Red Flag Differentials — Do Not Miss
-
Endometrial carcinoma — any woman > 40 with new AUB or AUB not responding to treatment. Any postmenopausal bleeding. Risk factors: obesity, PCOS, tamoxifen, nulliparity, Lynch syndrome.
-
Pregnancy complications — always check β-hCG. Ectopic pregnancy can be life-threatening.
-
Cervical carcinoma — especially with PCB/IMB. Check smear history. Examine cervix.
-
Coagulopathy (especially vWD) — underdiagnosed. Think about it in adolescents with HMB since menarche.
-
PID/endometritis — can cause AUB with pain and discharge. May progress to tubo-ovarian abscess.
High Yield Summary
Step 1: Confirm bleeding is uterine (not cervical, vaginal, vulvar, or non-genital). Speculum examination is essential.
Step 2: Exclude pregnancy in ALL reproductive-age women (β-hCG).
Step 3: Determine the bleeding pattern — heavy regular (structural: fibroids, adenomyosis; or AUB-E/coagulopathy) vs heavy irregular (ovulatory dysfunction, polyps, hyperplasia/malignancy) vs IMB (surface lesions) vs PCB (cervical pathology).
Key differentials for regular HMB: Fibroids (commonest structural cause, especially submucosal), adenomyosis (dysmenorrhoea + boggy tender uterus), coagulopathy (especially vWD — 10–15% of HMB), endometrial haemostatic defect (AUB-E: ↑tPA, ↑PGE₂), copper IUD.
Key differentials for irregular HMB: Anovulation (PCOS, perimenopause, adolescence), endometrial hyperplasia/carcinoma, polyps.
Must-not-miss: Endometrial carcinoma (> 40, risk factors), pregnancy, cervical carcinoma, coagulopathy (menarche onset), PID.
Age-based thinking: Adolescents → anovulation + coagulopathy; reproductive → fibroids + pregnancy; perimenopausal → anovulation + exclude malignancy; postmenopausal → carcinoma until proven otherwise.
Active Recall - Differential Diagnosis of HMB
References
[1] Lecture slides: Adrian Lui Gynecology Notes.pdf (p11, p13) [3] Senior notes: Ryan Ho Haemtology.pdf (p113–114, p117, p128, p137–138, p161) [4] Senior notes: Ryan Ho Haemtology.pdf (p128 — vWD clinical features and HMB association) [5] Senior notes: Ryan Ho Fundamentals.pdf (p404 — approach to bleeding disorders) [6] Senior notes: Maksim Medicine Notes.pdf (p153, p160–161 — IDA causes including menorrhagia, platelet/clotting disorders)
Diagnostic Criteria, Diagnostic Algorithm, and Investigations for HMB
HMB does not have traditional "diagnostic criteria" in the way that, say, rheumatic fever has Jones criteria. Instead, the diagnosis rests on two pillars:
-
Clinical (patient-centred) criterion: Excessive menstrual blood loss that interferes with the woman's physical, social, emotional, and/or material quality of life [1]. If the patient says her periods are heavy and they impair her life, that is HMB.
-
Objective assessment tools (supportive, not mandatory):
- Pictorial Blood Assessment Chart (PBAC): score ≥ 100 correlates with MBL > 80 mL (sensitivity ~80%, specificity ~80%)
- Alkaline haematin method: research gold standard for quantifying MBL (> 80 mL = HMB), but impractical for clinical use
In practice, you diagnose HMB based on history and then your job shifts to identifying the underlying cause using the PALM-COEIN framework, and assessing the consequences (iron deficiency anaemia).
When Is HMB Diagnosed?
There is no blood test or imaging study that "diagnoses" HMB. The diagnosis is clinical — the woman reports heavy periods with QoL impact. The investigations are directed at finding the CAUSE and assessing CONSEQUENCES, not at confirming the diagnosis itself.
Not every woman with HMB needs extensive investigation. The decision tree depends on age, risk factors, clinical findings, and response to empirical treatment.
The goal of investigation is to:
- Exclude pregnancy
- Assess consequences (anaemia)
- Identify structural causes
- Exclude malignancy/hyperplasia
- Identify non-structural causes (coagulopathy, thyroid, anovulation)
Investigations — Detailed Breakdown
I will organise these by category, explaining what each test is looking for, why you order it, and how to interpret the findings.
A. Bedside and First-Line Blood Tests
- 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:
| Finding | Interpretation | Pathophysiological Basis |
|---|---|---|
| ↓Hb with ↓MCV, ↓MCH (microcytic hypochromic anaemia) | Iron deficiency anaemia [6] — the most common consequence of chronic HMB | Chronic blood loss → iron stores depleted → insufficient iron for haemoglobin synthesis → small, pale red cells |
| ↓Hb with normal MCV | Could be early IDA (iron stores depleted but MCV not yet dropped), or mixed deficiency, or anaemia of chronic disease | Iron depletion precedes changes in MCV; see staged progression below |
| Reactive thrombocytosis (↑platelet count) | ↑EPO stimulates platelet precursors [6] — common in IDA | Thrombopoietin and EPO share structural homology; EPO stimulates megakaryocyte progenitors |
| ↓Platelet count | Suggests ITP, DIC, or bone marrow pathology as underlying cause of HMB | Reduced platelet count → impaired primary haemostasis → mucocutaneous bleeding including HMB |
| ↑WBC | Consider PID/endometritis, or haematological malignancy | Infection → neutrophilia; malignancy → abnormal differential |
- Why: provides morphological information that CBC numbers alone cannot
- Key findings:
Fe profile: for Fe def anaemia [1]
Understanding iron studies from first principles is essential. Let me walk you through the stages of iron deficiency [7]:
| Stage | Serum Iron | TIBC | Transferrin Saturation | Serum Ferritin | Hb / MCV | Clinical State |
|---|---|---|---|---|---|---|
| 1. Depletion of iron stores | Normal | Normal | Normal | LOW | Normal | Asymptomatic; stores exhausted but functional iron sufficient |
| 2. Functional iron deficiency | ↓ | ↑ | ↓ (< 16%) | ↓ | Normal | Iron-restricted erythropoiesis begins; BM staining ↓ |
| 3. Iron deficiency anaemia | ↓ | ↑ | ↓ (< 16%) | ↓ | Hb < 12, MCV < 80 | Frank anaemia with microcytosis |
Interpretation of individual markers [7]:
| Marker | What It Measures | Key Points |
|---|---|---|
| Serum ferritin | Body iron stores (intracellular storage iron) | Most sensitive and specific marker [7]; Low serum ferritin is diagnostic of iron deficiency [7]; BUT it is an acute phase reactant — falsely elevated in inflammation, liver disease, malignancy |
| Serum iron | Circulating iron bound to transferrin | CANNOT be used alone [7] — fluctuates with diurnal variation, meals, inflammation |
| TIBC | Total binding capacity of transferrin in plasma | ↑ in IDA (body tries to maximise iron capture), ↓ in inflammation |
| Transferrin saturation (TSAT) | Serum iron / TIBC × 100% | CANNOT be used alone [7]; < 16% suggests iron-restricted erythropoiesis |
Clinical decision cut-offs for serum ferritin [7]:
- Adults: < 34 pmol/L (15 μg/L) = diagnostic of iron deficiency
- Hospitalised elderly: < 100 pmol/L (45 μg/L)
- Community-based elderly: < 49 pmol/L (22 μg/L)
- Disease-specific thresholds exist (e.g., renal dialysis patients)
Ferritin Pitfall
A "normal" ferritin does NOT exclude iron deficiency in the presence of concurrent inflammation, infection, liver disease, or malignancy. In these settings, ferritin can be falsely elevated because it is an acute phase reactant. Use TSAT and clinical context alongside ferritin. Some guidelines use a higher cut-off (e.g., < 100 μg/L) in the context of chronic disease or CKD.
± Clotting profile: if HMB since menarche, or FHx +ve [1]
Not routine for all women with HMB — only when clinical suspicion exists.
