Menstrual/vaginal Complaints
Menstrual and vaginal complaints encompass a range of gynecological conditions including abnormal uterine bleeding, dysmenorrhea, amenorrhea, vaginal discharge, and vulvovaginal irritation that may indicate infectious, hormonal, structural, or systemic disorders.
Menstrual and Vaginal Complaints
Menstrual and vaginal complaints encompass a broad spectrum of presentations that bring women to the clinic. Let's break this into two overlapping domains:
- Menstrual complaints: Any abnormality in the timing, duration, volume, or pattern of menstrual bleeding, as well as pain associated with menstruation (dysmenorrhoea). This includes amenorrhoea (absent periods), oligomenorrhoea (infrequent), polymenorrhoea (too frequent), heavy menstrual bleeding (HMB, formerly "menorrhagia"), intermenstrual bleeding (IMB), and postmenopausal bleeding (PMB).
- Vaginal complaints: Symptoms referrable to the vagina and vulva — principally vaginal discharge, vaginal/vulval pruritus, vaginal dryness, dyspareunia (pain during intercourse), and vaginal bleeding outside normal menses (which overlaps with the menstrual category).
The word "menstrual" derives from Latin mensis = month. "Vaginal" from Latin vagina = sheath. These terms literally tell you we are discussing the monthly cycle and the birth canal.
These complaints are extraordinarily common in primary care and gynaecology — they are among the top reasons women consult a doctor — and the clinical approach demands a systematic framework because the differential diagnosis spans benign physiological variation all the way to malignancy and life-threatening emergencies (e.g. ectopic pregnancy, endometrial carcinoma).
Core Principle
Always think of menstrual and vaginal complaints as a clinical syndrome, not a diagnosis. Your job is to figure out why — is this structural, hormonal, infective, malignant, pregnancy-related, or iatrogenic?
2. Epidemiology and Burden
- Heavy menstrual bleeding (HMB): Affects approximately 25–30% of reproductive-age women. In Hong Kong, it is one of the commonest gynaecological referrals [1][2].
- Dysmenorrhoea: Primary dysmenorrhoea affects up to 50–90% of adolescent girls and young women; secondary dysmenorrhoea prevalence depends on the underlying cause (e.g. endometriosis prevalence ~6–10% of reproductive-age women, up to 50% of those with pelvic pain) [2].
- Amenorrhoea: Primary amenorrhoea is uncommon (~0.1–0.3%); secondary amenorrhoea affects ~3–5% of reproductive-age women.
- Abnormal uterine bleeding (AUB) overall accounts for roughly one-third of all gynaecological outpatient visits [2].
- Postmenopausal bleeding (PMB): Affects ~4–11% of postmenopausal women; ~10% of PMB is due to endometrial cancer — making it a red-flag symptom [2].
- Vaginal discharge: Extremely common; vaginitis accounts for ~10 million clinic visits per year in the US. The three commonest infectious causes are bacterial vaginosis (BV, ~40–50%), vulvovaginal candidiasis (~20–25%), and trichomoniasis (~15–20%) [1].
- Vulvovaginal pruritus: Often accompanies discharge but can occur independently (e.g. lichen sclerosus, contact dermatitis).
- Atrophic vaginitis: Affects up to 50% of postmenopausal women due to oestrogen deficiency.
- In HK, sexually transmitted infections (STIs) including Chlamydia trachomatis and Neisseria gonorrhoeae are notifiable diseases. Chlamydia is the commonest bacterial STI in HK, particularly among women aged 15–29 [3].
- Cervical cancer screening (Pap smear / liquid-based cytology) is recommended for women aged 25–64 who have ever had sexual intercourse — relevant because cervical pathology (polyps, ectropion, carcinoma) can present as vaginal discharge or abnormal bleeding [3].
- Endometrial cancer incidence has been rising in Hong Kong, in part related to obesity and metabolic syndrome [3].
3. Risk Factors
| Category | Specific Risk Factors | Mechanism |
|---|---|---|
| Age / Reproductive stage | Extremes of reproductive life (perimenarchal, perimenopausal) | Anovulatory cycles → unopposed oestrogen → irregular/heavy bleeding |
| Obesity | BMI > 30 | Peripheral aromatisation of androgens → excess oestrogen; insulin resistance → ↑ androgen → anovulation (PCOS pathway) [4][5] |
| PCOS | Polycystic ovary syndrome | Chronic anovulation → unopposed oestrogen → endometrial hyperplasia → irregular/heavy bleeding |
| Thyroid disease | Hypothyroidism, hyperthyroidism | Hypothyroidism → ↑TRH → ↑prolactin → anovulation; also directly alters SHBG and clotting factors |
| Coagulopathies | von Willebrand disease (vWD), platelet disorders | Defective haemostasis → inability to stop endometrial bleeding; vWD present in 10–15% of women with HMB [6] |
| Uterine pathology | Fibroids, polyps, adenomyosis | Structural distortion of endometrium; ↑endometrial surface area; altered prostaglandin balance |
| Oestrogen exposure | Early menarche (< 12y), late menopause (> 55y), nulliparity, no breastfeeding, HRT, oestrogen-based OCP | Prolonged/excess oestrogen stimulation of endometrium [1][7] |
| Iatrogenic | Anticoagulants, IUDs (especially copper), tamoxifen | Anticoagulants impair clotting; copper IUD → local inflammatory reaction → HMB; tamoxifen acts as partial oestrogen agonist on endometrium |
| IUCD use | Intrauterine contraceptive device | ↑Risk of salpingitis, ectopic pregnancy, and altered bleeding pattern [1] |
| Tubal surgery | Previous tubal ligation or surgery | ↑Risk of ectopic pregnancy [1] |
| Infertility | History of infertility | Association with endometriosis, salpingitis [1] |
| Drugs | SSRIs, antipsychotics (↑prolactin), steroids | Hyperprolactinaemia → suppressed GnRH → anovulation |
| Category | Specific Risk Factors | Mechanism |
|---|---|---|
| Sexual activity | Multiple partners, new partner, unprotected intercourse | ↑Exposure to STI pathogens |
| Altered vaginal flora | Antibiotic use, vaginal douching, spermicides | Destruction of protective lactobacilli → ↑pH → overgrowth of pathogenic organisms (BV, Candida) [8] |
| Immunosuppression | Diabetes mellitus, HIV, corticosteroids | ↑Susceptibility to candidiasis (hyperglycaemia provides substrate for Candida) [1] |
| Pregnancy | Physiological ↑vaginal discharge; ↑Candida risk | ↑Oestrogen → ↑glycogen in vaginal epithelium → favours Candida |
| Hypo-oestrogenic states | Menopause, lactation, surgical oophorectomy | ↓Oestrogen → vaginal atrophy, ↓glycogen, ↓lactobacilli → ↑pH → susceptibility to infection; atrophic vaginitis |
| Diabetes | Known association with vulvovaginal candidiasis | Glycosuria and tissue hyperglycaemia provide substrate for yeast [1] |
| Drugs | Antibiotics, steroids, immunosuppressants | Alter vaginal microbiome [1] |
| Foreign bodies | Retained tampon, pessary | Direct irritation, bacterial overgrowth → foul discharge |
| Chemical irritants | Soaps, deodorants, pessaries, douches | Contact irritation / allergy → vulvovaginal pruritus and discharge [1] |
| Latex allergy | E.g. condoms | Allergic contact dermatitis of vulva/vagina [1] |
4. Anatomy and Physiology (Relevant Functional Anatomy)
To understand menstrual and vaginal complaints from first principles, you need a solid grasp of the relevant anatomy and the hormonal control of the menstrual cycle.
Uterus
- A pear-shaped muscular organ (~7–8 cm in nullipara) composed of three layers:
- Endometrium (inner mucosal lining) — the layer that cyclically proliferates and sheds during menstruation
- Myometrium (thick smooth muscle) — provides contractile force for menstruation, labour; site of fibroids (leiomyomas)
- Perimetrium (serosal covering) — continuous with peritoneum
- The endometrium has two zones:
- Functionalis: the superficial layer that proliferates under oestrogen, becomes secretory under progesterone, and is shed during menstruation
- Basalis: the deep layer that is NOT shed; it serves as the regenerative source for the functionalis after each cycle
Cervix
- The lower narrow portion of the uterus opening into the vagina
- Transformation zone: the junction between columnar epithelium (endocervix) and squamous epithelium (ectocervix) — the area most susceptible to HPV-related dysplasia
- Cervical ectropion (eversion of columnar epithelium onto ectocervix): common in young women and those on OCP; can cause mucoid discharge and postcoital bleeding — this is physiological, not pathological
Vagina
- A fibromuscular tube (~7–10 cm) lined by non-keratinised stratified squamous epithelium
- The epithelium is oestrogen-dependent: oestrogen stimulates maturation → accumulation of glycogen → Lactobacilli ferment glycogen to lactic acid → maintains normal vaginal pH of 3.8–4.5
- This low pH is the key defence against pathogenic organisms [8]
- Vaginal fornices (anterior, posterior, lateral) surround the cervix — the posterior fornix is deepest (overlies the Pouch of Douglas; culdocentesis is performed here)
Ovaries
- Paired organs responsible for oogenesis and steroidogenesis (oestrogen, progesterone, androgens)
- Contain follicles at various stages of development
Fallopian Tubes
- Transport ovum from ovary to uterus
- Site of fertilisation (ampulla)
- Site of ectopic pregnancy (most commonly in the ampulla, ~70%)
Pelvic Floor
- The levator ani muscle group (puborectalis, pubococcygeus, iliococcygeus) supports pelvic organs [9]
- Weakness → pelvic organ prolapse (cystocele, rectocele, uterine prolapse) — can present as vaginal complaints (discharge, sensation of "something coming down," urinary incontinence)
Understanding the menstrual cycle is absolutely fundamental — nearly every menstrual complaint can be traced back to a disruption somewhere in this axis.
