Abnormal Vaginal Bleeding — Terminology & Causes

A structured framework for classifying abnormal uterine bleeding in non-pregnant reproductive-age patients. Pregnancy must be excluded before any further assessment.

Key definitions
Heavy menstrual bleeding (HMB / menorrhagia)
Excessive cyclical menstrual bleeding interfering with physical, emotional, social, or material quality of life. Does NOT include intermenstrual or postcoital bleeding.
Abnormal uterine bleeding (AUB)
Broader term — menstrual bleeding of abnormal quantity, duration, or schedule. Classified by the FIGO PALM-COEIN system.
Intermenstrual bleeding and postcoital bleeding require separate investigation — they are not managed as HMB. Pregnancy must be excluded first in all cases.
PALM-COEIN classification (FIGO)
PALM — Structural
P — Polyp
Hysteroscopic polypectomy; often causes intermenstrual bleeding or HMB
A — Adenomyosis
HMB with dysmenorrhoea; bulky tender uterus; hysterectomy is definitive
L — Leiomyoma (fibroids)
Affects 30% of individuals with HMB; submucosal particularly implicated
M — Malignancy & hyperplasia
Risk factors: age >45, obesity, PCOS, unopposed oestrogen, tamoxifen, family history
COEIN — Non-structural
C — Coagulopathy
HMB from menarche; e.g. von Willebrand disease; screen adolescents
O — Ovulatory dysfunction
Irregular cycles; PCOS most common; also hypothyroidism, hyperprolactinaemia
E — Endometrial
Primary haemostatic disorder of the endometrium; diagnosis of exclusion
I — Iatrogenic
IUCDs, anticoagulants, tamoxifen, exogenous oestrogens; some herbal supplements
N — Not otherwise classified
AVM, caesarean scar defect (isthmocele), enhanced myometrial vascularity
Fibroids are the most common uterine pathology. Abnormal endometrial haemostasis is the most common functional cause but is a diagnosis of exclusion.
Normal menstrual parameters (FIGO System 1)
ParameterNormalAbnormal
Frequency≥24 and ≤38 daysAbsent (amenorrhoea); frequent (<24d); infrequent (>38d)
Duration≤8 daysProlonged (>8 days)
RegularityShortest-to-longest cycle variation ≤7–9 daysVariation ≥10 days
Flow volumePatient-determined (normal)Patient-determined (heavy or light)
IntermenstrualNoneRandom or cyclic (early/mid/late) — separate workup

History & Red Flags

Structured history focused on distinguishing HMB from other bleeding patterns, identifying underlying causes, and flagging features that require early referral.

History — structured approach
Bleeding pattern & volume
Age / LNMPConfirm age; date of last normal menstrual period
ContraceptionCurrent method; possibility of pregnancy/miscarriage
PatternRegular or irregular — and how many years since menarche
VolumeFlooding, clot size, double protection, nocturnal changes; PBAC score
TypeHMB vs intermenstrual vs postcoital — different workups
Impact & associated symptoms
QoL impactWork, sleep, activities, relationships
Pelvic painEndometriosis / fibroids / adenomyosis suggestive
DysmenorrhoeaSevere at baseline = early referral indication
Iron deficiencyFatigue, hair loss, pica, restless legs — with or without anaemia
Bleeding elsewhereEpistaxis, bruising, dental bleeding — coagulopathy clue
Reproductive & gynaecological
ParityPrevious pregnancies; desire for future fertility
Cervical screeningStatus — take at consultation if due
Family historyEndometrial, bowel (Lynch), ovarian cancer
Prior surgeryCaesarean (isthmocele), fibroid treatment
Medical & medication history
ComorbiditiesDiabetes, obesity, thyroid, PCOS, bleeding disorders
MedicationsAnticoagulants, tamoxifen, exogenous oestrogens, IUCD
OTC / herbalGinseng, ginkgo, soya — may affect oestrogen / coagulation
Approximately two-thirds of patients on oral anticoagulants experience AUB — this typically unmasks underlying pathology rather than causing it. Always investigate.
Red flags — indications for EARLY referral (before 6 months)
Concurrent severe dysmenorrhoea at baseline
Or dysmenorrhoea not settling after 3 months of pharmacotherapy — suggests endometriosis or adenomyosis.
Suspected fertility-threatening pathology
Individuals wishing to conceive in whom endometriosis or adenomyosis is suspected.
Fibroids >3 cm or endometrial polyps
Specialist assessment for surgical options (myomectomy, hysteroscopic resection, UAE).
Elevated endometrial cancer risk
Oligomenorrhoea, PCOS, personal/family history of endometrial or colon cancer, unopposed oestrogen, tamoxifen, obesity (especially with diabetes/hypertension), age >45 years.
Radiological findings
Endometrial thickness >12 mm premenopausal or ≥5 mm perimenopausal (measured first half of cycle).
Acute severe bleeding / haemodynamic instability
Send to emergency department. Exclude pregnancy-related bleeding first.
Postcoital or intermenstrual bleeding
Require separate investigation — NOT treated as HMB. Cervical, endometrial, or infective causes.
Examination
Abdominal
Suprapubic/pelvic mass (fibroids); palpable uterine fundus above pelvic brim; tenderness
Speculum
Visualise cervix; exclude visible lesions; take CST if due
Bimanual
Uterine size, shape, mobility; adnexal masses/tenderness; fixed retroverted uterus or uterosacral nodularity (endometriosis)
General
Pallor, tachycardia (anaemia); BMI, BP; thyroid, PCOS (hirsutism, acne), bleeding disorder (bruising, petechiae)