- HMB since menarche — this is the single most important screening question
- Family history of bleeding disorder
- Other mucocutaneous bleeding symptoms (easy bruising, epistaxis, gum bleeding, post-surgical/dental bleeding)
- Suspected coagulopathy on clinical grounds
What to order and interpretation [3][5]:
| Test | What It Assesses | Expected in vWD | Expected in ITP | Expected in Haemophilia Carrier |
|---|---|---|---|---|
| PT (and INR) | Extrinsic pathway (factor VII) + common pathway | Normal | Normal | Normal |
| aPTT | Intrinsic pathway (factors VIII, IX, XI, XII) + common pathway | Isolated ↑aPTT (but can be normal in mild disease) [4] | Normal | May be mildly ↑ |
| Platelet count | Quantitative platelet assessment | Normal (except type 2B → ↓) | ↓↓↓ | Normal |
| Fibrinogen, D-dimer | DIC screen | Normal | Normal | Normal |
If initial screen abnormal or high clinical suspicion despite normal screen [5]:
- vWF antigen (vWF:Ag): < 30% (< 30 IU/dL) consistent with vWD [4]
- vWF activity (vWF:Act / Ristocetin cofactor assay, vWF:RiCof): measures functional binding to platelet GPIb [4]
- Factor VIII activity: moderately ↓ in types 1, 2A, 2B, 2M; significantly ↓ in types 2N, 3 [4]
- vWF Act:Ag ratio: < 0.5–0.7 indicates qualitative defect (type 2) [4]
- Further: multimer analysis, RIPA for subtype differentiation [4]
vWD Testing Pitfall
aPTT can be normal in vWD due to: (1) mild deficiency, (2) stress-induced ↑vWF/F8 during phlebotomy, inflammation, infection, malignancy, (3) hormonal factors — vWF levels rise during the menstrual cycle and with OCP/pregnancy [4]. A normal aPTT does NOT exclude vWD. If clinical suspicion is high, proceed directly to vWF-specific assays.
± TFT: only when clinically symptomatic (uncommon) [1]
- Why not routine? Because thyroid disease is an uncommon cause of HMB in isolation. However, when thyroid symptoms are present (fatigue, weight changes, cold/heat intolerance, tremor, constipation, etc.), TFTs should be checked.
- Interpretation: ↑TSH + ↓fT4 = hypothyroidism → can cause HMB through anovulation (↑TRH → ↑prolactin → GnRH suppression) and altered endometrial physiology
± Further workup on anovulation: hormonal profile: LH, FSH, E2; endocrine profile: TFT, PRL; PCOS: (US), testosterone, OGTT [1]
Indicated when the bleeding pattern is irregular (suggesting ovulatory dysfunction):
| Test | What It Tells You | Key Findings |
|---|---|---|
| LH, FSH | Hypothalamic-pituitary function | ↑LH:FSH ratio (> 2:1) in PCOS; ↑FSH in perimenopause/ovarian failure; ↓ both in hypothalamic cause |
| Oestradiol (E2) | Ovarian function | ↓ in ovarian failure/menopause; variable in PCOS |
| Prolactin (PRL) | Hyperprolactinaemia screen | ↑ in prolactinoma, drug-induced, hypothyroidism; causes anovulation via GnRH suppression |
| Testosterone | Hyperandrogenism screen | ↑ in PCOS (mild-moderate); significantly ↑ consider adrenal/ovarian androgen-secreting tumour |
| OGTT | Insulin resistance/diabetes in PCOS | PCOS is associated with insulin resistance → screen with 75g OGTT |
| TFT | As above | Hypothyroidism can cause anovulation |
F. Imaging Studies
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:
| Modality | When to Use | Advantages | Limitations |
|---|---|---|---|
| Transvaginal USS (TVUS) | First-line; better resolution for endometrium, small fibroids, adenomyosis | High resolution for endometrial thickness, cavity assessment, adnexal structures | Cannot visualise very large uteri that extend beyond probe range |
| Transabdominal USS (TAS) | Large uteri (> 12-week size), overview assessment | Wider field of view | Lower resolution for endometrial detail |
Key findings and interpretation:
| USS Finding | Diagnosis | Description |
|---|---|---|
| Single or multiple well-circumscribed hypoechoic mass [1] | Fibroid (leiomyoma) | Well-defined, rounded, usually hypoechoic with posterior acoustic shadowing; pseudocapsule visible from surrounding compressed myometrium [1] |
| Heterogeneous echoes | Complicated fibroid | E.g., complicated by bleeding (uncommon) [1]; may also represent degeneration (red, hyaline, cystic) |
| Cystic areas within fibroid | Cystic degeneration | E.g., cystic degeneration [1] |
| Asymmetric myometrial thickening, heterogeneous myometrium, myometrial cysts, indistinct endo-myometrial junction | Adenomyosis | Sub-endometrial cysts (ectopic glands), "Venetian blind" shadowing, globular uterus |
| Echogenic focal mass within endometrial cavity ± feeder vessel | Endometrial polyp | Best seen with saline infusion sonography (SIS) which distends the cavity |
| Thickened endometrium | Endometrial hyperplasia or carcinoma | Post-menopausal: should be ≤ 4 mm [1]; pre-menopausal: interpret in context of cycle phase |
| High-velocity, low-resistance flow on Doppler | Uterine AVM | Tangle of vessels with arteriovenous shunting; colour Doppler shows characteristic "aliasing" |
| Myometrial niche at C/S scar | Isthmocele (C/S scar defect) | Triangular hypoechoic defect at previous scar site |
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
G. Endometrial Sampling
This is the critical investigation for excluding endometrial hyperplasia and malignancy.
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:
| Result | Interpretation | Action |
|---|---|---|
| Proliferative endometrium | Normal — consistent with follicular phase | Reassuring; no further action for endometrial pathology |
| Secretory endometrium | Normal — confirms ovulation occurred | Reassuring |
| Disordered proliferative endometrium | Suggests anovulation/hormonal imbalance | Supports AUB-O; medical management |
| Endometrial hyperplasia without atypia | Low malignant potential (~1–3% over 20 years) | Progestogen therapy; follow-up EA in 3–6 months |
| Atypical hyperplasia / EIN | High malignant potential (~25–30% progression) | Refer gynaecology-oncology; consider hysterectomy |
| Endometrial carcinoma | Malignancy confirmed | Staging investigations + gynaecology-oncology management |
| Insufficient sample | Non-diagnostic — cavity not adequately sampled | Consider hysteroscopy + targeted biopsy |
| Chronic endometritis | Plasma cells in stroma → consider PID | Antibiotic treatment; investigate for STI |
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:
| Hysteroscopic Finding | Diagnosis | Significance |
|---|---|---|
| Smooth, pedunculated or sessile mass within cavity | Endometrial polyp | Can be removed during same procedure (polypectomy) |
| Rounded mass distorting cavity, covered by endometrium | Submucosal fibroid | Assess % intracavitary protrusion → determines if hysteroscopic myomectomy is feasible |
| Generalised thickened, friable, vascular endometrium | Endometrial hyperplasia | Biopsy for histopathology |
| Irregular, necrotic, bleeding mass | Suspicious for malignancy | Urgent biopsy → histology |
| Pale, thin, atrophic endometrium with petechial haemorrhages | Atrophic endometrium (PMB) | Reassuring if biopsy confirms |
Note any cervical pathology and perform a cervical smear if (1) due for screening (2) look suspicious but no obvious lesion [1]
- Cervical cytology (Pap smear / liquid-based cytology): should be performed if due for screening or if cervical abnormality noted on speculum
- In Hong Kong, cervical screening is recommended every 3 years for women aged 25–64 who have ever been sexually active (transitioning to HPV-based primary screening)
- If AGC (atypical glandular cells) found on Pap → consider EA + colposcopy [1]
| Investigation | When to Order | What You're Looking For |
|---|---|---|
| Pregnancy test | ALL reproductive-age women | Exclude pregnancy-related bleeding |
| CBC | ALL women with HMB | Anaemia (Hb, MCV), thrombocytopenia |
| Iron profile | When anaemia detected or suspected | Confirm iron deficiency; stage of depletion |
| Clotting profile | HMB since menarche, FHx +ve, other bleeding symptoms | Coagulopathy (↑aPTT in vWD, ↓platelets in ITP) |
| vWF assay + FVIII | Suspected vWD (above features) | vWD subtypes |
| TFT | Only when clinically symptomatic | Hypo-/hyperthyroidism |
| Hormonal profile | Irregular cycles suggesting anovulation | PCOS, hyperprolactinaemia, ovarian failure |
| Pelvic USS (TVUS ± TAS) | Structural pathology suspected on exam | Fibroids, adenomyosis, polyps, endometrial thickness |
| EA (Pipelle) | Age ≥ 45 with regular HMB; age ≥ 40 with IMB/irregular; RFs for endometrial pathology; failed treatment | Endometrial hyperplasia / malignancy |
| Hysteroscopy ± biopsy | Suspected polyp/submucosal fibroid; EA failed/inconclusive; irregular bleeding on hormonal Tx > 3m | Direct visualisation + targeted biopsy/treatment |
| MRI pelvis | Complex surgical planning, UAE planning, suspicious for sarcoma | Fibroid mapping, adenomyosis confirmation, sarcoma exclusion |
| Cervical smear | Due for screening or suspicious cervix | Cervical dysplasia / malignancy |
This is a critical exam point. The age thresholds determine when endometrial sampling is indicated:
Age ≥ 45y with regular heavy period → EA indicated [1] Age ≥ 40y with persistent IMB or irregular bleeding → EA indicated [1] Any age with RFs for endometrial pathology (obesity, PCOS, tamoxifen, failed treatment) → EA indicated [1] All cases of postmenopausal bleeding → EA mandatory [1]
Endometrial Sampling Indications — Exam Favourite
The logic behind the age cut-offs: as women age, the probability of endometrial hyperplasia/carcinoma increases. By age 45, even regular heavy periods warrant endometrial sampling because perimenopausal anovulation → unopposed oestrogen → hyperplasia risk. By age 40, irregular/intermenstrual bleeding raises more concern for endometrial pathology. At any age, additional risk factors (obesity, PCOS, tamoxifen, failed treatment) lower the threshold for sampling.
