In one line
Heavy menstrual bleeding is excessive menstrual loss that impairs a woman's quality of life, classified by cause through FIGO PALM-COEIN; once pregnancy and malignancy are excluded and there is no structural lesion, the most effective medical treatment is the levonorgestrel intrauterine system, and the consultant's task is to match the intervention to the cause, the woman's fertility wishes, and — in South Africa — to what the service can actually deliver before her anaemia and her time run out.
Mechanism & pathophysiology
Menstruation is the controlled shedding of the secretory endometrium when the corpus luteum fails and progesterone withdrawal triggers it. The volume lost is set by a balance the endometrium itself controls: vasoconstriction of the spiral arterioles, platelet plug formation, and a brisk local fibrinolytic response that liquefies clot so the cavity does not obliterate. Normal loss is roughly 30–40 mL per cycle; loss above ~80 mL is the volume historically defined as menorrhagia and the level above which iron-deficiency anaemia becomes likely. The modern definition is deliberately not a millilitre count — it is bleeding that interferes with physical, social, emotional or material quality of life — because women do not measure their loss and the clinical problem is the impact, not the assay.
Two mechanisms produce heavy loss, and they map onto the management. Disordered local haemostasis is the dominant pathway in heavy bleeding from an anatomically normal uterus: the endometrium of women with heavy menstrual bleeding shows relative deficiency of the vasoconstrictors (endothelin, prostaglandin F2α) and an excess of vasodilatory prostaglandins (PGE2) and of plasminogen activators, so the vessels constrict poorly and the clot dissolves too fast. This is precisely why the two non-hormonal first-line drugs work where they do: tranexamic acid is an antifibrinolytic that blocks plasminogen activation and stems the excess clot lysis, and the NSAID mefenamic acid inhibits cyclo-oxygenase and rebalances the prostaglandin ratio. The drugs are not symptomatic afterthoughts — each corrects a specific limb of the deranged endometrial physiology.
The second mechanism is structural or systemic disruption of that haemostatic environment: a submucosal fibroid or polyp increasing endometrial surface area and distorting vascular architecture; adenomyosis enlarging the uterus and disrupting junctional-zone contractility; a coagulopathy removing the systemic clotting reserve; or anovulation removing progesterone so the endometrium proliferates unopposed under oestrogen, becomes thick and fragile, and sheds erratically and heavily. Anovulatory bleeding dominates at the two ends of reproductive life — the adolescent with an immature hypothalamic–pituitary–ovarian axis and the perimenopausal woman with failing follicular recruitment — and unopposed oestrogen is also the thread linking persistent anovulation to endometrial hyperplasia and carcinoma, which is why the same anovulatory pattern that looks benign in a 16-year-old is a malignancy concern in a 52-year-old. The mechanistic groundwork on the menstrual cycle, ovulatory physiology and the pathological lesions is assumed here from the Intermediate heavy-menstrual-bleeding chapters; the level above is reasoning from that physiology to a structured cause and a defensible plan.
FIGO PALM-COEIN is the structured classification that organises all of this and is the language an examiner expects. It separates causes into structural (assessable by imaging or histology) and non-structural:
- PALM — Polyp; Adenomyosis; Leiomyoma (subclassified by location, the clinically critical split being submucosal versus other); Malignancy and hyperplasia.
- COEIN — Coagulopathy; Ovulatory dysfunction; Endometrial (a primary disorder of endometrial haemostasis or inflammation, a diagnosis of exclusion); Iatrogenic (anticoagulants, copper IUD, exogenous hormones, and the breakthrough bleeding of progestin-only methods); Not otherwise classified (arteriovenous malformation, isthmocele/niche after caesarean). A woman can carry more than one category at once — a fibroid uterus in a woman who is also anovulatory — so the classification is annotated, not forced into a single box, and the discipline it imposes is that you assign each category present rather than stopping at the first lesion you find.
Assessment
The first job is to confirm the bleeding really is heavy and is menstrual, and the second is to exclude the two things that change everything — pregnancy and malignancy — before reaching for the PALM-COEIN work-up.
- Quantify by impact, not by volume. Ask about flooding, clots, double sanitary protection, changing protection at night, restriction of work, school or social activity, and the symptoms of anaemia (fatigue, breathlessness, pica). The Pictorial Blood Assessment Chart can support the history but the clinical anchor is the effect on the woman's life.
- A bleeding and coagulopathy screen from the history is mandatory, not optional. Heavy bleeding since menarche, a family history of bleeding disorder, postpartum haemorrhage, bleeding with dental work or surgery, or easy bruising/epistaxis should trigger investigation for an inherited bleeding disorder. Von Willebrand disease is the one to remember: in women presenting with menorrhagia its prevalence is around 13%, far higher than in the general population, and it is routinely missed because the bleeding is attributed to a gynaecological cause. The corollary is that coagulopathy is disproportionately the answer in the adolescent with heavy bleeding from the first period — she earns a coagulation screen, von Willebrand factor antigen and activity, and factor VIII before she earns a hormonal label.
- Examination is directed at the structural categories: abdominal and bimanual examination for an enlarged, bulky or irregular uterus (fibroids, adenomyosis), and speculum examination of the cervix — a friable or visible cervical lesion is biopsied, not smeared, exactly as for any suspected genital-tract cancer. A normal examination does not exclude a submucosal lesion.
- Baseline bloods: full blood count in every woman (the prevalence and consequence of iron deficiency make this non-negotiable) and a pregnancy test in anyone of reproductive age. Ferritin is added where iron deficiency is suspected or the blood indices are equivocal rather than as a universal test, since the guideline mandates the blood count for all women but not routine ferritin. Thyroid function and a coagulation screen are directed by the history, not reflexive.
- Transvaginal ultrasound is the first-line structural investigation — it sizes and locates fibroids, raises adenomyosis, measures endometrial thickness and identifies a focal mass. Its weakness is the submucosal lesion in a thickened endometrium, where it under-reads polyps and intracavitary fibroids; saline-infusion sonography (sonohysterography) or hysteroscopy resolves the cavity directly and is the investigation when ultrasound is equivocal, when there is persistent intermenstrual bleeding, or when a structural cause is suspected but not seen.
- Endometrial sampling is targeted, not universal. It is taken to exclude hyperplasia and carcinoma in the women whose pre-test probability justifies it, and the framework is risk-based rather than a single age cut-off: persistent intermenstrual or irregular bleeding, unopposed-oestrogen risk (obesity, PMOS — polyendocrine/metabolic ovarian syndrome, previously PCOS — tamoxifen, a strong family history), and failure of medical treatment. Any postmenopausal bleeding is evaluated and sampled regardless of the scan. Rising age raises the pre-test probability, and the SA STG sets an explicit age threshold for sampling that is worth following where it applies, but that is a separate document from the risk-based NICE framework and the two should not be merged. A blind office biopsy that misses a focal lesion is a false reassurance; where a focal abnormality is suspected, sampling is done under hysteroscopic vision so the lesion is actually hit. The principle that organises sampling thresholds is simple: you sample whenever the risk of an endometrial neoplasm is high enough that a normal scan is not enough to rest on.