Investigations

A tiered approach to investigating HMB/AUB — from essential baseline tests, through targeted add-ons based on clinical assessment, to specialist investigations.

1
First-line — all patients
Essential baseline — order for every HMB presentation
β-hCG (pregnancy)
Exclude pregnancy BEFORE all other investigations
Full blood examination (FBE)
Identify anaemia, thrombocytopenia
Serum ferritin
Assess for iron deficiency in ALL individuals with HMB — may have deficiency without anaemia
Cervical screening test
If due
2
Consider — targeted based on clinical features
Add these when history or examination suggests the underlying cause
Coagulation profile + von Willebrand screen
Especially in adolescents with irregular bleeding from menarche, or family history of clotting disorders. Severe HMB in adolescents from menarche should always prompt coagulopathy screening.
Serum TSH
If clinical features suggest thyroid dysfunction; hypothyroidism is a recognised ovulatory dysfunction cause.
Pelvic ultrasound
Indicate menopausal status on the request. Perform days 5–10 of cycle if possible. Transvaginal preferred (better detail); transabdominal if TVS unavailable or declined.
Indications: increased endometrial cancer risk, polyps suspected, uterine fibroids suspected, endometriosis/adenomyosis suspected, OR symptoms unresponsive after 6 months of medical therapy (3 months if concurrent dysmenorrhoea).
Do NOT routinely order sex hormone testing (oestradiol, FSH, LH) in individuals with cyclical bleeding — ovarian and pituitary function will be normal.
3
Specialist investigations
After referral, or if endometrial cancer suspected
Saline-infused sonography
Enhanced visualisation of endometrial cavity; polyps, submucosal fibroids
Hysteroscopy
Direct visualisation; diagnostic + operative (polypectomy, myomectomy)
Endometrial biopsy
Exclude hyperplasia/malignancy
Biopsy indications: bleeding unresponsive to medical therapy; other endometrial cancer risk factors (age >45, unopposed oestrogen, obesity, PCOS, Lynch syndrome, tamoxifen); endometrial thickness >12 mm premenopausal or >5 mm perimenopausal. A normal cervical screening test does NOT exclude endometrial cancer.

HMB Management

Treatment depends on fertility intentions, contraceptive needs, and coexisting symptoms. All doses below are from Therapeutic Guidelines (eTG).