Since PMB is covered as a differential and shares investigation principles, here is the protocol for completeness [1]:
PMB: any uterine bleeding > 1y after last natural menstrual period [1] Must r/o CA endometrium [1]
- Cervical cytology if no regular screening [1]
- Endometrial aspirate: mandatory in all cases of PMB [1]
- NOT routinely performed in asymptomatic patients with incidental finding of thickened endometrium unless > 11 mm and associated with other USS findings or RFs [1]
- TVUS for endometrial thickness: should be ≤ 4 mm in post-menopausal women [1]
- Hysteroscopy ± endometrial biopsy: if on tamoxifen, endometrial thickness > 4 mm, recurrent/refractory symptoms despite treatment for atrophic changes [1]
High Yield Summary
Diagnosis of HMB is clinical — based on patient-reported excessive menstrual blood loss interfering with quality of life. There are no lab/imaging criteria for "diagnosing" HMB itself. Investigations find the CAUSE and assess CONSEQUENCES.
Baseline for ALL: Pregnancy test + CBC (Hb, platelets). This is non-negotiable.
Iron profile: Ferritin is the single most sensitive and specific marker for iron deficiency. Low ferritin = diagnostic. But it is an acute phase reactant — can be falsely normal/elevated in inflammation. Use TSAT alongside in ambiguous cases.
Coagulation screen: Only if HMB since menarche, FHx positive, or other mucocutaneous bleeding. vWD is the key target — aPTT can be NORMAL in mild disease; if suspicion is high, go directly to vWF:Ag, vWF:Act, FVIII.
Pelvic USS (TVUS ± TAS): First-line for structural causes. Fibroids = well-circumscribed hypoechoic mass with pseudocapsule. Adenomyosis = heterogeneous myometrium, myometrial cysts, globular uterus. Endometrial thickness ≤ 4 mm in postmenopausal women has NPV 99.4–100% for CA.
Endometrial aspirate (EA): Simple office procedure. Indications: age ≥ 45 with regular HMB, age ≥ 40 with IMB/irregular bleeding, any age with RFs (obesity, PCOS, tamoxifen, failed Tx), ALL PMB.
Hysteroscopy: Superior to EA but limited availability. Indicated when EA fails/inconclusive, suspected polyp/submucosal fibroid, or persistent bleeding on hormonal Tx > 3 months. Allows targeted biopsy and therapeutic intervention.
MRI: Second-line. For complex surgical planning, UAE planning, sarcoma suspicion, adenomyosis confirmation.
Active Recall - Diagnosis and Investigation of HMB
References
[1] Lecture slides: Adrian Lui Gynecology Notes.pdf (p13–14, p20, p22, p91, p97) [3] Senior notes: Ryan Ho Haemtology.pdf (p113–114 — approach to bleeding disorders, platelet clumping) [4] Senior notes: Ryan Ho Haemtology.pdf (p128 — vWD pathogenesis, clinical features, laboratory features) [5] Senior notes: Ryan Ho Fundamentals.pdf (p404 — approach to bleeding disorders, standard evaluation) [6] Senior notes: Maksim Medicine Notes.pdf (p153 — IDA causes, laboratory findings, management) [7] Senior notes: Ryan Ho Chemical Path.pdf (p53 — iron deficiency stages, ferritin interpretation, clinical cut-offs)
Management of Heavy Menstrual Bleeding (HMB)
Before diving into specific treatments, let me lay out the core management principles. Think of HMB management as answering four questions in sequence:
- Is there an underlying cause that needs specific treatment? (e.g., polyp → remove it; malignancy → oncological management; coagulopathy → haematological treatment; thyroid disease → correct it)
- What does the patient want? — particularly regarding fertility preservation vs completed family
- How severe is the HMB? — is there haemodynamic compromise requiring emergency management, or is this a chronic outpatient problem?
- Are there contraindications to specific treatments (e.g., oestrogen in VTE risk)?
Management of underlying cause as appropriate [1] Polyp can be observed (1/4 chance to spontaneously resolve if < 1 cm) [1]
Section A: Medical Treatment of HMB
Medical treatment is the first-line approach for most women with HMB, regardless of cause (unless surgery is specifically indicated). I will go through each option with its mechanism, efficacy, dosing, side effects, and contraindications.
1. Non-Hormonal Treatments
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
Why Tranexamic Acid Works for HMB
The endometrium in HMB has increased local tPA activity → premature clot lysis at spiral artery stumps → continued bleeding. Tranexamic acid blocks this enhanced fibrinolysis. It is the pharmacological answer to the "AUB-E" pathophysiology. This is why it is effective across multiple causes of HMB, not just endometrial causes — any bleeding benefits from clot stabilisation.
± 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
2. Hormonal Treatments
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].
Iron replacement is a critical adjunct — remember, HMB is the leading cause of IDA in premenopausal women.
Iron supplement: FeSO₄ 300 mg BD × 12 weeks [1] 2nd line: ferrum hausmann chewable tablet BD or 3 mL droplet QD × 12 weeks [1] 3rd line: IV iron [1]
For fibroid-related HMB: Iron supplementation: FeSO₄ 300 mg TDS PO × 6 months (if Hb < 10 g/dL) [1]
- FeSO₄ 300 mg contains ~65 mg elemental iron per tablet
- Expect Hb ↑1 g/dL every 7–10 days [6]
- Give with vitamin C (promotes reduction of Fe³⁺ → Fe²⁺ → enhances absorption) and without food (2h before, 4h after) [6]
Side effects [6]: N/V, constipation, epigastric discomfort, metallic taste, black stool
- If intolerant: switch to elixir form or take with meals (note ↓absorption) [6]
IV iron indications [8]:
- Those who tolerate oral iron poorly, with severe ongoing blood loss, or malabsorption
- Options: ferric carboxymaltose (Ferinject), iron sucrose, ferric gluconate
- Advantage: effective, rapid correction, ensure good compliance, no GI side effects [8]
Transfusion: If angina, heart failure, cerebral hypoxia, or Hb < 7 g/dL [8]
Section B: Surgical Treatment of HMB
Surgery is indicated when:
- Medical treatment has failed or is contraindicated
- The patient has completed childbearing
- Structural pathology requires surgical intervention
- Malignancy is present
1. Hysteroscopic Procedures
- 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
Myomectomy: laparoscopic, trans-abdominal, hysteroscopic (± endometrial ablation) [1]
Principle: surgical removal of fibroids while preserving the uterus — fertility-sparing.