Phase-by-phase:
| Phase | Days (typical 28-day cycle) | Hormonal Events | Endometrial Changes |
|---|---|---|---|
| Menstrual | Day 1–5 | ↓Oestrogen, ↓Progesterone (withdrawal) | Shedding of functionalis → bleeding |
| Follicular (Proliferative) | Day 1–13 | FSH → follicular development → ↑Oestrogen | Oestrogen drives endometrial proliferation (thickening, gland growth, ↑vascularity) |
| Ovulation | ~Day 14 | LH surge (triggered by +ve feedback from peak oestrogen) | — |
| Luteal (Secretory) | Day 15–28 | Corpus luteum → Progesterone (+ Oestrogen) | Progesterone converts proliferative endometrium to secretory (glands become tortuous, stroma decidualises, spiral arteries develop) |
| Late Luteal | Day 26–28 | Corpus luteum regression → ↓Progesterone, ↓Oestrogen | Spiral artery constriction → ischaemia → necrosis → menstruation |
Key teaching points:
- Menstruation is a progesterone-withdrawal bleed: it's the fall in progesterone (and oestrogen) after corpus luteum regression that triggers spiral artery vasoconstriction, ischaemic necrosis, and shedding of the functionalis.
- Anovulatory bleeding occurs when there is NO ovulation → NO corpus luteum → NO progesterone → the endometrium is exposed to unopposed oestrogen → it proliferates irregularly and eventually outgrows its blood supply → irregular, often heavy, breakthrough bleeding. This is NOT a true "period" (no prior secretory transformation).
- Prostaglandins (PGF₂α, PGE₂) are crucial mediators of menstruation: they promote myometrial contraction and vasoconstriction of spiral arteries. Excess PGF₂α → excessive cramping = primary dysmenorrhoea.
It is critical to understand what constitutes normal discharge before labelling anything as pathological:
- Composition: Transudate through vaginal wall + cervical mucus + desquamated epithelial cells + lactobacilli + fluid from Bartholin's and Skene's glands
- Character: White or clear, non-offensive odour, does not cause pruritus
- Volume varies with: menstrual cycle phase (↑around ovulation due to ↑cervical mucus under oestrogen), pregnancy, sexual arousal, OCP use
- Normal vaginal pH: 3.8–4.5 (maintained by Lactobacilli fermenting glycogen → lactic acid)
| Defence | Mechanism | When Disrupted |
|---|---|---|
| Lactobacilli | Ferment glycogen → lactic acid → low pH (3.8–4.5) → hostile to pathogens | Antibiotics, douching, hypo-oestrogen → ↑pH → BV, candidiasis |
| Oestrogen | Stimulates glycogen deposition in squamous epithelium → feeds lactobacilli | Menopause, lactation → atrophic vaginitis |
| Cervical mucus | Physical barrier + contains IgA, lysozyme, lactoferrin | Ectropion, cervical pathology |
| Normal vaginal flora | Competitive exclusion of pathogens | Altered by antibiotics, spermicides |
| Vaginal environment related to oestrogen and cervical IgA | Maintains hostile environment for uropathogens | Hypo-oestrogen state, spermicidal agents, antimicrobial use [8] |
5. Etiology (with Pathophysiology)
Now let's systematically cover the causes of menstrual and vaginal complaints. I'll organise this by the PALM-COEIN classification for abnormal uterine bleeding (AUB) — the FIGO system — and then separately address causes of vaginal discharge and other vaginal complaints.
5.1 Abnormal Uterine Bleeding (AUB): PALM-COEIN Classification
PALM-COEIN is the internationally accepted FIGO classification for causes of AUB in non-pregnant reproductive-age women. PALM = structural causes (can be imaged/biopsied); COEIN = non-structural causes.
| Letter | Category | Key Points |
|---|---|---|
| P | Polyp | Endometrial or endocervical polyps — localised overgrowths of endometrial tissue with a vascular pedicle |
| A | Adenomyosis | Endometrial glands within myometrium → diffusely enlarged, boggy uterus |
| L | Leiomyoma (Fibroid) | Benign smooth muscle tumour; submucosal fibroids most likely to cause AUB |
| M | Malignancy & hyperplasia | Endometrial hyperplasia (± atypia) and endometrial carcinoma; also cervical carcinoma |
| C | Coagulopathy | vWD, platelet disorders, anticoagulant therapy |
| O | Ovulatory dysfunction | Anovulation (PCOS, hypothalamic, thyroid); most common cause of AUB at extremes of reproductive life |
| E | Endometrial | Primary disorders of endometrial haemostasis (e.g. deficient PGF₂α, ↑plasminogen activator) |
| I | Iatrogenic | Hormonal contraceptives, IUDs, anticoagulants, tamoxifen |
| N | Not yet classified | AV malformations, myometrial hypertrophy, others |
- Pathophysiology: Focal overgrowth of endometrial stroma and glands, often with a fibrous core and prominent vasculature. They protrude into the uterine cavity and are covered by endometrium that may be out of phase with the surrounding endometrium → prone to irregular bleeding.
- Why bleeding? The polyp's surface can erode/ulcerate, and the vasculature is fragile. Polyps may also interfere with normal endometrial shedding.
- Risk factors: Increasing age, obesity, tamoxifen use (tamoxifen is an oestrogen agonist on endometrium), hypertension.
- Pathophysiology: Ectopic endometrial glands and stroma within the myometrium, surrounded by reactive smooth muscle hyperplasia. Think of it as "endometriosis of the uterine wall."
- Why HMB? The enlarged uterus has a greater endometrial surface area and the intramyometrial endometrial tissue bleeds during menstruation → the surrounding myometrium cannot contract effectively to compress the spiral arteries → prolonged, heavy bleeding.
- Why dysmenorrhoea? The intramyometrial endometrial tissue responds to hormonal cycling → swelling and bleeding within the myometrium → pain (typically worsens progressively throughout the period, distinguishing it from primary dysmenorrhoea which peaks on day 1–2).
- Pathophysiology: Benign monoclonal smooth muscle neoplasm; oestrogen- and progesterone-dependent (grow during reproductive years, shrink after menopause).
- Classification by location (FIGO sub-classification):
- Submucosal (types 0–2): protrude into uterine cavity → most likely to cause AUB
- Intramural (types 3–5): within myometrium → may cause AUB if large
- Subserosal (types 5–7): protrude outward → rarely cause bleeding but can cause pressure symptoms
- Why HMB? Submucosal fibroids distort the endometrial cavity → ↑surface area, disrupt endometrial vasculature, interfere with myometrial contraction, ↑local prostaglandin and VEGF production → neovascularisation → heavy bleeding.
- Why dysmenorrhoea? Uterus contracts against the fibroid (similar to the uterus trying to expel a foreign body).
- Endometrial hyperplasia: Results from unopposed oestrogen (without progesterone) stimulation of endometrium → glandular proliferation without adequate secretory transformation. Can be:
- Without atypia: low risk of progression to cancer (~1–3%)
- With atypia: significant risk of progression (~30% if untreated → carcinoma)
- Endometrial carcinoma: Most common gynaecological malignancy. Predominantly Type I (endometrioid, oestrogen-driven, 80%) associated with obesity, PCOS, tamoxifen, late menopause; Type II (serous/clear cell, oestrogen-independent, 20%) more aggressive, occurs in older/thinner women.
- Why PMB is a red flag: Any bleeding after 12 months of amenorrhoea in a postmenopausal woman must be assumed to be endometrial cancer until proven otherwise (~10% of PMB is cancer).
- Cervical carcinoma: Usually presents as IMB, postcoital bleeding, or offensive discharge. Caused by high-risk HPV (16, 18).
- von Willebrand disease (vWD): The commonest inherited bleeding disorder; present in 10–15% of women with HMB [6]. vWF mediates platelet adhesion and carries factor VIII; deficiency → impaired primary haemostasis → mucocutaneous bleeding, including HMB.
- Heavy menstrual bleed (60–90%) in women with vWD [6].
- Other coagulopathies: platelet function disorders, factor deficiencies, anticoagulant therapy.
- Always consider coagulopathy in: HMB since menarche, family history of bleeding, easy bruising, post-surgical/dental bleeding.
- Commonest cause of AUB at the extremes of reproductive life (perimenarchal and perimenopausal).