Decision framework
Trying to conceive?
Yes → non-hormonal (tranexamic acid ± NSAID)
No → consider contraception question
Contraception required?
Yes → LNG-IUD / COC / vaginal ring / DMPA
No → LNG-IUD still first-line
Dysmenorrhoea?
Tranexamic acid is NOT effective for dysmenorrhoea. NSAIDs and all hormonal therapies help both.
Most effective drug therapy: 52 mg levonorgestrel-releasing intrauterine device (LNG-IUD) — first-line even when contraception is not required.
Hormonal therapy — dosing (eTG)
Levonorgestrel-releasing IUD 52 mg
Inserted into uterus. Replace every 5 years. Most effective medical therapy for HMB. Some irregular bleeding expected in first few months — refer if not settled at 6 months. Note: the 19.5 mg LNG-IUD is not indicated for HMB.
Combined oral contraceptive (COC)
Once daily. Extended or continuous use recommended to avoid/minimise withdrawal bleeding. Estradiol valerate + dienogest has indication for heavy/prolonged bleeding but no head-to-head data to favour over other formulations.
Ethinylestradiol + etonogestrel vaginal ring 2.7/11.7 mg
Intravaginally; extended/continuous use, OR 3 weeks in then 7 days out. Likely effective but less evidence than COCs.
Depot medroxyprogesterone acetate (DMPA)
150 mg deep IM every 12 weeks. Induces amenorrhoea in 50–70% at 1 year. Alternative if LNG-IUD and vaginal ring unsuitable.
Oral progestogens — REGULAR cycles (short-term only)
Medroxyprogesterone 5–10 mg orally, 1–3 times daily, days 1 to 21 of a 28-day cycle.
OR Norethisterone 5 mg orally, 2–3 times daily, days 5 to 26 of a 28-day cycle.
Review at 6 months. Must be given for ≥21 days of cycle — shorter courses do NOT reduce blood loss.
Oral progestogens — IRREGULAR cycles (short-term only)
Medroxyprogesterone 5–10 mg daily for the same 12 days each calendar month.
OR Norethisterone 5 mg once–twice daily for the same 12 days each calendar month.
OR Micronised progesterone 200–300 mg nightly for the same 12 days each calendar month (fewer adverse effects, more expensive).
POP is not recommended for HMB. Oral progestogens are short-term therapy only — long-term use risks hypoestrogenism (bone and potentially cardiovascular health).
Non-hormonal therapy — dosing (eTG)
Tranexamic acid (antifibrinolytic)
1 to 1.5 g orally, 6- to 8-hourly for the first 3 to 5 days of each cycle. Reduces blood loss more than NSAIDs or oral progestogens. Well tolerated. Caution if predisposed to thromboembolism.
Ibuprofen
200–400 mg orally, 3 times daily. Start just before/at onset of menses; continue up to 5 days.
Mefenamic acid
500 mg orally, 3 times daily; start just before/at menses onset; up to 5 days. (Aged 12+; use <14 years not a registered indication.)
Naproxen
500 mg initially, then 250 mg every 6–8 hours. Max 1250 mg/day. Up to 5 days from menses onset.
Tranexamic acid and NSAIDs can be combined, and can also be combined with hormonal therapy if required. NSAIDs reduce dysmenorrhoea but are less effective than tranexamic acid for blood loss control.

Acute Severe Heavy Uterine Bleeding

An episode in a non-pregnant reproductive-age patient in which the quantity of bleeding requires immediate intervention. Pregnancy-related haemorrhage must be excluded first.

Immediate priorities: Resuscitate haemodynamically unstable patients. Exclude pregnancy-related bleeding. Investigate causes once stable. Use lowest effective dose, especially in adolescents — but high doses may be needed short-term to control bleeding.
Hormonal regimens
Medroxyprogesterone (first-line)
10 mg orally, every 4 to 8 hours until bleeding stops. Taper over a few weeks after control. Expect withdrawal bleed when stopped.
Norethisterone (first-line)
5 to 10 mg orally, every 4 to 8 hours until bleeding stops. Taper similarly.
High-dose COC (if progestogens fail)
Ethinylestradiol 35 or 50 micrograms orally, every 6 hours until bleeding stops. Re-evaluate after 48 hours. Taper over a few weeks.
An antiemetic is recommended with hormonal therapy for acute severe bleeding (nausea is common with high-dose oestrogen). Caution with high-dose estrogen/progestogen in those at VTE risk.
Tranexamic acid — alternative to hormonal therapy
Tranexamic acid — oral (GP setting)
1 to 1.5 g orally, 6- to 8-hourly until bleeding stops. Tapering NOT required.
Tranexamic acid — intravenous (hospital)
10 mg/kg intravenously, every 8 hours until bleeding stops.
Caution in those with increased thromboembolism risk. Once acute bleeding is controlled, transition to standard HMB management to prevent recurrence in subsequent cycles.
Special considerations — adolescents
Severe bleeding from menarche
Always investigate for coagulation disorders (especially von Willebrand disease) — HMB may be the first manifestation.
Otherwise healthy adolescent
Severe bleeding usually reflects an immature hypothalamic–pituitary–ovarian axis with anovulatory cycles.

