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Hypermenorrhoea - Full Detailed Explanation
1. Understanding the Clinical Scenario
Hypermenorrhoea = Heavy menstrual blood loss (>80 mL per cycle) with normal cycle frequency.
Polymenorrhoea = Cycles coming every <21 days (if the "25 days" refers to cycle frequency, this is slightly frequent but near-normal).
In this patient:
- Heavy flow ("hypermenorrhoea")
- Cycles every 25 days (slightly frequent)
- Hysteroscopy (HSK) - no fibroids found (rules out submucosal leiomyoma)
- Doctor suggested OCPs but patient declined
- Wants future pregnancy (so fertility must be preserved)
2. CAUSES - Full Explanation Using PALM-COEIN
The old term "DUB (Dysfunctional Uterine Bleeding)" is no longer used. FIGO now classifies all heavy/abnormal uterine bleeding as AUB (Abnormal Uterine Bleeding) using the PALM-COEIN system.
PALM = Structural Causes
P - Polyps (AUB-P)
- Endometrial polyps are fleshy overgrowths of the endometrial lining
- They cause heavy menstrual bleeding AND intermenstrual spotting
- Important: Hysteroscopy is actually the gold standard to diagnose polyps. If HSK was done and no polyps were reported, this is largely ruled out - BUT small polyps can be missed
- Associated with tamoxifen use and infertility
- Treatment: Hysteroscopic polypectomy (fertility-preserving)
A - Adenomyosis (AUB-A)
- Endometrial glands and stroma embedded within the myometrium (uterine muscle)
- Causes the uterus to become bulky, boggy, and tender
- Classic presentation: Heavy, PAINFUL, regular cycles - "dysmenorrhoea + menorrhagia"
- NOT visible on hysteroscopy (hysteroscopy only sees the uterine cavity surface)
- Diagnosed on transvaginal ultrasound (heterogeneous myometrium, myometrial cysts) or MRI (most accurate)
- This is a commonly missed cause when hysteroscopy is done and called "normal"
L - Leiomyoma (Fibroids) - Ruled out by hysteroscopy in this patient (submucosal type especially causes HMB)
M - Malignancy / Hyperplasia (AUB-M)
- Endometrial hyperplasia from unopposed oestrogen can cause HMB
- Endometrial carcinoma - less likely in young women but must be considered if >35 years or risk factors (obesity, PCOS, nulliparity, diabetes)
- Diagnosed by endometrial biopsy
COEIN = Non-Structural Causes
C - Coagulopathy (AUB-C)
- 5-20% of women with menorrhagia have an undiagnosed bleeding disorder
- Most common: Von Willebrand Disease (VWD) - a deficiency/dysfunction of VWF protein needed for platelet plug formation
- Suspect if:
- Heavy bleeding since menarche (first period)
- Easy bruising, epistaxis (nosebleeds)
- Prolonged bleeding after dental work or surgery
- Family history of bleeding disorders
- Postpartum haemorrhage
- Also consider: Thrombocytopenia (low platelets), liver disease (reduced clotting factor production), anticoagulant drugs
O - Ovulatory Dysfunction (AUB-O) - MOST COMMON CAUSE
This is the most important one to understand:
In a normal ovulatory cycle, after ovulation the corpus luteum produces progesterone. Progesterone stabilises the endometrium by causing it to become secretory and structurally organised. When progesterone is withdrawn at the end of the cycle, the endometrium sheds in an orderly, synchronised way - with spiral arteriolar vasoconstriction that limits blood loss.
When there is no ovulation (anovulation), there is no progesterone. The endometrium is stimulated by oestrogen alone and keeps proliferating. When it eventually breaks down, it does so randomly, from different sites at different times, without vasoconstriction - so bleeding is heavy, irregular, and prolonged.