| Approach | Indication | Notes |
|---|---|---|
| Hysteroscopic | Submucosal fibroids (types 0, 1, 2 with > 50% protrusion) | Transcervical, no abdominal incision |
| Laparoscopic | Subserosal or intramural fibroids, limited number/size | Minimally invasive, faster recovery |
| Open (laparotomy) | Large or numerous fibroids, previous multiple surgeries | Best for very large or multiple fibroids |
Risks: haemorrhage (fibroids are vascular), adhesion formation, uterine rupture in subsequent pregnancy (risk depends on depth of myometrial entry — typically ~1% if myometrium was not breached through to cavity), recurrence (~15–30% over 5 years)
Hysterectomy: vaginal, abdominal, laparoscopic [1]
The only definitive cure for HMB — eliminates the source entirely.
Indications [1]:
- Acute haemorrhage not responding to other therapies
- Completed childbearing or no fertility wish
- ↑Risk for CA cervix, endometrium, ovaries: e.g., CIN, endometrial hyperplasia
- Patient preference
- Failed medical and conservative surgical treatments
Routes:
| Route | When Preferred | Advantages | Limitations |
|---|---|---|---|
| Vaginal | Mobile uterus ≤ 12 weeks, no significant adhesions, benign pathology | Least invasive, fastest recovery, lowest complication rate, no abdominal incision | Limited exposure for large/complex cases |
| Laparoscopic (TLH / LAVH) | Moderate uterine size, need for oophorectomy, adhesions, endometriosis | Minimally invasive, good visualisation | Longer operating time, requires skilled surgeon |
| Abdominal (TAH) | Large uterus (> 12–14 weeks), suspected malignancy, multiple previous surgeries | Best exposure, can handle any size | Larger incision, longer recovery |
| Robotic-assisted | Similar to laparoscopic | Enhanced dexterity | Cost, availability |
Extent:
- Total hysterectomy: removal of uterine body + cervix (standard)
- Subtotal/supracervical hysterectomy: removal of uterine body, cervix preserved — faster procedure, preserves pelvic floor support, but requires continued cervical screening
- ± Bilateral salpingo-oophorectomy (BSO): consider if perimenopausal, family history of ovarian/breast cancer, or BRCA carrier. Otherwise, ovarian conservation is recommended in premenopausal women (sudden surgical menopause → cardiovascular and osteoporosis risk)
Complications: haemorrhage, infection, injury to bladder/ureter/bowel, VTE, vaginal vault prolapse (long-term), early menopause (if ovaries removed)
Uterine artery embolization (UAE) [1] Transcatheter embolisation: embolic agents used to block specific blood vessels [9] Examples: Gelfoam, PVA particles, coil, glue [9] Uterine fibroid embolisation [9]
Principle: interventional radiology procedure — catheter inserted via femoral artery → selectively catheterise both uterine arteries → inject embolic particles (PVA particles, microspheres) → occlude blood supply to fibroids → ischaemic necrosis of fibroids → shrinkage + symptom improvement
Mechanism (from first principles):
- Fibroids derive their blood supply primarily from the uterine arteries
- Normal myometrium has dual supply (uterine + ovarian arteries) and can recruit collaterals
- Fibroids have a single end-artery supply without collateral network → selectively vulnerable to embolisation
- Post-embolisation: fibroid undergoes coagulative necrosis → shrinks by 40–60% over 3–6 months
Efficacy: ~85–90% symptomatic improvement; ~70% reduction in fibroid volume
Advantages: minimally invasive, uterus-preserving, no general anaesthesia needed, short hospital stay
Complications:
- Post-embolisation syndrome (most common): pain + fever + nausea/malaise lasting 1–2 weeks (inflammatory response to fibroid necrosis)
- Fibroid passage (necrotic fibroid expelled vaginally — especially submucosal types)
- Amenorrhoea/premature ovarian failure (~3% in women > 45; uterine artery embolisation may affect ovarian blood supply via utero-ovarian anastomoses)
- Rarely: uterine infection, uterine necrosis requiring hysterectomy
Contraindications:
- Pregnancy or desire for future pregnancy (relative — UAE is associated with ↑miscarriage, preterm labour, abnormal placentation; myomectomy preferred for fertility)
- Suspected malignancy (uterine sarcoma)
- Active pelvic infection
- Severe contrast allergy
- Coagulopathy
For adenomyosis [1]:
UAE: reserved for failure or C/I to medical + surgical therapy [1] Effect: ~2/3 had long-term ↓symptom severity, but high rate of additional intervention for persistent or recurrent symptoms [1]
High-intensity focused ultrasound (HIFU) [1]
- Non-invasive: focused ultrasound waves cause thermal ablation of fibroid tissue
- MRI-guided (MRgFUS) or USS-guided
- Investigational / limited availability [1]
- Advantages: completely non-invasive
- Limitations: limited to certain fibroid types/locations, variable long-term durability
Section C: Cause-Specific Management Summaries
Conservative management: if asymptomatic (esp for those approaching menopause) [1] Medical treatment: considered if heavy menstrual bleeding [1]
| Approach | Modality | Notes |
|---|---|---|
| Conservative | Observation | If asymptomatic, especially approaching menopause (fibroids shrink post-menopause as oestrogen declines) |
| Non-hormonal medical | Transamin ± Ponstan | Note: Ponstan does NOT reduce blood loss in fibroids specifically |
| Hormonal medical | Mirena (if fibroids < 3 cm, no cavity distortion); COCP; Cyclical Primolut N; GnRH agonists (pre-op) | Hormonal treatment a/w little efficacy except for some flow control in fibroids |
| Iron | FeSO₄ 300 mg TDS × 6 months if Hb < 10 | Correct anaemia |
| Pre-op shrinkage | GnRH agonists | 3–6 months pre-op to ↓fibroid size 30–50%, improve Hb |
| Surgical | Hysteroscopic myomectomy (submucosal); laparoscopic/open myomectomy (intramural/subserosal); hysterectomy | Choice depends on fertility wish, fibroid location/size |
| Interventional | UAE; HIFU | Uterus-preserving alternatives |
Surgical indications for fibroids [1]:
Indications: NOT dependent on anatomical factor
- Symptomatic: but warn patient that urinary frequency may not improve as it may be due to DUI [detrusor underactivity/instability]
- Rapid growth or post-menopausal growth → worrisome of malignancy
- Unexplained subfertility with significant submucosal component
Medical treatment: hormonal treatment generally similar to endometriosis (unlike fibroids, where they are generally ineffective) [1]
| Approach | Modality | Notes |
|---|---|---|
| Medical | Mirena (LNG-IUS), Depot Provera, COCP, GnRH agonists, aromatase inhibitors | Hormonal treatments more effective than in fibroids |
| Hysterectomy | Definitive treatment: only way to excise as there is no surgical plane for simple enucleation (even in adenomyoma) [1] | Subtotal hysterectomy as cervix and ovaries not affected |
| UAE | Reserved for failure or C/I to medical + surgical therapy [1] | ~2/3 benefit long-term but high re-intervention rate |
| Ablative | RFA, HIFU (investigational) [1] | Limited evidence |
Asymptomatic adenomyosis incidentally found does not require any Tx [1]
Combined OC pills: 1st line treatment unless C/I [1] High-dose progestogen: when C/I to COC pills [1]
The principle here is to provide the progesterone that is missing → convert the thick, fragile, unopposed-oestrogen-stimulated endometrium into an organised, stable endometrium → produce regular, lighter withdrawal bleeds.