Referral & Follow-up

When to refer, what surgical options exist, and the essential safety-netting and monitoring points for patients managed in general practice.

When to refer
After 6 months of unsuccessful pharmacotherapy
Refer for specialist assessment and consideration of surgical options.
Early referral (before 6 months)
Red-flag features: severe dysmenorrhoea, fibroids >3 cm, polyps, fertility concerns with suspected endometriosis/adenomyosis, endometrial cancer risk factors.
Emergency department
Severe anaemia, acute heavy bleeding, haemodynamic instability.
Haematology
Suspected bleeding disorder (HMB from menarche, family history, other bleeding symptoms); complex thrombosis risk affecting treatment choice.
For any patient with an indication for specialist referral, arrange an ultrasound before referral.
Surgical options — specialist-led
Uterine-preserving (fertility preserved)
• Hysteroscopic resection of polyps / small fibroids
• Laparoscopic resection of fibroids
• Fibroid-necrosing procedures (e.g., uterine artery embolisation)
Non-fertility-preserving
• Endometrial ablation — fertility NOT preserved; contraception still needed (risk of pregnancy very low)
• Hysterectomy — definitive; indicated for hyperplasia with atypia or genetic predisposition to endometrial cancer
Safety-netting & follow-up
Review at 6 months (or 3 months if dysmenorrhoea)
If symptoms not controlled → arrange ultrasound and refer. If oral progestogens are working, still review at 6 months to consider changing to other therapies (avoid long-term risks).
LNG-IUD — expected bleeding pattern
Some irregular bleeding is expected in the first few months after insertion. If not settled at 6 months, specialist referral is required to investigate underlying causes.
Iron deficiency — treat and monitor
Reassess FBE and ferritin as clinically indicated. Treat deficiency with oral or IV iron per guidelines.
Patient warning signs
• Bleeding worsens, becomes unmanageable, or associated with dizziness, breathlessness, chest pain → urgent care
• New intermenstrual or postcoital bleeding → separate workup
• New pelvic pain, fever, or infection symptoms (especially post IUD insertion)
• Withdrawal bleed expected after stopping oral progestogen or high-dose COC regimens for acute bleeding

PCOS — Overview & Pathophysiology

A common reproductive and metabolic disorder in females of reproductive age, characterised by menstrual irregularity, hyperandrogenism, and sometimes polycystic ovarian morphology.

Epidemiology & scope
Prevalence
8–13% of females of reproductive age globally (Rotterdam criteria). Similar across ethnicities; may be higher in South East Asian and Eastern Mediterranean regions.
Nature of condition
Lifelong — clinical and biochemical hyperandrogenism may persist postmenopause. Menstrual irregularity often improves after age 40.
GP relevance
Most cases diagnosed and managed in general practice; leading cause of anovulatory infertility; significant metabolic, CVD, and psychological impact.
Pathophysiology — four interconnected mechanisms
1
Insulin resistance
Exacerbates ovarian androgen overproduction and suppresses sex hormone-binding globulin (SHBG), increasing bioavailability of free androgens.
2
LH / FSH imbalance
Elevated LH relative to FSH stimulates theca cell androgen production while impairing granulosa cell aromatisation, driving hyperandrogenism and anovulation.
3
Unopposed oestrogen
Anovulatory cycles → prolonged oestrogenic stimulation of the endometrium without progesterone-induced shedding → endometrial hyperplasia and cancer risk.
4
Obesity amplification
Present in majority of patients — amplifies insulin resistance and hyperandrogenism, creating a self-perpetuating cycle. Even 5% weight loss improves outcomes.
Clinical features
Symptoms (patient-reported)Signs (on examination)
Menstrual irregularity — oligomenorrhoea, amenorrhoea Clinical hyperandrogenism — hirsutism, acne, female-pattern hair loss
Excess body/facial hair, acne, scalp hair thinning Obesity / central adiposity (majority)
Subfertility / difficulty conceiving PCOM on ultrasound (≥20 follicles per ovary in adults)
Weight gain Insulin resistance signs — acanthosis nigricans, raised BMI
Psychological — depression, anxiety, eating disorders, body image concerns Virilisation (rare) — clitoromegaly, voice deepening, increased muscle mass. NOT consistent with PCOS — investigate for androgen-secreting tumour.