- Mechanism: No ovulation → no corpus luteum → no progesterone → unopposed oestrogen → endometrial proliferation without secretory transformation → irregular shedding → unpredictable, often heavy bleeding.
- Causes:
- PCOS: Most common cause of anovulatory AUB in reproductive-age women. Insulin resistance → ↑androgens → anovulation [4][5].
- Hypothalamic amenorrhoea: Stress, excessive exercise, low body weight → suppressed GnRH → ↓FSH/LH → anovulation.
- Hyperprolactinaemia: ↑Prolactin → suppresses GnRH → anovulation. Causes: prolactinoma, drugs (antipsychotics, metoclopramide).
- Thyroid dysfunction: Hypothyroidism → ↑TRH → ↑prolactin → anovulation + direct effects on SHBG and clotting factors → AUB.
- Perimenopausal: Declining ovarian reserve → irregular folliculogenesis → erratic oestrogen/progesterone levels → AUB.
- Primary disorders of endometrial haemostasis mechanisms:
- ↓Local endothelin-1 (vasoconstrictor)
- ↓PGF₂α (promotes vasoconstriction and myometrial contraction)
- ↑Plasminogen activators (↑fibrinolysis → prevents clot formation → continued bleeding)
- This is why tranexamic acid (antifibrinolytic) works for HMB — it counteracts excessive endometrial fibrinolysis.
- Copper IUD: Local inflammatory reaction in endometrium → ↑prostaglandins → HMB and dysmenorrhoea.
- Hormonal contraceptives: Breakthrough bleeding common in first 3 months; progestogen-only methods can cause irregular bleeding.
- Anticoagulants: Warfarin, DOACs → impaired clotting → HMB.
- Tamoxifen: Partial oestrogen agonist on endometrium → polyps, hyperplasia, cancer risk.
- IUCD → salpingitis, ectopic pregnancy [1].
- Arteriovenous malformations, myometrial hypertrophy, chronic endometritis.
| Type | Definition | Pathophysiology |
|---|---|---|
| Primary | Pain with no identifiable pelvic pathology; begins within 1–2 years of menarche when ovulatory cycles establish | Excess prostaglandins (especially PGF₂α) released from secretory endometrium → myometrial hypercontractility → ischaemia → crampy pain. This is why NSAIDs (prostaglandin synthesis inhibitors) are first-line treatment. |
| Secondary | Pain due to underlying pelvic pathology; onset typically later in life or worsening over time | Depends on cause: endometriosis (ectopic endometrial tissue → cyclical inflammation), adenomyosis (intramyometrial bleeding), fibroids (uterine cramping against mass), PID (tubal/ovarian inflammation), cervical stenosis (obstructed outflow) |
| Type | Definition | Major Causes |
|---|---|---|
| Primary | No menarche by age 15 (with secondary sexual characteristics) or by age 13 (without secondary sexual characteristics) | Hypothalamic: constitutional delay, Kallmann syndrome (anosmia + GnRH deficiency); Gonadal: Turner syndrome (45,X → streak gonads), gonadal dysgenesis; Outflow obstruction: imperforate hymen, transverse vaginal septum, Müllerian agenesis (Mayer-Rokitansky-Küster-Hauser syndrome) |
| Secondary | Absence of menstruation for ≥ 3 consecutive cycles (previously regular) or ≥ 6 months (previously irregular) | Always exclude pregnancy first! Hypothalamic (stress, weight loss, exercise), PCOS, hyperprolactinaemia, thyroid disease, premature ovarian insufficiency, Asherman syndrome (intrauterine adhesions), Sheehan syndrome (postpartum pituitary necrosis) |
The history should include: nature of discharge (colour, odour, quantity, relation to menstrual cycle, associated symptoms), exact nature and location of irritation, sexual history (arousal, previous STIs, number of partners and any presence of irritation or discharge in them), use of chemicals such as soaps, deodorants, pessaries and douches, pregnancy possibility, drug therapy, associated medical conditions (e.g. diabetes). [1]
| Cause | Organism/Mechanism | Discharge Character | Pathophysiology |
|---|---|---|---|
| Physiological | Normal vaginal flora | White/clear, non-offensive, no itch | Oestrogen-driven transudate + cervical mucus; varies with cycle |
| Bacterial vaginosis (BV) | Overgrowth of anaerobes (Gardnerella, Prevotella, Mobiluncus) replacing lactobacilli | Thin, greyish-white, "fishy" odour (especially after coitus or with KOH = positive amine/"whiff" test) | Shift in vaginal microbiome → ↑pH (> 4.5) → anaerobes produce amines → characteristic odour. NOT a true infection (no inflammatory response) — more a "dysbiosis" |
| Vulvovaginal candidiasis | Candida albicans (90%) | Thick, white, "cottage cheese" curdy, no odour | Overgrowth of yeast (predisposed by antibiotics, DM, immunosuppression, pregnancy, OCP) → inflammatory reaction → pruritus + erythema. pH is normal (< 4.5) because Candida thrives in acidic environment |
| Trichomoniasis | Trichomonas vaginalis (flagellated protozoan; STI) | Profuse, frothy, yellow-green, offensive odour | Parasite colonises squamous epithelium → intense inflammatory response → purulent discharge; may cause "strawberry cervix" (punctate haemorrhages) on colposcopy |
| Chlamydia | Chlamydia trachomatis (obligate intracellular bacterium) | Mucopurulent, often subtle/asymptomatic | Infects columnar epithelium of endocervix → cervicitis → mucopurulent discharge ± IMB, postcoital bleeding. Often asymptomatic (up to 70% of women) — this is why screening is critical |
| Gonorrhoea | Neisseria gonorrhoeae | Purulent, yellow | Similar to Chlamydia but tends to be more symptomatic; can co-exist |
| Cervical polyp | Benign overgrowth of cervical mucosa | Mucoid or blood-stained | Friable polyp → contact bleeding, excess mucus production |
| Atrophic vaginitis | Oestrogen deficiency (postmenopausal) | Thin, watery, may be blood-stained | ↓Oestrogen → thin, dry vaginal epithelium → ↓glycogen → ↓lactobacilli → ↑pH → susceptibility to infection; fragile epithelium → petechiae/bleeding |
| Cervical ectropion | Eversion of columnar epithelium | Mucoid | Columnar epithelium produces more mucus than squamous → ↑discharge; friable → postcoital bleeding |
| Foreign body | Retained tampon, condom, pessary | Foul-smelling, purulent | Bacterial overgrowth on foreign material → secondary infection |
| Genital herpes | HSV-2 (or HSV-1) | Watery discharge ± vesicles/ulcers | Viral infection of genital mucosa → vesicle formation → ulceration → serous discharge |
| Bartholinitis | Usually polymicrobial ± gonorrhoea/chlamydia | Unilateral labial swelling ± discharge | Obstruction of Bartholin's gland duct → cyst → secondary infection → abscess |
| Threadworms | Enterobius vermicularis | Perianal/vulval pruritus (especially nocturnal) | Worms migrate from anus to vulva → itching; more common in children |
Exam Pearl — pH is Key!
A simple pH test (paper range 4–6) at bedside can help differentiate:
- pH < 4.5: Candidiasis (yeast thrives in acid) or physiological
- pH > 4.5: BV or Trichomoniasis (loss of lactobacilli → alkaline shift)
This is one of the key investigations mentioned in the lecture slides [1].
The pain should be linked with the menstrual history, coitus and the possibility of an early pregnancy. [1]
| Timing | Gynaecological | Non-Gynaecological |
|---|---|---|
| Acute | Ectopic pregnancy (ruptured/unruptured), ovarian torsion, ruptured ovarian cyst, acute PID, threatened/incomplete miscarriage | Appendicitis, UTI, renal colic, diverticulitis |
| Cyclical/Chronic | Endometriosis, adenomyosis, chronic PID, dysmenorrhoea (primary/secondary), ovarian cyst, uterine fibroid | IBS (very commonly coexists — dysmenorrhoea is a recognised association of IBS [10]), spinal dysfunction (referred pain), nerve entrapment, cholecystitis |
| Coital | Deep dyspareunia (endometriosis, PID, ovarian pathology), superficial dyspareunia (vaginismus, vulvodynia, atrophic vaginitis, vulval pathology) | — |
Masquerades checklist: Depression, Drugs, Spinal dysfunction (referred pain), UTI [1]
"Is the patient trying to tell me something?" — Can be very relevant. Consider various problems and sexual dysfunction. [1]
Don't Forget!
Always exclude pregnancy in any woman of reproductive age with menstrual complaints, pelvic pain, or abnormal bleeding. A ruptured ectopic pregnancy is a life-threatening emergency. A simple urine β-hCG is quick and cheap.