- If PCOS: address insulin resistance (metformin, lifestyle), manage hyperandrogenism, weight loss
- If hypothyroidism: levothyroxine
- If hyperprolactinaemia: cabergoline/bromocriptine
Refer to haematology for condition-specific management. Key adjuncts for HMB in coagulopathies:
- Tranexamic acid — effective across all coagulopathies as adjunct
- DDAVP — for vWD (type 1, 2A, 2M) and mild haemophilia A: ↑factor VIII and vWF release from storage pools in endothelium and platelets [4]
- vWF concentrates — for major bleeding or DDAVP-inadequate cases [4]
- Hormonal treatments — COCP or LNG-IUS to reduce menstrual blood loss
- Antifibrinolytic agents: alone or with DDAVP/vWF in mucosal bleeds [4]
- Hyperplasia without atypia: high-dose cyclical or continuous progestogens (e.g., medroxyprogesterone acetate 10–20 mg/day for 14 days/cycle, or LNG-IUS) → repeat EA at 3–6 months to confirm regression
- Atypical hyperplasia/EIN: strong consideration for hysterectomy (25–30% coexist with or progress to carcinoma); fertility-sparing option with high-dose progestogens + close surveillance is possible in young women desiring fertility but carries risk
- Endometrial carcinoma: surgical staging (hysterectomy + BSO ± lymph node assessment) → adjuvant therapy as indicated
When a woman presents with acute, heavy menstrual bleeding with haemodynamic compromise:
-
ABCs + Resuscitate:
- Large-bore IV access (≥ 16G)
- Bloods: CBC, clotting, crossmatch, β-hCG
- IV fluid resuscitation (crystalloid) → blood transfusion if Hb < 7 or symptomatic anaemia
- Tranexamic acid 1g IV
-
High-dose hormonal therapy to stop bleeding:
- High-dose oestrogen: conjugated equine oestrogen (Premarin) 25 mg IV every 4–6 hours (up to 24 hours) — stabilises the endometrium by promoting rapid proliferation and clotting factor synthesis
- OR High-dose oral progestogen: norethisterone 5 mg TDS or medroxyprogesterone 10 mg TDS
- OR Monophasic COCP: one pill every 6–8 hours until bleeding slows, then taper
-
If bleeding uncontrolled:
- Intrauterine balloon tamponade (e.g., Foley catheter with 30 mL balloon)
- Emergency hysteroscopy + targeted haemostasis
- UAE for acute haemorrhage
- Hysterectomy: acute haemorrhage not responding to other therapies [1]
| Step | What | Details |
|---|---|---|
| 1 | Treat underlying cause | Polyp → polypectomy; thyroid → levothyroxine; coagulopathy → haematology |
| 2 | Iron supplementation | FeSO₄ 300 mg BD × 12 weeks (or TDS × 6 months if Hb < 10) |
| 3 | 1st line medical | COCP (if no C/I) or LNG-IUS (Mirena) |
| 4 | Adjuncts / alternatives | Tranexamic acid ± mefenamic acid; cyclical progestogens if C/I to COCP |
| 5 | 2nd line / failed medical | Endometrial ablation (if family complete); GnRH agonist (bridge) |
| 6 | Surgical | Myomectomy (fibroids); hysterectomy (definitive) |
| 7 | Interventional | UAE, HIFU |
High Yield Summary
First-line medical treatment for HMB without structural cause: COCP (1st line unless C/I) or LNG-IUS (Mirena) — Mirena is the single most effective medical treatment (~90–95% ↓MBL).
Non-hormonal options: Tranexamic acid 1g TDS during menses (↓MBL ~40–50%); mefenamic acid (↓MBL ~20–30% + treats dysmenorrhoea) but does NOT work for fibroid-related HMB.
Mirena requirements for fibroids: only if fibroids < 3 cm with no cavity distortion.
Hormonal treatments have little efficacy for fibroid-specific HMB (unlike adenomyosis where they are more effective) — medical treatment mainly provides flow control while definitive surgical management is planned.
GnRH agonists: pre-operative shrinkage only (3–6 months max due to menopausal side effects and bone loss). Not for long-term use.
Surgical indications for fibroids: symptomatic, rapid/postmenopausal growth, unexplained subfertility with submucosal element — NOT based on size alone.
Hysterectomy is the only definitive cure — indicated for completed family, failed medical/conservative Tx, acute uncontrolled haemorrhage, malignancy.
Adenomyosis: hysterectomy is definitive — no surgical plane for excision. Hormonal Tx (Mirena, Depot Provera) more effective than for fibroids.
Iron supplementation: FeSO₄ 300 mg BD × 12 weeks (1st line); ferrum hausmann (2nd line); IV iron (3rd line). Expect Hb ↑1 g/dL every 7–10 days.
UAE: minimally invasive alternative for fibroids (not ideal if fertility desired) and adenomyosis (reserve for failed medical/surgical); ~85–90% symptomatic improvement.
Active Recall - Management of HMB
References
[1] Lecture slides: Adrian Lui Gynecology Notes.pdf (p13, p15, p20, p51, p91–92) [4] Senior notes: Ryan Ho Haemtology.pdf (p128–129 — vWD management, DDAVP, vWF concentrates, antifibrinolytics) [6] Senior notes: Maksim Medicine Notes.pdf (p153 — IDA laboratory findings, iron supplementation) [8] Senior notes: Ryan Ho Haemtology.pdf (p19 — IDA management, oral iron, IV iron, transfusion indications) [9] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p85 — transcatheter embolisation, UAE, uterine fibroid embolisation)
Complications of Heavy Menstrual Bleeding (HMB)
Complications of HMB fall into two broad categories: consequences of the chronic blood loss itself (the most common) and complications arising from the underlying cause or its treatment. Let me walk you through each systematically, always explaining why each complication occurs from first principles.
1. Iron Deficiency Anaemia (IDA) — The Cardinal Complication
This is, by far, the most common and most important complication of HMB. Every single menstrual cycle in which blood loss exceeds the body's capacity to replenish iron brings the woman closer to frank anaemia.