Monash 2023 Diagnostic Approach

The 2023 Monash International Evidence-based Guideline updates the Rotterdam criteria to an evidence-based framework with a clearer stepwise algorithm. AMH is added as an alternative to ultrasound in adults; both are removed for adolescents.

Historical context — Rotterdam criteria (2003)
Historically, PCOS was diagnosed with the Rotterdam criteria — 2 of 3 features, after exclusion of other causes:
1. Menstrual disturbance
Ovulatory dysfunction
2. Hyperandrogenism
Clinical or biochemical
3. Polycystic ovarian morphology
On ultrasound
The criteria were controversial and have been refined. Monash 2023 keeps the core structure but provides a stepwise algorithm, adds AMH, and sharpens adolescent criteria.
Monash 2023 stepwise algorithm (adults)
1
Irregular cycles + clinical hyperandrogenism
Both present → diagnosis made (after excluding other causes)
Ultrasound and AMH are NOT required. Diagnosis is made on clinical grounds alone. This is the most common presentation and saves the patient unnecessary imaging.
↓
2
No clinical hyperandrogenism → check biochemistry
Test for biochemical hyperandrogenism; if positive → diagnosis
If irregular cycles are present but no clinical hyperandrogenism, test for biochemical hyperandrogenism (total + free testosterone, LC-MS/MS preferred). If positive and other causes excluded → diagnosis confirmed.
↓
3
Only ONE feature (irregular cycles OR hyperandrogenism)
Use ultrasound for PCOM OR AMH — not both
If positive (and other causes excluded) → diagnosis confirmed. Use ultrasound OR AMH, never both — to limit overdiagnosis.
Adolescents — different rules
BOTH hyperandrogenism AND ovulatory dysfunction are required
Unlike adults, adolescents must have both features — a single feature is insufficient for diagnosis.
Ultrasound and AMH are NOT used
Multi-follicular ovaries are common in normal adolescents — poor specificity would lead to overdiagnosis.
Features present but criteria not met → "at risk of PCOS"
Label as "at risk" and reassess at or before full reproductive maturity — 8 years post-menarche. Includes adolescents with PCOS features before commencing COCP, persisting features, or significant weight gain.
Menstrual irregularity in adolescents is defined by years post-menarche: >1 to <3 years: <21 or >45 days; >3 years post-menarche: <21 or >35 days or <8 cycles/year; >1 year post-menarche: >90 days for any one cycle is abnormal.
Exclusion of other causes — required at EVERY step
Baseline exclusions (always test)
TSHExclude thyroid disease
ProlactinExclude hyperprolactinaemia
17-OHPExclude NCCAH (early morning, follicular phase)
FSH (+ LH)Exclude POI and hypogonadotrophic hypogonadism
If clinically indicated
Cushing'sSevere features, purple striae, easy bruising
TumoursAndrogen-secreting; rapid-onset virilisation
Hypo-gonLow BMI, intensive exercise → LH/FSH low
β-hCGAlways exclude pregnancy
Overt virilisation is NOT consistent with PCOS — clitoromegaly, voice deepening, rapid hirsutism → investigate for androgen-secreting tumour.

Hyperandrogenism — Clinical & Biochemical

Hyperandrogenism can be clinical (visible) or biochemical (measured). The Monash 2023 guideline prioritises clinical assessment and uses biochemistry when clinical findings are unclear.