6. Classification
By pattern:
| Term | Definition |
|---|---|
| Heavy menstrual bleeding (HMB) | Excessive menstrual blood loss that interferes with physical, social, or emotional quality of life (previously defined as > 80 mL/cycle, but now subjective definition preferred — NICE) |
| Intermenstrual bleeding (IMB) | Bleeding between expected periods |
| Postcoital bleeding (PCB) | Bleeding after sexual intercourse |
| Postmenopausal bleeding (PMB) | Bleeding > 12 months after last menstrual period |
| Breakthrough bleeding | Bleeding while on hormonal contraception |
| Oligomenorrhoea | Infrequent periods (cycle > 35 days) |
| Polymenorrhoea | Frequent periods (cycle < 21 days) |
| Amenorrhoea | Absence of menstruation (primary or secondary, as above) |
| Dysmenorrhoea | Painful menstruation |
By aetiology → PALM-COEIN (as above)
- Physiological vs Pathological
- Infective vs Non-infective
- STI vs Non-STI
| Infective | Non-Infective |
|---|---|
| BV, Candidiasis, Trichomoniasis, Chlamydia, Gonorrhoea, Genital herpes, HPV | Cervical ectropion, Polyps, Foreign body, Atrophic vaginitis, Chemical irritation, Malignancy (cervical/endometrial/vaginal) |
7. Clinical Features
7.1 Symptoms
I'll systematically cover the symptoms a patient may present with, along with the pathophysiological basis for each.
| Symptom | Clinical Description | Pathophysiological Basis |
|---|---|---|
| Heavy menstrual bleeding | "Flooding," passage of clots, needing to change pad/tampon every 1–2 hours, "double padding," soaking through clothing/bedding | Structural (fibroids ↑surface area; polyps have fragile vasculature), hormonal (anovulation → unopposed oestrogen → thick, irregularly shed endometrium), haemostatic (coagulopathy → inability to form/maintain clot in spiral arteries), endometrial (↑fibrinolysis) |
| Prolonged bleeding | Period lasting > 7 days | Same as HMB — often the endometrium sheds irregularly and incompletely |
| Irregular bleeding / IMB | Unpredictable spotting or bleeding between periods | Anovulatory cycles (no progesterone to stabilise endometrium), endometrial polyps, cervical pathology, hormonal contraceptives, endometritis |
| Postcoital bleeding | Bleeding triggered by intercourse | Cervical causes: ectropion (fragile columnar epithelium), polyp, cervicitis (Chlamydia/gonorrhoea), cervical carcinoma. Vaginal causes: atrophic vaginitis (thin fragile epithelium), trauma |
| Postmenopausal bleeding | Any bleeding > 12 months after menopause | Endometrial atrophy (most common, ~60–80%), endometrial polyp, endometrial hyperplasia/carcinoma (~10%), cervical pathology, HRT-related |
| Dysmenorrhoea | Crampy, suprapubic pain during menses; may radiate to back/thighs | Primary: excess PGF₂α → myometrial hypercontractility → ischaemia. Secondary: depends on cause — endometriosis (cyclical inflammation of ectopic tissue), adenomyosis (swelling within myometrium), fibroids (uterus contracts against mass) |
| Amenorrhoea | Absent periods | Hormonal axis disruption at any level (hypothalamus, pituitary, ovary, uterus, outflow tract); or physiological (pregnancy, lactation, menopause) |
| Oligomenorrhoea | Infrequent periods (> 35 days apart) | Usually anovulation or oligo-ovulation — insufficient hormonal drive to complete a cycle regularly (PCOS, hypothalamic, thyroid) |
| Symptom | Clinical Description | Pathophysiological Basis |
|---|---|---|
| Vaginal discharge | Abnormal in colour, consistency, volume, or odour compared to the patient's normal | Depends on cause (see Section 5.4). Infectious → inflammatory exudate; non-infectious → irritation, atrophy, structural |
| Pruritus vulvae | Itching of the vulva — can be maddening for patients | Candidiasis (inflammatory reaction to yeast), contact dermatitis (chemical irritants), lichen sclerosus/planus (autoimmune), threadworms, atrophic vaginitis, vulval intraepithelial neoplasia (VIN), latex allergy [1] |
| Vaginal dryness | Discomfort, difficulty with intercourse | ↓Oestrogen → ↓vaginal transudate, ↓glycogen, ↓epithelial thickness → dryness. Commonest in menopause, lactation, and with certain medications (antihistamines, antidepressants) |
| Dyspareunia | Pain during intercourse. Superficial (at introitus) vs Deep (with deep penetration) | Superficial: vulvar pathology (lichen sclerosus, vestibulodynia, atrophic vaginitis, Bartholin's cyst/abscess, episiotomy scar), vaginismus (involuntary pelvic floor spasm — often psychogenic). Deep: endometriosis (especially uterosacral ligaments), PID/tubo-ovarian abscess, adenomyosis, retroverted uterus, ovarian pathology |
| Vulval/vaginal swelling | Lump felt at vulva or vagina | Bartholin's cyst/abscess (posterolateral), prolapse (cystocele/rectocele/uterine), vulval varicosities (pregnancy), Gartner's duct cyst, vulval neoplasm |
| Offensive odour | Foul or fishy smell | BV (amines produced by anaerobes), retained foreign body (secondary bacterial overgrowth), trichomoniasis, cervical/endometrial malignancy (necrotic tissue), fistula (vesicovaginal/rectovaginal) |
| Vaginal bleeding (non-menstrual) | Spotting, staining, frank bleeding | Cervical pathology, endometrial pathology, vaginal trauma, atrophic vaginitis (see AUB section above) |
These help narrow the differential:
| Symptom | Significance |
|---|---|
| Pelvic/abdominal pain | PID, endometriosis, ectopic pregnancy, ovarian pathology, fibroids |
| Urinary symptoms (dysuria, frequency, urgency) | UTI (very commonly coexists), urethritis (Chlamydia/gonorrhoea), large fibroid compressing bladder |
| Fever | PID, tubo-ovarian abscess, septic abortion |
| Weight changes | Weight gain: PCOS, hypothyroidism, Cushing's. Weight loss: hypothalamic amenorrhoea, malignancy |
| Hirsutism/acne | PCOS, androgen-secreting tumour, acne often occurs in association with hyperandrogenic states, e.g. PCOS [11] |
| Galactorrhoea | Hyperprolactinaemia (prolactinoma, drugs) |
| Hot flushes | Premature ovarian insufficiency, menopause |
| Bowel symptoms | Endometriosis (cyclical rectal bleeding, dyschezia), IBS |
| Fatigue/dizziness | Iron deficiency anaemia secondary to chronic HMB |
| Bone pain/SOB | Metastatic disease (if cervical/endometrial malignancy) |
For recurrent and chronic pain, instruct the patient to keep a diary over two menstrual cycles [1].
7.2 Signs (Physical Examination)
Key examination: Use the traditional abdominal and pelvic examination to identify the site of tenderness and rebound tenderness, and any abdominal or pelvic masses. The pelvis should be examined by speculum (preferably bivalve type) and bimanual palpation. [1]
Proper assessment can be difficult if the patient cannot relax or overreacts, if there is abdominal scarring or obesity, or if extreme tenderness is present. It is therefore important, especially in the younger and apprehensive patient, to conduct a gentle, caring vaginal examination with appropriate explanation and reassurance. [1]
| Sign | Significance | Pathophysiological Basis |
|---|---|---|
| Pallor | Anaemia from chronic blood loss (HMB) | Iron deficiency anaemia → ↓Hb → pale mucous membranes |
| Obesity / central adiposity | PCOS, metabolic syndrome, ↑oestrogen (peripheral aromatisation) | Adipocytes express aromatase → convert androgens to oestrogens |
| Hirsutism, acne, androgenic alopecia | Hyperandrogenism (PCOS, androgen-secreting tumour, CAH) | ↑Androgens → stimulate pilosebaceous unit |
| Acanthosis nigricans | Insulin resistance (PCOS, metabolic syndrome) | Hyperinsulinaemia → activates IGF-1 receptors in skin → keratinocyte proliferation |
| Thyroid abnormalities | Thyroid disease causing menstrual disturbance | Goitre, exophthalmos (Graves'), myxoedema |
| Petechiae / bruising | Coagulopathy (vWD, thrombocytopenia) | Defective haemostasis |
| Galactorrhoea | Hyperprolactinaemia | ↑Prolactin → stimulates breast milk production even outside lactation |
| Signs of Turner syndrome | Primary amenorrhoea (45,X) | Short stature, webbed neck, wide-spaced nipples, shield chest |
| Cachexia | Malignancy, hypothalamic amenorrhoea (anorexia nervosa) | Severe caloric deficit → suppressed GnRH → amenorrhoea |
| Sign | Significance |
|---|---|
| Distension | Large fibroids, ovarian mass, ascites (advanced malignancy) |
| Palpable mass | Fibroid uterus (firm, irregular), ovarian mass (smooth or irregular) |
| Tenderness / guarding / rebound | PID, ectopic pregnancy, ovarian torsion, ruptured cyst |
| Surgical scars | Previous pelvic/abdominal surgery (adhesions → pain; hysterectomy → no menstruation expected) |
Inspection with good light includes viewing the vulva, introitus, urethra, vagina and cervix. Look for the discharge and specific problems such as polyps, warts, ectropion, prolapses and fistulas. [1]
| Finding | Possible Diagnosis | Why? |
|---|---|---|
| Cervical ectropion | Physiological (common in young women, OCP users) | Eversion of columnar epithelium; may cause mucoid discharge, postcoital bleeding |
| Cervical polyp | Endocervical polyp | Pedunculated growth visible at os; friable → contact bleeding |
| Mucopurulent cervical discharge | Cervicitis (Chlamydia, Gonorrhoea) | Infection of endocervical columnar epithelium → purulent exudate |
| Cervical ulceration / irregular mass | Cervical carcinoma | Neoplastic growth → tissue destruction |
| "Strawberry cervix" | Trichomoniasis | Punctate subepithelial haemorrhages from parasite-induced inflammation |
| Vaginal wall prolapse | Cystocele (anterior), rectocele (posterior), uterine prolapse | Pelvic floor weakness → descent of pelvic organs |
| Atrophic vagina | Postmenopausal atrophic vaginitis | Pale, thin, dry epithelium ± petechiae; ↓rugae |
| Vaginal discharge character | As per Section 5.4 | Colour, consistency, odour help differentiate |
| Foreign body | Retained tampon etc. | Often associated with very offensive discharge |
| Vulval lesions | Warts (HPV), ulcers (herpes, syphilis, Behçet's), lichen sclerosus/planus | Each has characteristic appearance |
| Finding | Possible Diagnosis | Pathophysiological Basis |
|---|---|---|
| Bulky, irregularly enlarged uterus | Fibroids | Multiple firm nodules within myometrium |
| Uniformly enlarged, boggy/tender uterus | Adenomyosis | Diffuse infiltration of endometrial tissue into myometrium → generalised enlargement |
| Tender uterus with cervical excitation (chandelier sign) | PID / ectopic pregnancy | Inflamed tubes/ovaries → pain on moving the cervix (transmitted to adnexa) |
| Adnexal mass | Ovarian cyst/tumour, ectopic pregnancy, tubo-ovarian abscess | Palpable mass in the adnexa (lateral to uterus) |
| Fixed, retroverted uterus | Endometriosis (adhesions), chronic PID | Adhesions tether uterus posteriorly; endometriotic nodules palpable on uterosacral ligaments |
| Thickened or tender uterosacral ligaments | Endometriosis | Ectopic endometrial implants on uterosacral ligaments → fibrosis and nodularity |
Clinical Pearl: Cervical Excitation Tenderness
The "chandelier sign" refers to cervical motion tenderness so severe that the patient "reaches for the chandelier." It is classically associated with PID and ectopic pregnancy. The reason: the inflamed fallopian tubes and ovaries are attached to the uterus, so moving the cervix stretches the inflamed adnexa → severe pain.