Recall the staged progression [7]:
| Stage | What Happens | Lab Findings | Clinical State |
|---|---|---|---|
| 1. Iron store depletion | Total body iron stores (ferritin) exhausted, but circulating iron adequate for erythropoiesis | ↓Ferritin; normal Hb, MCV, serum iron, TIBC | Asymptomatic |
| 2. Functional iron deficiency | Circulating iron insufficient to meet erythropoietic demand; BM cannot make enough haemoglobin | ↓Ferritin, ↓serum iron, ↑TIBC, ↓TSAT (< 16%); Hb still normal | May have fatigue, ↓exercise tolerance |
| 3. Iron deficiency anaemia | Frank anaemia with microcytic hypochromic red cells | ↓Hb (< 12 F), ↓MCV (< 80), ↓ferritin, ↓serum iron, ↑TIBC, ↓TSAT | Symptomatic (see below) |
- The average woman loses ~30–40 mL of blood per cycle, containing ~15–20 mg of iron
- Normal dietary iron absorption is ~1–2 mg/day (matching the ~1 mg/day basal iron loss from skin/GI desquamation)
- If menstrual blood loss exceeds ~60–80 mL/cycle, iron losses outstrip dietary absorption → negative iron balance → progressive depletion
- Menorrhagia is the most common cause of iron deficiency in premenopausal women [6][8]
Symptoms of anaemia: due to ↓O₂ delivery, depends on onset and severity of anaemia [10][11]
| Symptom/Sign | Pathophysiological Mechanism |
|---|---|
| Fatigue, ↓exercise tolerance, SOBOE [10] | ↓Haemoglobin → ↓oxygen-carrying capacity → tissues (especially exercising muscle) cannot meet metabolic demand |
| Palpitations [1][10] | Compensatory ↑heart rate and stroke volume (hyperdynamic circulation) to maintain cardiac output with reduced oxygen-carrying capacity |
| Dizziness, syncope (may be postural) [10] | ↓Cerebral oxygen delivery; if acute blood loss → ↓intravascular volume → orthostatic hypotension |
| Pallor (conjunctival, palmar crease) [10] | ↓Haemoglobin → ↓red colouration of blood → visible through mucous membranes and skin |
| Headache [1] | Cerebral vasodilation as compensatory mechanism to maintain cerebral oxygen delivery |
| Pica (appetite for non-food substances) [6] | Mechanism poorly understood but highly specific to iron deficiency; pagophagia (ice craving) is most common |
| Koilonychia (spoon-shaped nails) [6] | Severe iron deficiency → impaired keratin formation in the nail matrix → thin, brittle nails that curve upward |
| Glossitis (smooth, red tongue) [6] | Rapid epithelial cell turnover on the tongue requires iron; deficiency → papillary atrophy → smooth, painful tongue |
| Angular cheilitis (cracks at mouth corners) [6] | Epithelial thinning from iron deficiency → vulnerable to minor trauma and secondary infection |
| Restless leg syndrome [6] | Iron is a cofactor for tyrosine hydroxylase, the rate-limiting enzyme in dopamine synthesis; ↓iron → ↓dopamine in basal ganglia → uncomfortable leg sensations and urge to move |
| Plummer-Vinson/Paterson-Kelly syndrome (oesophageal web + IDA + glossitis) [6] | Extremely rare; iron deficiency → mucosal changes in upper oesophagus → web formation → dysphagia |
| Flow murmur (ejection systolic murmur) | Hyperdynamic, low-viscosity blood flow across normal valves → audible turbulence |
Anemic symptoms: headache, palpitation, SOB, dizziness, fatigue, pica [1]
- CBC: MicHyp anaemia, reactive thrombocytosis (↑EPO stimulates platelet precursors) [6]
- Why? Erythropoietin (EPO) and thrombopoietin (TPO) share structural homology and cross-react with each other's receptors to some extent. In iron deficiency, ↑EPO production (to drive erythropoiesis despite limited iron) can stimulate megakaryocyte precursors → ↑platelet count
- This is usually mild and clinically insignificant but is a useful laboratory clue pointing to IDA
When IDA is severe or develops in the context of pre-existing cardiovascular disease, the compensatory mechanisms become pathological:
| Complication | Mechanism |
|---|---|
| High-output cardiac failure | Chronic severe anaemia → persistent ↑cardiac output (↑heart rate + ↑stroke volume) → eventually the heart cannot maintain this → decompensation → heart failure with ↑JVP, peripheral oedema, hepatomegaly, pulmonary congestion |
| Cardiac ischaemia / angina [10] | ↓Oxygen-carrying capacity → myocardial oxygen demand exceeds supply, especially in those with co-existing coronary artery disease → anginal chest pain; can precipitate acute MI |
| Exacerbation of pre-existing cardiac conditions | Anaemia worsens any condition where myocardial oxygen supply is marginal — e.g., aortic stenosis, heart failure |
| ↑Mortality [10] | Severe untreated anaemia carries ↑mortality, particularly in elderly and those with cardiovascular comorbidities |
When Anaemia Becomes Dangerous
Chronic anaemia is usually well tolerated in young, otherwise healthy women because compensatory mechanisms (↑cardiac output, ↑2,3-DPG → rightward shift of Hb-O₂ dissociation curve) maintain tissue oxygenation. However, in elderly patients or those with IHD, even moderate anaemia (Hb 8–10) can precipitate angina or heart failure. Always consider the patient's baseline cardiovascular reserve.
While most HMB is chronic and outpatient, occasionally bleeding can be acute and torrential — particularly in the context of:
- Ruptured submucosal fibroid polyp
- Uterine AVM
- Coagulopathy (e.g., acute ITP, DIC)
- Anticoagulant use
Hypovolaemic shock is characterised by ↑sympathetic outflow [12]:
- Vasoconstriction → pallor, peripheral cyanosis, cold extremities, delayed capillary refill [12]
- Empty peripheral veins [12]
- Tachycardia [12]
- Sweating [12]
Causes of haemorrhagic hypovolaemic shock include uterine or vaginal haemorrhage and spontaneous haemorrhage due to bleeding diathesis [12].
Management follows standard resuscitation principles [12]:
- Large-bore IV access (14/16G)
- Bloods: CBC, clotting, crossmatch
- Rapid IV crystalloid then transfusion if needed
- Transfusion usually indicated when Hb < 7 g/dL (< 8 g/dL in IHD patient) [12]
- Treat underlying cause (hormonal haemostasis, surgical intervention, UAE)
This is arguably the most underappreciated complication, yet it is embedded in the very definition of HMB.
| Domain | Impact | Mechanism |
|---|---|---|
| Physical | Fatigue, exercise limitation, inability to work | Chronic anaemia + disruption of daily activities by heavy bleeding |
| Social | Avoidance of social activities, embarrassment from accidents (staining), school/work absenteeism | Fear of flooding, inability to predict or control bleeding |
| Emotional/psychological | Anxiety, depression, low self-esteem, feelings of loss of control | Biopsychosocial problem: impact on ADL [1]; chronic illness burden, body image concerns |
| Sexual | Avoidance of sexual intercourse, dyspareunia (if adenomyosis/endometriosis) | Fear of bleeding during intercourse; pain from underlying pathology |
| Financial/material | Cost of sanitary products, medical visits, lost wages | Direct economic burden — particularly relevant in lower socioeconomic settings |
| Fertility | Difficulty conceiving (if submucosal fibroids, anovulation, or endometriosis) | Structural distortion of cavity (implantation failure), anovulation (no oocyte release) |
5. Complications of Underlying Causes
HMB is a symptom, not a disease. The underlying causes carry their own complications:
Pressure symptoms: due to irregularly enlarged uterus, usually in > 12-week uterus [1]
| Complication | Mechanism |
|---|---|
| Urinary frequency [1] | Anterior fibroid compresses bladder → ↓capacity → frequent urge to void |
| Acute urinary retention (AROU) [1] | Classically a 12-week uterus with a cervical fibroid or a posterior fibroid pushing onto a retroverted uterus → kinking of urethra [1] |
| Hydronephrosis [1] | Large fibroid compresses ureter → obstructive uropathy |
| Tenesmus [1] | Posterior fibroid compresses rectum → sensation of incomplete evacuation [1] |
| Venous compression → ↑risk of VTE [1] | Very large uteri may compress vena cava [1] → venous stasis → ↑DVT/PE risk |
| Infertility [1] | Association is controversial but appear to be ↑in those distorting the cavity [1] — submucosal fibroids impair implantation and placentation |
| Miscarriage and preterm labour [1] | Due to adverse effect by submucosal fibroids on implantation, placentation and increase in uterine contractility [1] |
| Malpresentation and obstructed labour [1] | Due to distortion of shape of birth canal [1] |
| PPH [1] | ↑Risk by ↓force and coordination of uterine contractions → ↑risk of atony [1] |
| Red degeneration [1] | Classically occur in mid-2nd trimester of pregnancy — rapid fibroid growth outstrips blood supply → ischaemic necrosis → acute pain, fever, ↑WCC. Treatment is conservative (analgesia, hydration) |
| Torsion of pedunculated fibroid [1] | A/w acute pain ± fever [1] — pedunculated subserosal fibroid twists on its stalk → ischaemia → acute abdomen |
| Fibroid degeneration (other types) | Hyaline, cystic, calcific degeneration — generally asymptomatic but may confuse imaging |
| Sarcomatous change (leiomyosarcoma) | Extremely rare (< 0.5%); rapid growth or post-menopausal growth → worrisome of malignancy [1] |
| Complication | Mechanism |
|---|---|
| Progressive dysmenorrhoea | Ectopic endometrial tissue within myometrium undergoes cyclical swelling → pain worsens over time |
| Infertility / subfertility | Disrupted junctional zone → impaired uterine peristalsis and implantation |
| Adverse pregnancy outcomes | ↑Risk of preterm birth, preterm PROM, malpresentation, C/S |
| Complication | Mechanism |
|---|---|
| Progression to endometrial carcinoma | Atypical hyperplasia: ~25–30% progression to carcinoma — chronic unopposed oestrogen → accumulated genetic mutations → neoplastic transformation |
| Delayed diagnosis of malignancy | If HMB is attributed to a benign cause and endometrial sampling is not performed, early carcinoma may be missed |
| Complication | Mechanism |
|---|---|
| Post-partum bleeding (62% in vWD) [4] | vWF levels decline precipitously after delivery [4] → loss of haemostatic protection → PPH |
| Surgical bleeding risk | Undiagnosed coagulopathy → unexpected haemorrhage during any surgical procedure (including gynaecological surgery for HMB) |
| Chronic anaemia from multiple mucocutaneous sites | HMB is just one manifestation; concurrent epistaxis, GI bleeding, gum bleeding compound blood loss |
6. Complications of HMB Treatment
Treatments themselves carry complications — this is important for exam questions that ask about "complications of management."