Clinical hyperandrogenism
Adults — assess for:
• Hirsutism — predictive of biochemical hyperandrogenism and PCOS
• Acne
• Female-pattern hair loss
Adolescents — assess for:
• Severe acne
• Hirsutism
(Higher threshold applied to avoid overdiagnosis.)
Hirsutism alone predicts biochemical hyperandrogenism and PCOS. Female-pattern hair loss and acne in isolation (without hirsutism) are relatively weak predictors of biochemical hyperandrogenism.
Negative psychosocial impact is important regardless of apparent clinical severity. Patient-reported concerns about hair growth or hair loss should be taken seriously even if examination appears mild.
Assessment tools
Modified Ferriman–Gallwey score (mFG)
Standardised visual hirsutism score. mFG ≥ 4–6 = hirsutism (threshold varies by ethnicity).

Caveat: self-treatment (waxing, laser, etc.) is common and can limit clinical assessment — ask specifically.

View mFG reference chart (PDF)
Ludwig (or Olsen) visual scale
Preferred for assessing female-pattern hair loss. Grades I–III based on crown and parietal thinning.

No universally accepted visual scale exists for acne.

View Ludwig scale reference (PDF)
Biochemical hyperandrogenism
A
Main tests — first line
Total testosterone AND free testosterone
Free testosterone can be estimated by the calculated free androgen index (FAI). Use LC-MS/MS tandem mass spectrometry — direct free testosterone immunoassays have poor sensitivity and precision and are NOT preferred. Use lab reference ranges.
B
Second line — if testosterone not elevated
Androstenedione and DHEAS
If total or free testosterone is not elevated, androstenedione and DHEAS may be considered — but they have poorer specificity and DHEAS shows age-associated decrease. Limited role in PCOS diagnosis.
Biochemical hyperandrogenism is of greatest value when clinical hyperandrogenism is unclear. If clinical signs are obvious, biochemistry adds little.
COCP interferes with biochemical assessment. The COCP increases SHBG and reduces gonadotrophin-dependent androgen production. If assessment is essential, withdraw the COCP for ≥ 3 months with alternative contraception.
If androgen levels are markedly above lab reference ranges, consider other causes: androgen-secreting neoplasms, ovarian hyperthecosis, CAH, Cushing's syndrome, severe insulin resistance syndromes, iatrogenic. History of onset and progression is critical — some tumours produce only mild-to-moderate elevations.
In adolescents, androgen levels reach adult ranges at 12–15 years. Repeated androgen measures in ongoing PCOS assessment have a limited role in adults.

Ultrasound & AMH — When and How

Imaging and AMH are reserved for adults with only one cardinal feature (irregular cycles OR hyperandrogenism). Either may be used — not both. Neither is used in adolescents.

When imaging / AMH is NOT needed
If irregular cycles AND hyperandrogenism are both present (with other causes excluded), the diagnosis is made on clinical grounds — neither ultrasound nor AMH is required. This is the most common clinical scenario.
Ultrasound is NOT used for PCOS diagnosis in adolescents — multi-follicular ovaries are common and normal in this life stage.
AMH is NOT recommended in adolescents and should NOT be used as a single test for diagnosis at any age.
Ultrasound — PCOM thresholds (adults only)
Preferred marker
Follicle number per ovary (FNPO) — the most effective ultrasound marker in adults.
Modern equipment (≥8 MHz)
FNPO ≥ 20 in at least one ovary — counting 2–9 mm follicles.
Older equipment OR inadequate image quality
Ovarian volume ≥ 10 mL OR FNPS ≥ 10 in at least one ovary.
Transabdominal approach
Primarily report OV ≥ 10 mL or FNPS ≥ 10 — accurate follicle counts difficult by this route.
Avoid corpora lutea, cysts, and dominant follicles (≥ 10 mm) in ovarian volume calculations — rely on contralateral ovary FNPO if dominant follicle present. Transvaginal approach is most accurate and preferred if acceptable to the individual.
Minimum reporting standards: LMP (stage of cycle), transducer bandwidth, route, 2–9 mm follicles per ovary, measurements in 3 dimensions or volume, other ovarian features (cysts, corpora lutea, dominant follicles), uterine features (endometrial thickness and pattern).
Anti-Mullerian Hormone (AMH)
Alternative to ultrasound — not additive
In adults, serum AMH may be used to define PCOM as an alternative to pelvic ultrasound. Either US OR AMH may be used — NEVER both, to avoid overdiagnosis.
Not a single diagnostic test
AMH should NOT be used as the sole test for PCOS. It only defines PCOM (one of the three cardinal features), not the diagnosis itself.
Not used in adolescents
Insufficient specificity in this life stage.
Factors affecting AMH levels:
• Age — peaks at 20–25 years in the general population
• BMI — lower AMH at higher BMI
• COCP — recent or current use may suppress levels
• Menstrual cycle day — some variation across cycle
Labs should use population- and assay-specific cut-offs.