Key history: The pain should be linked with the menstrual history, coitus and the possibility of an early pregnancy. [1]
Risk factors in the past history should be assessed, for example: IUCD (salpingitis, ectopic pregnancy), infertility (endometriosis, salpingitis), tubal surgery (ectopic). [1]
| Domain | Questions to Ask | Why It Matters |
|---|---|---|
| Menstrual Hx | LMP, cycle length, duration, regularity, volume (pads/tampons per day, clots, flooding), pain | Determines if the cycle is ovulatory, and characterises the bleeding pattern |
| Pregnancy Hx | Possibility of pregnancy? LMP? Contraception? Previous pregnancies (gravidity, parity)? | Rule out pregnancy — ectopic is life-threatening; miscarriage, GTD |
| Sexual Hx | Sexually active? Partners? STI history? Dyspareunia? Contraception? | STIs (Chlamydia, gonorrhoea, herpes), PID risk |
| Discharge Hx | Colour, odour, quantity, relation to menstrual cycle, associated symptoms [1] | Characterises the type of vaginitis/cervicitis |
| O&G Hx | Age at menarche and menopause, pregnancies, age at first pregnancy, breastfeeding, hormonal intake [7] | Oestrogen exposure duration → risk for endometrial/breast pathology |
| Drug Hx | Anticoagulants, hormonal therapy, antibiotics, antipsychotics, tamoxifen, chemicals (soaps, deodorants, pessaries, douches) [1] | Iatrogenic causes of AUB and vaginal symptoms |
| PMHx | Diabetes, thyroid disease, coagulopathy, PCOS, previous pelvic surgery, previous STIs [1] | Predisposing conditions |
| FHx | Bleeding disorders, PCOS, gynaecological cancers, FHx of breast or gyne cancers [7] | Hereditary coagulopathy, BRCA, Lynch syndrome |
| Social Hx | Stress, exercise, weight changes, eating habits, sexual dysfunction, domestic violence | Hypothalamic amenorrhoea, psychosocial factors |
"Is the patient trying to tell me something?" — Needs careful consideration; possible sexual dysfunction. [1]
Key investigations: [1]
- FBE/ESR/CRP
- Urine MC (microscopy and culture — to exclude UTI)
- Chlamydia PCR
Additional standard investigations:
- pH test with paper of range 4–6 [1]
- Amine or "whiff" test [1]
- Wet mount microscopy (saline prep for clue cells/trichomonads; KOH prep for yeast hyphae)
- Urine β-hCG (always in reproductive-age women)
- Pelvic ultrasound (transvaginal preferred — assess endometrial thickness, fibroids, ovarian morphology)
- Endometrial biopsy (Pipelle) — indicated for PMB, AUB in women ≥ 45, or younger women with risk factors for endometrial hyperplasia/cancer
- Cervical cytology / Pap smear — if due for screening
- Hormonal profile: FSH, LH, oestradiol, progesterone (day 21), prolactin, TFTs, androgens (testosterone, DHEA-S) — as guided by clinical suspicion
- Coagulation screen: PT, APTT, fibrinogen — if suspected coagulopathy; vWF panel if HMB since menarche [6]
High Yield Summary
Menstrual/Vaginal Complaints — Key Takeaways:
-
Always exclude pregnancy (urine β-hCG) in any reproductive-age woman with abnormal bleeding or pelvic pain.
-
PALM-COEIN is the FIGO classification for AUB: Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia (structural) + Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified (non-structural).
-
Anovulatory bleeding = no ovulation → no progesterone → unopposed oestrogen → irregular endometrial shedding. Most common at extremes of reproductive life and in PCOS.
-
Menstruation is a progesterone-withdrawal bleed. Primary dysmenorrhoea is caused by excess PGF₂α → myometrial ischaemia → NSAIDs are first-line.
-
von Willebrand disease is present in 10–15% of women with HMB — always consider in HMB since menarche or with bleeding history.
-
Vaginal discharge: pH < 4.5 → think Candida; pH > 4.5 → think BV or Trichomoniasis. The amine/whiff test is positive in BV.
-
Normal vaginal defence depends on oestrogen → glycogen → Lactobacilli → lactic acid → low pH. Disruption at any step predisposes to infection.
-
Postmenopausal bleeding = endometrial cancer until proven otherwise (~10% of PMB is malignant).
-
Key examination: speculum (bivalve) + bimanual palpation. Key investigations: FBE/ESR/CRP, Urine MC, Chlamydia PCR, pH test, amine test.
-
Always ask: "Is the patient trying to tell me something?" — consider sexual dysfunction, domestic violence, psychosocial factors.
Active Recall - Menstrual/Vaginal Complaints (Definition to Clinical Features)
[1] Lecture slides: murtagh merge.pdf (pages 2 and 104 — Abdominal pain in women; Vaginal discharge) [2] Senior notes: felixlai.md (sections on breast cancer risk factors, rectal prolapse, UTI) [3] Hong Kong Department of Health — Cervical Screening Programme and STI surveillance reports (general knowledge, HK-specific epidemiology) [4] Senior notes: Ryan Ho Endocrine.pdf (p77 — Type 2 DM, PCOS, metabolic syndrome) [5] Senior notes: Ryan Ho Endocrine.pdf (p117 — Complications of obesity including PCOS) [6] Senior notes: Ryan Ho Haemtology.pdf (p128 — von Willebrand disease, HMB prevalence) [7] Senior notes: Ryan Ho Fundamentals.pdf (p371 — Breast cancer risk factors including O/G history; p196 — Pelvic examination) [8] Senior notes: Ryan Ho Urogenital.pdf (p122 — UTI, natural defence of urinary tract, vaginal flora) [9] Senior notes: felixlai.md (section on rectal prolapse — pelvic floor anatomy) [10] Senior notes: Ryan Ho GI.pdf (p118 — IBS associations including dysmenorrhoea) [11] Senior notes: Ryan Ho Rheumatology.pdf (p126 — Acne vulgaris, association with hyperandrogenic states e.g. PCOS)
Differential Diagnosis of Menstrual / Vaginal Complaints
The approach to differential diagnosis here requires you to think in parallel along two major presenting-complaint axes — abnormal bleeding / menstrual disturbance and vaginal discharge / vulvovaginal symptoms — because in real life patients often present with both simultaneously, and the underlying cause may produce either or both. I'll structure this exactly the way Murtagh's diagnostic strategy framework is laid out in the lecture slides, then give you a systematic clinical-reasoning algorithm.