- Low oestrogen levels = irregular light/prolonged bleeding
- High sustained oestrogen = episodes of amenorrhoea followed by sudden heavy bleeding
Causes of ovulatory dysfunction include:
| Cause | Mechanism |
|---|
| PCOS (most common in reproductive age) | Excess androgens, anovulation, insulin resistance |
| Hypothyroidism | Elevated TRH stimulates prolactin; also direct effect on menstrual cycle |
| Hyperprolactinaemia | Suppresses GnRH → suppresses ovulation |
| Hyperthyroidism | Graves' disease → elevated oestrogen → oligomenorrhoea/AUB |
| Hypothalamic dysfunction | Stress, excessive exercise, eating disorders, chronic illness |
| Premature Ovarian Insufficiency (POI) | Waning ovarian function before age 40 |
| Perimenopause | Erratic ovulation as ovarian reserve declines |
E - Endometrial Causes (AUB-E)
- In ovulatory women, the endometrium itself can be the problem
- Imbalance between local vasoconstrictors (prostaglandin F2α, endothelin-1) and vasodilators (prostaglandin E2, prostacyclin I2)
- When vasodilators dominate, more blood loss occurs during menstruation
- This is why NSAIDs work - they block prostaglandin synthesis, shifting the balance toward vasoconstriction
- Chronic endometritis (e.g., from Chlamydia infection) can also cause menorrhagia
I - Iatrogenic (AUB-I)
- Copper IUD causes heavier periods
- Anticoagulants (heparin, warfarin, NOACs)
- Steroids, tamoxifen
- Breakthrough bleeding with progestin-only pills / implants
N - Not Yet Classified (AUB-N)
- Arteriovenous malformations
- Myometrial hypertrophy
- Rare and poorly understood causes
3. Why the Doctor Suggested OCPs
OCPs (combined oral contraceptive pills) work by:
- Suppressing ovulation (no LH surge)
- Providing cyclical progestogen that stabilises the endometrium
- Thinning the endometrium (reduced blood loss)
- Regularising cycles
They are very effective for AUB-O (anovulatory bleeding) and AUB-E. However, this patient declined them - possibly due to side effects, religious/personal reasons, or preference for a non-daily method.
4. NEXT STEP OF MANAGEMENT (OCP Declined, Fertility Desired)
Step 1 - Investigations That Should Be Done First
Before changing treatment, ensure these are completed:
| Test | Why |
|---|
| CBC | Check for anaemia (iron deficiency from chronic blood loss); check platelet count |
| TSH | Hypothyroidism is a common, treatable cause of menorrhagia |
| Prolactin | Hyperprolactinaemia causes anovulation |
| Day 21 serum progesterone | Confirms whether cycles are ovulatory (>5 nmol/L = ovulatory) |
| Coagulation screen (PT, aPTT, VWF antigen, ristocetin cofactor) | If HMB since menarche or bleeding history suggests coagulopathy |
| Transvaginal ultrasound (TVUS) | To look for adenomyosis (missed by HSK), endometrial polyps, thickness |
| Endometrial biopsy | If age >35, obese, PCOS, or not responding to treatment |
| Pelvic exam + cervical swab | Rule out cervicitis (Chlamydia), cervical lesions |
Step 2 - Medical Treatment Options (Fertility-Preserving, No OCP)
Option A: Levonorgestrel-IUS (LNG-IUS / Mirena) - BEST FIRST-LINE CHOICE
Mechanism:
- A small T-shaped device placed inside the uterus
- Releases a tiny, steady dose of levonorgestrel (a progestogen) directly into the uterine cavity
- This causes: local endometrial gland atrophy → thins the endometrium → dramatically reduces menstrual flow
- Systemic absorption is minimal (avoids most hormonal side effects)
Effectiveness:
- Up to 96% reduction in blood loss at 12 months
- About 50% of women become completely amenorrhoeic (no periods) at 12 months
- As effective as surgical endometrial ablation
Why ideal for this patient:
- No systemic hormonal effects
- Fertility fully restored when removed (woman can get pregnant shortly after removal)
- Lasts up to 5-7 years
- Does not interfere with the HPO axis in the same way OCPs do
- First-line non-pill option per ACOG and FIGO guidelines
Side effects to warn about:
- Irregular/unpredictable spotting in first 3-6 months (counsel the patient about this upfront)
- Cramping at insertion
- Small risk of expulsion or perforation
Option B: Tranexamic Acid (TXA)
Mechanism:
- The endometrium normally breaks down fibrin clots through fibrinolysis (via plasminogen activators)
- In women with HMB, there is excess fibrinolytic activity in the endometrium
- Tranexamic acid is an antifibrinolytic - it blocks the conversion of plasminogen to plasmin, preventing clot breakdown
- This helps blood clots form and stay at the bleeding site, reducing blood loss
Dose: 1g orally 3 times a day, taken only during menstruation (days 1-5)
Effectiveness: Reduces menstrual blood loss by approximately 40-50%
Why useful here:
- No hormonal effects at all - does not affect fertility or ovulation
- Only taken during periods (not a daily medication)
- Can be combined with NSAIDs for additive effect
Side effect: Nausea, GI upset; theoretical thrombosis risk (very low in young healthy women)
Option C: NSAIDs (e.g., Mefenamic Acid, Ibuprofen)
Mechanism:
- Block COX enzymes → reduce prostaglandin synthesis
- Shift endometrial prostaglandin balance toward vasoconstrictors (PGF2α > PGE2)
- Reduce both blood loss AND dysmenorrhoea (pain)
Effectiveness: Reduce blood loss by 20-30%
Dose: Mefenamic acid 500mg TDS, started 1-2 days before the period and continued during bleeding
Best used when: Patient also has dysmenorrhoea; can be combined with tranexamic acid
Option D: Cyclic Oral Progestogens
Mechanism:
- Artificially replaces the progesterone that is absent in anovulatory cycles
- Stabilises the endometrium so it sheds in an organised, controlled manner
Drugs:
- Norethisterone 5mg 3 times a day, days 5 to 26 of the cycle
- Medroxyprogesterone acetate (MPA) 10mg OD, days 12-26
Important points:
- Works best for anovulatory AUB (AUB-O)
- Does NOT provide contraception (unlike OCPs)
- Fertility is preserved
- Side effects: Bloating, mood changes, breast tenderness
Option E: Depot Medroxyprogesterone Acetate (DMPA / Depo-Provera)
- IM injection every 3 months
- Eventually induces amenorrhoea in most women
- Downside: Fertility return may be delayed by 6-18 months after stopping - relevant for this patient who wants to conceive
Step 3 - If Medical Treatment Fails (Surgical Options)
| Procedure | How it works | Suitable for this patient? |
|---|
| Hysteroscopic polypectomy | Remove any polyp found | Yes, if polyp found |
| Endometrial ablation | Destroys endometrium by heat/laser/microwave | NO - permanently impairs fertility |
| D&C (Dilatation & Curettage) | Scrapes out endometrium; only temporary benefit | Diagnostic value; not definitive treatment |
| GnRH agonists (e.g., Leuprolide, Goserelin) | Induce hypo-oestrogenic state → amenorrhoea | Short-term only (max 6 months); bone loss risk; used as bridge before surgery |
| Hysterectomy | Removes uterus; permanent cure | Only if family is complete; NOT appropriate here |
5. The Big Picture - Putting It Together
Patient: Hypermenorrhoea, HSK = no fibroids, wants future pregnancy, OCP refused
↓
First: Investigate → TSH, CBC, Day 21 progesterone, TVUS, coag screen if indicated
↓
Is there an identifiable cause?
├─ Hypothyroidism → Treat with levothyroxine
├─ PCOS → Metformin ± progestogens
├─ Adenomyosis on TVUS → LNG-IUS best option
├─ Polyp on TVUS → Hysteroscopic polypectomy
├─ VWD/Coagulopathy → TXA + DDAVP + haematology referral
└─ No clear cause (AUB-E or AUB-O) → Proceed to treatment below
↓
Medical Treatment (OCP declined, fertility desired):
FIRST CHOICE → LNG-IUS (Mirena) - 96% reduction, reversible
ALTERNATIVE → Tranexamic acid + NSAID during periods
IF ANOVULATORY → Add cyclic norethisterone day 5-26
↓
No response after 3-6 months?
↓
Surgical review (ablation only if family complete; GnRH agonist as bridge)
Sources: Berek & Novak's Gynecology (PALM-COEIN, AUB-O mechanism, AUB-C); Swanson's Family Medicine Review (LNG-IUS 96% efficacy, management algorithm)