PCOS Management

Multifaceted approach targeting reproductive, metabolic, dermatologic, and psychological features. Lifestyle is the foundation; pharmacological therapy is targeted at specific manifestations. Doses from Therapeutic Guidelines (eTG).

Lifestyle — foundation of management
5% weight loss is transformative
In overweight individuals, losing 5% of total body weight reduces insulin resistance and hyperandrogenism, and improves ovulatory function, fertility, and psychological wellbeing.
Diet — no single regimen superior
Any diet consistent with general healthy-eating guidelines has benefits. A high-protein, low-glycaemic-load hypocaloric diet may help in overweight/obese women. Tailor to patient preference.
Exercise improves insulin sensitivity
Even without weight loss. Adults: 150–300 min/week moderate or 75–150 min/week vigorous aerobic activity + muscle strengthening 2 days/week.
Weight stigma — be aware
Seek permission to weigh; use weight-inclusive language. Acknowledge weight as one indicator of health alongside other factors.
If lifestyle measures are not effective after 6 months, consider adding metformin.
Pharmacological therapy — dosing (eTG)
Combined oral contraceptive (COC) — first-line
Once daily; consider extended/continuous use. First-line for menstrual regulation; also suppresses ovarian androgen production and addresses hyperandrogenism symptoms. No clinical advantage of high-dose (≥30 mcg EE) over low-dose for hirsutism. Use lowest effective oestrogen dose.
Metformin immediate-release
Start 500 mg; increase by 500 mg every 1–2 weeks; max 1500 mg/day (Monash guideline max: 2.5 g adults, 2 g adolescents). Daily (evening meal) initially; then 2–3 divided doses. Take with food. Review 3–6 monthly.
Metformin modified-release
Start 500 mg; increase by 500 mg every 1–2 weeks; max 1500 mg/day. Once daily with evening meal. Use if IR not tolerated due to GI effects.
Levonorgestrel-releasing IUD 52 mg
Single insertion; replace every 5 years. Use if COC contraindicated — provides endometrial protection and contraception. Does not address hyperandrogenism symptoms.
Additional notes:
• COCs with antiandrogenic progestogens (cyproterone, dienogest, drospirenone) may provide added benefit for hyperandrogenism; insufficient head-to-head data to favour specific preparations.
• 35 µg EE + cyproterone acetate — consider as second-line over other COCPs, balancing benefits vs VTE risk.
• Oral cyclical progestogens — short-term alternative if COC/LNG-IUD contraindicated; less effective; do not address hyperandrogenism.
• Metformin is NOT recommended for managing menstrual disturbance alone — poor control of bleeding and inadequate endometrial protection. Use for metabolic indications or subfertility.
• Anti-androgens (spironolactone 25–100 mg/day) — consider if suboptimal response after ≥6 months of COCP/cosmetic therapy. Must be combined with effective contraception (risk of male fetal undervirilisation).
• Cyproterone acetate ≥10 mg NOT advised (meningioma risk). Finasteride, flutamide, bicalutamide — liver toxicity risks.
Fertility & ovulation induction (specialist-initiated)
First-line: Letrozole
Aromatase inhibitor. Superior to clomiphene citrate for ovulation, clinical pregnancy, and live birth rates. Off-label in many countries.
Second-line: Clomiphene ± metformin
Clomiphene + metformin can be used over clomiphene alone to improve ovulation and pregnancy rates.
Second-line alternatives
Gonadotrophins (risk of multiple pregnancy), laparoscopic ovarian surgery.
Third-line: IVF
If first- and second-line therapies fail. Risk of ovarian hyperstimulation syndrome — counsel before starting.
Preconception optimisation: weight management, folate, blood pressure, OGTT, smoking cessation, alcohol, mental health.
Monitoring & review
Metformin
Review titration every 1–2 weeks until target dose; clinical response 3–6 monthly. Monitor B12 if risk factors.
COC
Review efficacy and tolerability at 3 months, then annually.
Cardiometabolic screen
Repeat every 1–3 years: OGTT (preferred), lipids, BP, BMI/waist circumference.
Heavy menstrual bleeding persisting >6 months
Investigate to exclude endometrial cancer — earlier if additional risk factors. PCOS alone raises endometrial cancer risk.
Screen mental health at each review
Depression, anxiety, eating disorders, body image — high prevalence in PCOS.