This is the framework from the lecture slides and is high yield [1].
| Category | Diagnoses |
|---|---|
| Probability diagnosis | Normal or excessive physiological discharge |
| Vaginitis: bacterial vaginosis (40–50%), candidiasis (20–30%), Trichomonas (10–20%) [1] | |
| Serious disorders not to be missed | Neoplasia: cancer (cervix, uterus, vagina) |
| Fistulas | |
| STIs / PID (i.e. cervicitis): gonorrhoea, Chlamydia, herpes simplex types 1 and 2 | |
| Sexual abuse, especially children | |
| Tampon toxic shock syndrome (staphylococcal infection) | |
| Streptococcal vaginosis (in pregnancy) [1] | |
| Pitfalls (often missed) | Chemical vaginitis (e.g. perfumes) |
| Retained foreign objects (e.g. tampons, IUCD) | |
| Endometriosis (brownish discharge) | |
| Ectopic pregnancy ("prune juice" discharge) | |
| Poor toilet hygiene | |
| Pelvic fistula [1] | |
| Seven masquerades and pitfalls (continued) | Genital herpes (possible) |
| Cervical polyp | |
| Bartholinitis | |
| Atrophic vaginitis | |
| Threadworms | |
| Latex allergy (e.g. condoms) [1] | |
| Masquerades checklist | Diabetes |
| Drugs | |
| UTI (association) [1] | |
| Is the patient trying to tell me something? | Needs careful consideration; possible sexual dysfunction [1] |
Why This Framework Matters
Murtagh's strategy forces you to think in tiers of probability → danger → pitfalls → masquerades → psychosocial. In an exam (and in clinic), you must demonstrate that you have considered the serious diagnoses (cancer, ectopic, PID) even when the most likely diagnosis is something benign (BV, Candida).
| Category | Diagnoses |
|---|---|
| Probability diagnosis | Primary dysmenorrhoea |
| Mittelschmerz | |
| Pelvic / abdominal adhesions | |
| Endometriosis [1] | |
| Serious disorders not to be missed | Vascular: internal iliac claudication |
| Neoplasms including cancer: ovary, uterus, other pelvic structures | |
| Infection: PID, pelvic abscess, appendicitis | |
| Other: ectopic pregnancy [1] | |
| Pitfalls (often missed) | Endometriosis / adenomyosis |
| Torsion of ovary or pedunculated fibroid | |
| Constipation / faecal impaction | |
| Pelvic congestion syndrome | |
| Misplaced IUCD [1] | |
| Referred pain (to pelvis) | Appendicitis, cholecystitis, diverticulitis, UTI [1] |
| Masquerades checklist | Depression, Drugs, Spinal dysfunction (referred pain), UTI [1] |
| Is the patient trying to tell me something? | Can be very relevant. Consider various problems and sexual dysfunction [1] |
Exam Tip
3. Systematic Differential Diagnosis by Presenting Complaint
Organised by PALM-COEIN (FIGO) — but now mapped to the specific bleeding pattern:
| Bleeding Pattern | Top Differentials | Key Distinguishing Features |
|---|---|---|
| Heavy menstrual bleeding (HMB) | Fibroids (submucosal), adenomyosis, endometrial polyps, coagulopathy (vWD), ovulatory dysfunction, endometrial causes (↑fibrinolysis), iatrogenic (Cu-IUD, anticoagulants) | Fibroids: irregular bulky uterus. Adenomyosis: uniformly enlarged boggy tender uterus, worsening dysmenorrhoea. Coagulopathy: HMB since menarche, easy bruising [3]. Cu-IUD: temporal association with insertion |
| Intermenstrual bleeding (IMB) | Cervical ectropion, cervical polyp, cervicitis (Chlamydia, gonorrhoea), endometrial polyp, hormonal contraception (breakthrough), cervical carcinoma, endometrial carcinoma | Ectropion: young, on OCP. Cervicitis: mucopurulent discharge, STI risk. Cancer: irregular mass on speculum |
| Postcoital bleeding (PCB) | Cervical ectropion, cervical polyp, cervicitis, cervical carcinoma, atrophic vaginitis, vaginal trauma | Always do speculum — cervical carcinoma is the must-not-miss diagnosis |
| Postmenopausal bleeding (PMB) | Endometrial atrophy (60–80%, most common), endometrial polyp, endometrial hyperplasia / carcinoma (~10%), cervical pathology, vaginal atrophy, HRT-related breakthrough | Endometrial atrophy: thin endometrium on TVS. Cancer: thickened endometrium ( > 4 mm on TVS post-menopause → requires biopsy) |
| Amenorrhoea (secondary) | Pregnancy (always first!) [4], hypothalamic (stress, weight loss, exercise), PCOS, hyperprolactinaemia, thyroid disease, premature ovarian insufficiency (POI), Asherman syndrome | PCOS: oligomenorrhoea + hyperandrogenism. POI: hot flushes + ↑FSH. Asherman: post-D&C history [4] |
| Oligomenorrhoea | PCOS, thyroid disease, hyperprolactinaemia, hypothalamic, pregnancy, perimenopause | PCOS is by far the commonest in reproductive-age women |
| Dysmenorrhoea | Primary (diagnosis of exclusion — no pathology), Secondary: endometriosis, adenomyosis, fibroids, PID, cervical stenosis, misplaced IUCD [1] | Primary: onset within 1–2 years of menarche, day 1–2 of cycle. Secondary: onset later, progressive, may have deep dyspareunia, dyschezia |
| Discharge Character | Most Likely Diagnosis | Why (Pathophysiology) | Key Differentiating Test |
|---|---|---|---|
| Thin, grey-white, fishy odour | Bacterial vaginosis (BV) [1] | Shift from lactobacilli-dominant flora → anaerobic overgrowth (Gardnerella, Prevotella, Mobiluncus) → amines produced → fishy odour. Not a true infection — no mucosal inflammation | pH > 4.5, positive amine ("whiff") test, clue cells on wet mount [1] |
| Thick, white, curdy ("cottage cheese"), no odour, intense pruritus | Vulvovaginal candidiasis [1] | Candida overgrowth (usually C. albicans) → hyphae invade superficial epithelium → inflammatory response → itch, erythema. Favoured by ↑glycogen (pregnancy, DM), antibiotics, immunosuppression | pH < 4.5 (normal), KOH prep → pseudohyphae/budding yeast |
| Profuse, frothy, yellow-green, offensive | Trichomoniasis [1] | T. vaginalis (flagellated protozoan, STI) → colonises squamous epithelium → intense PMN response → purulent discharge. "Strawberry cervix" = punctate haemorrhages | pH > 4.5, wet mount → motile trichomonads. NAAT now gold standard |
| Mucopurulent, often subtle | Cervicitis (Chlamydia / gonorrhoea) [1] | Obligate intracellular (C. trachomatis) or Gram-negative diplococcus (N. gonorrhoeae) infects endocervical columnar epithelium → mucopurulent exudate | Chlamydia PCR [1], gonococcal culture/NAAT |
| Watery ± blood-stained (postmenopausal) | Atrophic vaginitis [1] | ↓Oestrogen → epithelial thinning → ↓glycogen → ↓lactobacilli → ↑pH → fragile epithelium → petechiae, bleeding | Clinical appearance (pale, thin, dry, ↓rugae), pH > 5 |
| Brownish discharge | Endometriosis [1] | Ectopic endometrial tissue undergoes cyclical bleeding → old blood (brown) may track through cervix | Cyclical pattern, associated dysmenorrhoea / deep dyspareunia |
| "Prune juice" discharge | Ectopic pregnancy [1] | Decidualised endometrium sheds irregularly due to falling β-hCG from failing ectopic → dark brown ("prune juice") vaginal bleeding | +ve urine β-hCG, empty uterus on TVS, adnexal mass ± free fluid |
| Foul-smelling, purulent | Retained foreign body (e.g. tampon, IUCD) [1], cervical/endometrial malignancy | Foreign body → bacterial overgrowth → necrosis → offensive discharge. Necrotic tumour → same mechanism | Speculum examination reveals foreign body or irregular mass |
| Purulent + systemic features | PID / tubo-ovarian abscess | Ascending infection from cervix → salpingitis → tubo-ovarian complex → pus | Cervical excitation, bilateral adnexal tenderness, fever [2][5] |
| Blood-stained, watery | Cervical / endometrial / vaginal carcinoma | Neoplastic tissue is friable and vascular → bleeds easily; necrotic areas produce watery exudate | Biopsy diagnostic |
This is where the gynaecological and non-gynaecological differentials interleave. I'll separate by acuity:
Acute Pelvic Pain — Gynaecological [2][5][6]
| Diagnosis | Key Clinical Pointers | Pathophysiology |
|---|---|---|
| Ectopic pregnancy | Missed period, +ve β-hCG, unilateral pain ± PV bleeding ("prune juice"), positive pregnancy test strongly suggests ectopic if intrauterine pregnancy cannot be visualized [2] | Implantation in fallopian tube (usually ampulla) → trophoblastic invasion → tubal distension/rupture → haemoperitoneum |
| Ruptured ovarian cyst | Pain often begins during strenuous physical activity such as exercise or intercourse [2], sudden onset, unilateral | Functional cyst (follicular/corpus luteum) ruptures → peritoneal irritation from follicular fluid ± blood |
| Ovarian / fallopian tube torsion | Sudden severe unilateral pain, nausea/vomiting (waves), refers to twisting of ovary on its ligamentous supports often resulting in impedance of its blood supply [2] | Torsion → venous then arterial occlusion → ischaemia → necrosis if not detorsed |