| Treatment | Complications | Mechanism |
|---|---|---|
| Tranexamic acid | Rarely: GI upset, headache; very rarely: seizures (high dose), thromboembolic events | Antifibrinolytic effect theoretically ↑thrombosis risk, but meta-analyses show no significant ↑ at therapeutic doses |
| COCP | CVS risk: ↑risk of MI, stroke, thromboembolism [1]; breakthrough bleeding; breast tenderness; minimal ↑risk in breast and cervical CA [1] | Oestrogen → ↑hepatic synthesis of clotting factors (II, VII, IX, X, fibrinogen) + ↓antithrombin, protein S |
| LNG-IUS (Mirena) | Irregular bleeding/spotting (first 3–6 months), functional ovarian cysts (~10%), expulsion (~5%), uterine perforation (rare, ~1:1000 at insertion) | Progestogen causes initial irregular endometrial shedding before full decidualisation; ovarian cysts from incomplete ovulation suppression |
| GnRH agonists | Climacteric symptoms (hot flushes, vaginal dryness), ↓bone mineral density [1]; irregular bleeding [1] | Medical menopause → ↓oestrogen → menopausal symptoms and ↑bone resorption via ↑RANKL:OPG ratio |
| Oral progestogens | Bloating, breast tenderness, mood changes, acne, weight gain; note: norethisterone at high doses has partial oestrogenic activity → thrombogenic potential | Progestogenic side effects; hepatic conversion to ethinylestradiol at high doses |
| Oral iron | N/V, constipation, epigastric discomfort, metallic taste, black stool [6] | Direct GI mucosal irritation by iron salts; black stool from unabsorbed iron (not melena) |
| Procedure | Key Complications | Mechanism |
|---|---|---|
| Endometrial ablation [1] | Uterine perforation and haemorrhage; haematometra; postablation tubal sterilisation syndrome; pelvic infections [1] | Perforation: instrument penetrates thinned myometrium; haematometra: remaining endometrium behind occlusion → cyclical bleeding → amenorrhoea with cyclical pain [1]; postablation tubal sterilisation syndrome: cyclical pain in those with ablation + tubal ligation — ?trapping of blood in uterine cornua [1] |
| Hysteroscopic myomectomy | Fluid overload/hyponatraemia (from glycine irrigation), uterine perforation, incomplete resection, adhesion formation (Asherman syndrome) | Glycine is a hypotonic non-electrolyte distension medium → absorbed into circulation → dilutional hyponatraemia → cerebral oedema (severe cases) |
| Hysterectomy | Haemorrhage, infection (wound, vault, pelvic abscess), injury to bladder/ureter/bowel, VTE, vaginal vault prolapse (long-term), premature menopause (if ovaries removed), psychological impact | Major abdominal/pelvic surgery → operative and postoperative complications; BSO → abrupt oestrogen withdrawal → menopausal symptoms, ↑cardiovascular and osteoporosis risk |
| Myomectomy | Haemorrhage (fibroids are highly vascular), adhesion formation, fibroid recurrence (~15–30% at 5 years), uterine rupture risk in subsequent pregnancy | Vascular bed of fibroid bleeds during excision; peritoneal injury → adhesion formation |
| UAE | Post-embolisation syndrome (pain, fever, nausea), fibroid passage (expulsion of necrotic tissue), premature ovarian failure (~3% if > 45y), uterine infection, rarely uterine necrosis requiring hysterectomy | Ischaemic necrosis of fibroid → inflammatory reaction (post-embolisation syndrome); utero-ovarian anastomoses → ovarian blood supply compromise → POF |
Post-Ablation Pregnancy Risk
Pregnancy is contraindicated after endometrial ablation [1]. Despite ablation, ~0.7% of women still become pregnant. These pregnancies carry significant risk including placenta accreta/increta (destroyed basalis cannot form normal decidua → trophoblast invades deeply into myometrium), preterm delivery, uterine rupture, and neonatal morbidity. Effective contraception is mandatory post-ablation.
| Scenario | Risk | Mechanism |
|---|---|---|
| Untreated anovulatory HMB | Endometrial hyperplasia → carcinoma | Chronic unopposed oestrogen drives endometrial proliferation → accumulation of genetic mutations → hyperplasia → atypia → carcinoma (the "oestrogen-to-cancer" pathway) |
| Untreated fibroids | Continued growth, worsening symptoms, very rarely leiomyosarcoma | Oestrogen-dependent growth continues until menopause; sarcomatous transformation is < 0.5% but must be considered if rapid growth, especially post-menopause |
| Undiagnosed coagulopathy | PPH, surgical bleeding, ↑transfusion risk | Without prior identification and peri-procedural management (DDAVP, factor replacement), coagulopathies cause unexpected bleeding during delivery or surgery |
| Category | Complication | Key Mechanism |
|---|---|---|
| Haematological | Iron deficiency anaemia (most common) | Chronic blood loss > dietary iron absorption → negative iron balance |
| Cardiovascular | High-output cardiac failure, angina, MI (in at-risk patients) | Compensatory ↑cardiac output overwhelms cardiac reserve |
| Haemodynamic | Hypovolaemic shock (acute severe HMB) | Rapid blood loss → ↓intravascular volume → ↓tissue perfusion |
| Quality of life | Physical, social, emotional, sexual, financial impairment | Chronic unpredictable heavy bleeding → activity limitation and psychological distress |
| Fertility | Subfertility (fibroids, anovulation), miscarriage, adverse pregnancy outcomes | Cavity distortion (fibroids), absent ovulation (anovulatory HMB), disrupted implantation |
| Obstetric | PPH (fibroids, vWD), red degeneration (pregnancy + fibroids) | Impaired myometrial contraction (fibroids); ↓vWF post-delivery (vWD); ischaemic necrosis of fibroid in pregnancy |
| Oncological | Endometrial hyperplasia → carcinoma | Unopposed oestrogen (anovulatory HMB, PCOS, obesity) |
| Iatrogenic | Treatment-related complications (see above) | Procedure-specific risks |
High Yield Summary
IDA is the most common and most important complication of HMB. It follows a staged progression: iron store depletion → functional iron deficiency → frank IDA (microcytic hypochromic anaemia). Menorrhagia is the leading cause of IDA in premenopausal women.
Cardinal anaemic symptoms: fatigue, SOBOE, palpitations, dizziness, headache. Signs: pallor, koilonychia, glossitis, angular cheilitis. Specific to iron deficiency: pica, restless leg syndrome, Plummer-Vinson syndrome.
Cardiovascular complications: in severe/chronic anaemia — high-output heart failure, angina, MI (especially in patients with pre-existing IHD).
Acute severe HMB can cause hypovolaemic shock — tachycardia, hypotension, cold peripheries, delayed capillary refill.
QoL impact is embedded in the definition of HMB and is an underappreciated but significant complication.
Fibroid-specific complications: pressure symptoms (urinary, bowel, venous), infertility, pregnancy complications (red degeneration, miscarriage, preterm labour, malpresentation, PPH), and very rarely sarcomatous transformation.
Anovulatory HMB carries oncological risk: chronic unopposed oestrogen → endometrial hyperplasia → atypical hyperplasia → carcinoma. This is why endometrial sampling is indicated in women ≥ 45 with regular HMB or ≥ 40 with irregular bleeding.
Undiagnosed coagulopathy (especially vWD) → risk of PPH and unexpected surgical bleeding.