Long-term Risks & Complications

PCOS is a lifelong condition with multisystem effects. Proactive screening and prevention are central to care — metabolic, cardiovascular, reproductive, and psychological domains all require attention.

Metabolic and cardiovascular
Type 2 diabetes / impaired glucose tolerance
Risk increased regardless of BMI. 75 g OGTT is the most accurate screening test. Reassess every 1–3 years based on risk. Screen all women with T1DM or T2DM for PCOS.
Cardiovascular disease
PCOS is an independent CVD risk factor. Lipid profile at diagnosis regardless of age/BMI. BP annually and when planning pregnancy. Overall premenopausal absolute CVD risk remains low.
MASLD (formerly NAFLD)
Driven by obesity, insulin resistance, and hyperandrogenism.
Reproductive & gynaecological
Subfertility
Anovulation is the major contributor. Conception can still occur with infrequent menstruation — contraception still needed if not desired.
High-risk pregnancy
Increased risk of: higher gestational weight gain, miscarriage, gestational diabetes, hypertensive disorders/preeclampsia, intrauterine growth restriction, preterm delivery, caesarean section.
Endometrial cancer
Markedly increased risk premenopausally — absolute risk remains low. Routine screening not recommended. Additional risk factors: long-standing untreated amenorrhoea, higher weight, T2DM, persistent thickened endometrium. Prevention: cycle regulation, weight management, regular progestogen therapy.
Sleep & psychological
Obstructive sleep apnoea
Higher prevalence independent of BMI. Screen for symptoms (snoring + unrefreshed sleep + daytime sleepiness/fatigue) using validated tools (e.g., Berlin questionnaire). Formal sleep study required for diagnosis.
Depression and anxiety
High prevalence of moderate-to-severe symptoms in adults and adolescents. Screen using regionally validated tools (e.g., PHQ-9, GAD-7). Screen at diagnosis and repeat based on clinical judgement and life events.
Eating disorders / disordered eating
Consider regardless of weight, especially in the context of weight management and lifestyle interventions.
Body image, quality of life, psychosexual function
Negative impact on body image common. Multiple factors influence psychosexual function: higher weight, hirsutism, mood disorders, infertility, medications.
Risks in relatives
Fathers and brothers of women with PCOS may have increased prevalence of metabolic syndrome, T2DM, and hypertension. Cardiometabolic risk in female first-degree relatives remains inconclusive. First-degree relatives should be aware of the increased diabetes risk and consider regular glycaemic assessment.
When to refer
Diagnostic uncertainty
Adolescents with features but not meeting criteria — label "at risk" and consider specialist input.
Refractory hirsutism
Not responding to antiandrogen therapy after 6–12 months.
Virilisation / rapid hirsutism
URGENT — androgen-secreting tumour evaluation.
Fertility treatment
Letrozole first-line; specialist-initiated.
Complex metabolic care
Poorly controlled T2DM, severe dyslipidaemia, bariatric surgery consideration.
Endometrial cancer suspected
Heavy bleeding not responding to 6 months of therapy.

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