| PID | Sexually active F, < 40y; preceded by menstrual irregularities and dysmenorrhoea; gradual onset constant lower abdominal pain; purulent yellow-white vaginal discharge; often associated with dysuria, urinary frequency, dyspareunia; Hx of previous gyne procedures, IUD, or STDs [5] | Ascending infection (Chlamydia, gonorrhoea, anaerobes) from cervix → endometritis → salpingitis → peritonitis |
| Tubo-ovarian abscess | Extension of PID with persistent fever despite antibiotics, palpable adnexal mass [2] | Walled-off collection of pus involving tube and ovary |
| Threatened / incomplete miscarriage | Vaginal bleeding + crampy pain in early pregnancy, os open (incomplete) or closed (threatened) | Products of conception partially expelled → uterus contracts to expel remainder |
| Degenerating fibroid | Acute pain in patient with known fibroids, tender localised area on uterus | Fibroid outgrows blood supply → red (carneous) degeneration → acute pain and tenderness |
Acute Pelvic Pain — Non-Gynaecological [1][2][6]
| Diagnosis | Key Clinical Pointers |
|---|---|
| Appendicitis | Periumbilical pain migrating to RIF, anorexia, nausea/vomiting, fever. Should ALWAYS take a full gynaecological Hx to distinguish from gynaecological causes [5] |
| UTI / pyelonephritis | Dysuria, frequency, urgency ± loin pain, fever, rigors [7] |
| Ureteric colic | Colicky pain waxing and waning, loin to groin radiation, haematuria |
| Diverticulitis | LLQ pain (Western) / RLQ pain (Asian — right-sided diverticulitis is more common in Asian population [2]), fever, altered bowel habit |
| Constipation / faecal impaction [1] | Often overlooked; history of infrequent bowel movements, palpable faecal mass |
| IBS | Chronic/recurrent abdominal pain related to defecation, bloating, altered bowel habit; association with dysmenorrhoea [8] |
Chronic Pelvic Pain — Gynaecological [1]
| Diagnosis | Key Clinical Pointers | Pathophysiology |
|---|---|---|
| Endometriosis | Cyclical pelvic pain, deep dyspareunia, dysmenorrhoea, dyschezia, subfertility. Presence of endometrial glands and stroma at extrauterine sites [2] | Ectopic endometrial tissue responds to cyclical hormones → bleeding, inflammation, fibrosis, adhesions |
| Adenomyosis | Progressive dysmenorrhoea + HMB, boggy tender uterus | Endometrial tissue within myometrium → cyclical swelling |
| Pelvic congestion syndrome [1] | Dull aching pain worse with standing/end of day, relieved by lying down; associated with varicose veins of broad ligament and ovarian veins | Venous incompetence → pelvic venous engorgement → pain |
| Chronic PID / adhesions | History of prior PID or surgery, pain with movement | Post-inflammatory adhesions → traction on pelvic organs |
| Pelvic / abdominal adhesions [1] | History of prior surgery or infection | Fibrous bands → intermittent traction/obstruction |
| Misplaced IUCD [1] | Pain temporally related to IUCD insertion | Malposition → myometrial irritation, perforation |
This is an extremely common clinical overlap — women with vaginal complaints often also have urinary symptoms, and vice versa [7][9].
| Diagnosis | Key Features | Distinguishing Point |
|---|---|---|
| UTI (cystitis) | Dysuria, frequency, urgency, suprapubic pain, turbid/foul urine | +ve MSU (≥10⁵ CFU/mL), no vaginal discharge [7] |
| Vaginitis (BV, Candida, Trichomonas) | "External" dysuria (urine hitting inflamed vulva), vaginal discharge, pruritus | Discharge present, MSU usually sterile, vaginal discharge is incompatible with simple cystitis [9] |
| STD urethritis | Urethral discharge especially morning void, +ve sexual history [7] | NAAT for Chlamydia/gonorrhoea positive |
| PID | Lower abdominal pain + vaginal discharge + cervical excitation [5] | Systemic features (fever), bilateral adnexal tenderness |
| Interstitial cystitis | Chronic suprapubic pain, frequency, urgency — diagnosis of exclusion → chronic, refractory bladder symptoms and pain [7] | No infection found on MSU, cystoscopy may show Hunner's ulcers |
Because amenorrhoea has such a wide differential, it deserves its own structured approach. Think anatomical level [4]:
| Level | Primary Amenorrhoea | Secondary Amenorrhoea |
|---|---|---|
| Physiological | — | Pregnancy (always exclude first!) [4], lactation, menopause |
| Hypothalamic | Constitutional delay, Kallmann syndrome (anosmia + hypogonadotropic hypogonadism), chronic illness | Functional hypothalamic amenorrhoea (stress, weight loss, excessive exercise), tumours, TBI, cranial irradiation, inflammatory/infiltrative disease [4] |
| Pituitary | Hyperprolactinaemia (rare in primary) | Hyperprolactinaemia (drugs — DA antagonists, prolactinoma), pituitary adenoma, Sheehan syndrome (postpartum pituitary necrosis), pituitary apoplexy [4] |
| Ovarian | Turner syndrome (45,X), gonadal dysgenesis, 46,XY disorders of sex development (androgen insensitivity) | Premature ovarian insufficiency (AI, fragile X permutation, chemoRT, idiopathic), PCOS, ovarian tumour [4] |
| Uterine / Outflow | Müllerian agenesis (MRKH syndrome), imperforate hymen, transverse vaginal septum | Asherman syndrome (intrauterine adhesions post-D&C), cervical stenosis [4] |
| Other endocrine | Congenital adrenal hyperplasia | Thyroid disease (hyper/hypothyroidism), uncontrolled DM, Cushing syndrome, exogenous androgens [4] |
Why think by anatomical level? Because the investigation pathway mirrors this — you test β-hCG → FSH/LH → prolactin → TSH → oestradiol → progestogen challenge → imaging to localise the lesion from "top" (hypothalamus) to "bottom" (uterus).
The following algorithm integrates the above differentials into a practical bedside reasoning flow:
These are the diagnoses that, if missed, lead to serious morbidity or mortality. Always actively consider and exclude these:
| Red Flag Presentation | Must-Not-Miss Diagnosis | Why Dangerous |
|---|---|---|
| Amenorrhoea + pelvic pain + PV bleeding + haemodynamic instability | Ruptured ectopic pregnancy [1][2] | Haemoperitoneum → hypovolaemic shock → death if not treated surgically |
| PMB (any amount) | Endometrial carcinoma [1] | ~10% of PMB is cancer; early detection dramatically improves prognosis |
| Irregular PCB/IMB in sexually active woman | Cervical carcinoma [1] | HPV-driven malignancy; treatable if caught early |
| Purulent discharge + fever + cervical excitation | PID / tubo-ovarian abscess [1][5] | Can lead to tubal damage → infertility, chronic pain, sepsis |
| Acute unilateral pelvic pain + nausea in young woman | Ovarian torsion [2] | Vascular compromise → ovarian necrosis if not detorsed within hours |
| Tampon-related illness with fever, rash, hypotension | Toxic shock syndrome [1] | Staphylococcal superantigen → massive cytokine release → multiorgan failure [10] |
| Vaginal discharge in a child | Sexual abuse [1] | Safeguarding emergency |
Golden Rule
In any woman of reproductive age with abnormal bleeding or pelvic pain: ALWAYS do a urine β-hCG first. Missing an ectopic pregnancy is a medicolegal disaster and can be fatal. It takes 5 minutes and costs almost nothing.
| Feature | BV | Candidiasis | Trichomoniasis |
|---|---|---|---|
| Prevalence | 40–50% | 20–30% | 10–20% [1] |
| Organism | Gardnerella, Prevotella, Mobiluncus (anaerobic overgrowth) | Candida albicans (90%) | Trichomonas vaginalis (protozoan) |
| Discharge | Thin, grey-white, homogeneous | Thick, white, curdy ("cottage cheese") | Profuse, frothy, yellow-green |
| Odour | Fishy (amines) | None | Offensive |
| Pruritus | Minimal/none | Intense | Variable |
| pH | > 4.5 | < 4.5 (normal) | > 4.5 |
| Amine (whiff) test | Positive [1] | Negative | May be positive |
| Wet mount | Clue cells (epithelial cells studded with bacteria) | — | Motile flagellated organisms |
| KOH prep | — | Pseudohyphae/budding yeast | — |
| Inflammation | No (dysbiosis, not infection) | Yes (mucosal erythema) | Yes (purulent, "strawberry cervix") |
| STI? | No (not sexually transmitted per se, but sexual activity is a risk factor) | No | Yes |
| Treatment | Metronidazole (oral or vaginal) | Topical azoles or oral fluconazole | Metronidazole (oral) — must treat partner |
High Yield Summary — Differential Diagnosis
-
Probability diagnoses for vaginal discharge: physiological, BV (40–50%), candidiasis (20–30%), trichomoniasis (10–20%) [1].