Treatment complications: COCP → VTE risk; GnRH agonists → bone loss and climacteric symptoms; endometrial ablation → haematometra, perforation, pregnancy contraindicated post-procedure; hysterectomy → surgical complications; UAE → post-embolisation syndrome, premature ovarian failure.
Active Recall - Complications of HMB
References
[1] Lecture slides: Adrian Lui Gynecology Notes.pdf (p11–13, p17, p19, p90, p92) [4] Senior notes: Ryan Ho Haemtology.pdf (p127–129 — vWD clinical features, PPH risk, management) [6] Senior notes: Maksim Medicine Notes.pdf (p153 — IDA clinical features, laboratory findings) [7] Senior notes: Ryan Ho Chemical Path.pdf (p53 — iron deficiency stages) [8] Senior notes: Ryan Ho Haemtology.pdf (p19 — IDA management, IV iron, transfusion indications) [10] Senior notes: Ryan Ho Haemtology.pdf (p10 — approach to anaemia, symptoms, signs, complications) [11] Senior notes: Ryan Ho Fundamentals.pdf (p380 — anaemia symptoms, signs, red cell indices) [12] Senior notes: Ryan Ho Critical Care.pdf (p20–21 — hypovolaemic shock causes, clinical features, management)
High Yield Summary
Definition: HMB = excessive menstrual blood loss interfering with physical, social, emotional, and/or material quality of life (NICE/FIGO — patient-centred). Old threshold was > 80 mL/cycle.
Normal menstruation: Cycle 24–38 days, flow ≤ 8 days, volume 5–80 mL. Controlled by spiral artery vasoconstriction, prostaglandin balance, local fibrinolysis, myometrial contraction, and endometrial regeneration.
PALM-COEIN (FIGO): Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia (structural) | Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified (non-structural).
Key pathophysiology: ↑endometrial surface area (fibroids, polyps), impaired myometrial contraction (adenomyosis, fibroids), altered local haemostasis (↑tPA, ↑PGE₂), unopposed oestrogen (anovulation), systemic coagulopathy.
Submucosal fibroids (FIGO types 0–2) cause HMB most — location > size. vWD in 10–15% of HMB; screen if HMB since menarche + mucocutaneous bleeding.
Always exclude pregnancy (β-hCG) and malignancy (age ≥ 45 with regular HMB, age ≥ 40 with IMB/irregular, any age with RFs).
Exam: Adenomyosis = uniformly enlarged, boggy, tender uterus. Fibroids = irregularly enlarged, firm, non-tender.
High Yield Summary — Differential Diagnosis
Step 1: Confirm bleeding is uterine (speculum essential). Step 2: Exclude pregnancy (β-hCG). Step 3: Use bleeding pattern to narrow DDx.
| Pattern | Key differentials |
|---|---|
| Heavy, regular | Fibroids (submucosal), adenomyosis, coagulopathy (vWD), AUB-E, copper IUD |
| Heavy, irregular | Anovulation (PCOS, perimenopause), polyps, hyperplasia, malignancy |
| IMB | Polyps, cervical pathology, hyperplasia/CA, PID, hormonal breakthrough |
| PCB | Cervical ectropion, polyp, cervicitis, cervical carcinoma |
Fibroids vs adenomyosis: Fibroids = irregular, firm, non-tender; adenomyosis = globular, boggy, tender + dysmenorrhoea.
Anovulation vs structural: Irregular unpredictable bleeding (AUB-O) vs regular but heavy (structural).
Must-not-miss: Endometrial carcinoma (> 40, RFs), pregnancy/ectopic, cervical CA, coagulopathy (menarche onset), PID.
Age-based: Adolescents → anovulation + vWD; reproductive → fibroids + pregnancy; perimenopausal → anovulation + exclude malignancy; postmenopausal → carcinoma until proven otherwise.
High Yield Summary — Diagnosis
HMB is a clinical diagnosis — investigations find the cause and assess consequences (anaemia), not confirm HMB itself.
Baseline for ALL: Pregnancy test + CBC (Hb, platelets).
| Investigation | When | Key point |
|---|---|---|
| Iron profile | Anaemia suspected | Ferritin most sensitive; falsely normal in inflammation (acute phase reactant) |
| Clotting + vWF assay | HMB since menarche, FHx, mucocutaneous bleeding | aPTT can be normal in vWD — go to vWF:Ag, vWF:Act, FVIII |
| Pelvic USS (TVUS ± TAS) | Structural cause suspected | Fibroid = hypoechoic + pseudocapsule; adenomyosis = heterogeneous myometrium |
| Endometrial aspirate (EA) | Age ≥ 45 regular HMB; age ≥ 40 IMB/irregular; any age with RFs; all PMB | Blind office procedure; ~90% sensitive for diffuse CA |
| Hysteroscopy ± biopsy | Suspected polyp/submucosal fibroid; EA failed; bleeding on hormonal Tx > 3 months | Superior for focal lesions — "see and treat" |
Postmenopausal ET: ≤ 4 mm on TVUS → NPV 99.4–100% for endometrial CA.
TFT: Only when clinically symptomatic (uncommon direct cause).
High Yield Summary — Management
Principles: Treat underlying cause; balance fertility vs completed family; assess severity (acute vs chronic); check contraindications.
First-line medical (no structural cause): COCP (unless C/I) or LNG-IUS (Mirena) — Mirena most effective (~90–95% ↓MBL).
| Agent | Dose / role |
|---|---|
| Tranexamic acid | 1g TDS during menses (↓MBL ~40–50%); antifibrinolytic — works across aetiologies |
| Mefenamic acid | 250–500 mg TDS; ↓dysmenorrhoea but does NOT reduce fibroid-related HMB |
| Cyclical progestogen | Norethisterone 5 mg TDS days 5–26 if C/I to COCP |
| Iron | FeSO₄ 300 mg BD × 12 weeks; IV iron if intolerant/severe |
Mirena for fibroids: Only if < 3 cm with no cavity distortion.
Fibroids: Hormonal Tx has little efficacy (flow control only); GnRH agonists pre-op only (3–6 months). Surgery if symptomatic, rapid/postmenopausal growth, subfertility with submucosal element. UAE if fertility not desired.
Adenomyosis: Hormonal Tx more effective than fibroids; hysterectomy definitive (no surgical plane).
Hyperplasia without atypia: Progestogen + repeat EA 3–6 months. Atypical: hysterectomy (25–30% progression).
Acute severe HMB: Resuscitate → IV TXA → high-dose oestrogen or progestogen → balloon tamponade → surgery if uncontrolled.
High Yield Summary — Complications
IDA is the cardinal complication — menorrhagia is the leading cause in premenopausal women. Stages: store depletion → functional iron deficiency → frank IDA (microcytic hypochromic). Symptoms: fatigue, SOBOE, palpitations, pica.
Cardiovascular: Severe/chronic anaemia → high-output cardiac failure, angina (especially with IHD).
Acute severe HMB: Hypovolaemic shock — resuscitate, transfuse if Hb < 7 or symptomatic.
QoL impact is embedded in the HMB definition itself.
Fibroid-specific: Pressure symptoms (urinary, bowel, VTE from vena cava compression), infertility, pregnancy complications (red degeneration, miscarriage, PPH), rare sarcomatous change (rapid/postmenopausal growth).
Anovulatory HMB: Chronic unopposed oestrogen → endometrial hyperplasia → carcinoma — why EA is indicated in at-risk women.
Undiagnosed vWD: PPH, unexpected surgical bleeding.
Treatment complications: COCP → VTE; GnRH agonists → bone loss; endometrial ablation → pregnancy contraindicated; hysterectomy → surgical morbidity; UAE → post-embolisation syndrome, premature ovarian failure.
Endometriosis
Endometriosis is a chronic gynecological condition in which endometrial-like tissue grows outside the uterine cavity, commonly on the ovaries, fallopian tubes, and pelvic peritoneum, causing inflammation, pain, and potential infertility.
Intermenstrual And Irregular Bleeding
Intermenstrual and irregular bleeding refers to uterine bleeding that occurs between expected menstrual periods or deviates from the normal cyclical pattern in timing, frequency, or duration, potentially indicating hormonal imbalance, structural lesions, or systemic pathology.