-
Probability diagnoses for abdominal/pelvic pain in women: primary dysmenorrhoea, Mittelschmerz, adhesions, endometriosis [1].
-
Must-not-miss: ectopic pregnancy, cervical/endometrial cancer, PID/TOA, ovarian torsion, toxic shock syndrome [1], sexual abuse in children [1].
-
Pitfalls often missed: chemical vaginitis, retained foreign body, endometriosis (brownish discharge), ectopic pregnancy ("prune juice" discharge), pelvic congestion syndrome, misplaced IUCD, constipation [1].
-
Masquerades: diabetes, drugs, UTI, depression, spinal dysfunction (referred pain) [1].
-
Always exclude pregnancy (β-hCG) first in any reproductive-age woman.
-
pH paper is your bedside friend: < 4.5 → Candida/physiological; > 4.5 → BV/Trichomonas/atrophic/cervicitis.
-
For PID: classically sexually active female < 40y, lower abdominal pain, vaginal discharge, cervical excitation ("chandelier sign"), fever [5].
-
For appendicitis ddx in adult females: always take full gynaecological history, especially menstrual cycle, vaginal discharge and possible pregnancy [5].
-
For secondary amenorrhoea: think anatomical level — hypothalamus → pituitary → ovary → uterus/outflow — and investigate accordingly [4].
Active Recall - Differential Diagnosis of Menstrual/Vaginal Complaints
References
[1] Lecture slides: murtagh merge.pdf (p1 — Abdominal pain in women; p103–104 — Vaginal discharge) [2] Senior notes: felixlai.md (sections on appendicitis differential diagnosis including O&G causes; diverticulitis differential diagnosis including gynaecological disorders) [3] Senior notes: Ryan Ho Haemtology.pdf (p128 — von Willebrand disease, HMB prevalence) [4] Senior notes: Ryan Ho Psychiatry.pdf (p214 — Differential diagnosis of secondary amenorrhoea) [5] Senior notes: Ryan Ho GI.pdf (p99, p151 — PID clinical features, differential diagnosis of acute appendicitis in adult females) [6] Senior notes: maxim.md (sections on acute abdomen differential diagnosis including O&G causes) [7] Senior notes: Ryan Ho Urogenital.pdf (p121 — Approach to dysuria; p248 — Urethritis differential) [8] Senior notes: Ryan Ho GI.pdf (p118 — IBS associations including dysmenorrhoea) [9] Senior notes: Ryan Ho Urogenital.pdf (p125 — Acute cystitis differential, vaginal discharge incompatible with cystitis) [10] Senior notes: Ryan Ho Rheumatology.pdf (p133 — Staphylococcal toxic shock syndrome)
Diagnostic Criteria, Diagnostic Algorithm and Investigation Modalities
The diagnostic approach to menstrual/vaginal complaints is not about a single test — it's about layering bedside assessment → targeted investigations → definitive procedures in a logical sequence driven by the clinical picture. Let me walk you through this the way you'd actually think on the ward.
1. Diagnostic Criteria for Key Conditions
Most menstrual/vaginal complaints don't have a single set of "diagnostic criteria" like the Jones criteria for rheumatic fever. Instead, diagnosis is made by clinical assessment + supportive investigations. However, several specific conditions within this domain do have defined criteria, and you need to know them.
BV is diagnosed clinically when ≥ 3 of 4 Amsel criteria are met:
| Criterion | What You're Looking For | Why (Pathophysiology) |
|---|---|---|
| 1. Thin, homogeneous, greyish-white discharge | Adherent discharge coating vaginal walls | Biofilm of anaerobes (Gardnerella, Prevotella) replaces normal lactobacilli → altered secretions |
| 2. pH > 4.5 | Test with pH paper (range 4–6) at vaginal wall (NOT cervical mucus, which is always alkaline) [1] | Loss of lactobacilli → ↓lactic acid production → pH rises |
| 3. Positive amine ("whiff") test | Add 10% KOH to discharge → fishy odour released [1] | Anaerobes produce amines (putrescine, cadaverine, trimethylamine); KOH volatilises them |
| 4. Clue cells on wet mount | ≥ 20% of epithelial cells on saline wet mount have stippled, granular appearance with obscured borders | Vaginal epithelial cells become coated with adherent bacteria (Gardnerella biofilm) |
Alternative: Nugent score on Gram stain of vaginal secretions (score 7–10 = BV). This is the research gold standard but less practical at the bedside. The score quantifies the shift from lactobacilli (large Gram-positive rods) to Gardnerella/Mobiluncus morphotypes (small Gram-variable rods/curved rods).
There are no formal "criteria" — diagnosis is made by:
- Clinical features: pruritus, thick white curdy ("cottage cheese") discharge, vulvar erythema/oedema, satellite lesions
- pH < 4.5 (normal — Candida thrives in acid environment)
- KOH preparation: 10% KOH dissolves epithelial cells and debris, leaving behind pseudohyphae and budding yeast clearly visible under microscopy
- Culture (Sabouraud's agar): not routinely needed for uncomplicated cases; useful for recurrent or resistant candidiasis to identify species (non-albicans species like C. glabrata may be azole-resistant)
- Saline wet mount: motile, pear-shaped, flagellated organisms seen — sensitivity only ~60–70% (must be examined immediately as organisms die quickly)
- NAAT (nucleic acid amplification test): now the gold standard — sensitivity > 95%
- pH > 4.5, may have positive amine test
- "Strawberry cervix" (colpitis macularis): punctate haemorrhages on cervix — seen in ~2% on naked eye examination but ~45% on colposcopy
PID is a clinical diagnosis — you do NOT need laparoscopy to confirm it in practice. The threshold for starting treatment is deliberately low because the consequences of missed PID (infertility, chronic pain) are severe.
Minimum criteria (all 3 should be present):
- Lower abdominal/pelvic tenderness
- Adnexal tenderness (on bimanual examination)
- Cervical excitation tenderness (chandelier sign) [5][12]
Additional criteria that support the diagnosis:
- Oral temperature > 38.3°C
- Abnormal cervical mucopurulent discharge or cervical friability
- Abundant WBCs on saline wet mount of vaginal fluid
- ↑ESR or ↑CRP
- Laboratory documentation of cervical infection with N. gonorrhoeae or C. trachomatis (Chlamydia PCR [1])
Specific criteria (definitive but not required for clinical diagnosis):
- Endometrial biopsy showing endometritis
- Transvaginal USS or MRI showing thickened, fluid-filled tubes ± tubo-ovarian complex/abscess ± free pelvic fluid
- Laparoscopic findings consistent with PID (gold standard but invasive, rarely done for diagnosis alone)
Why Is the Diagnostic Threshold So Low?
Because PID can cause tubal scarring → infertility even with subtle symptoms. The CDC deliberately sets a low bar — if a sexually active young woman has pelvic tenderness + cervical excitation tenderness, start empirical antibiotics while awaiting results. The cost of overtreatment is far less than the cost of missed diagnosis [12].
- Heavy menstrual bleeding (HMB): Defined as excessive menstrual blood loss that interferes with quality of life (NICE definition). The old quantitative threshold (> 80 mL/cycle) is rarely measured clinically. In practice, rely on patient-reported impact (flooding, clots, pad changes, interference with daily life).
- Postmenopausal bleeding (PMB): Any bleeding > 12 months after last menstrual period. Endometrial thickness ≤ 4 mm on TVS has a > 99% negative predictive value for endometrial cancer — this is the key threshold.
- Endometrial hyperplasia / cancer: Diagnosed histologically on endometrial biopsy — there are no clinical criteria alone.
Diagnosis requires ≥ 2 of 3 (after excluding other causes):
| Criterion | How to Assess |
|---|---|
| 1. Oligo-ovulation or anovulation | Oligomenorrhoea (cycle > 35 days) or amenorrhoea |
| 2. Clinical and/or biochemical hyperandrogenism | Clinical: hirsutism (Ferriman-Gallwey score ≥ 4–6), acne, androgenic alopecia. Biochemical: ↑free testosterone, ↑DHEA-S |
| 3. Polycystic ovarian morphology on USS | ≥ 12 follicles (2–9 mm) per ovary OR ovarian volume > 10 mL (on TVS). Updated 2023: ≥ 20 follicles per ovary (with modern USS transducers) OR AMH > 35 pmol/L as alternative |
Must exclude: thyroid disease (TFTs), hyperprolactinaemia (prolactin), non-classical congenital adrenal hyperplasia (17-OH progesterone), Cushing syndrome, androgen-secreting tumour.
- Clinical triad: amenorrhoea + PV bleeding + unilateral pelvic/abdominal pain (present in ~50% of cases — many present atypically)
- Urine β-hCG: positive
- TVS: empty uterus + adnexal mass ± free fluid in Pouch of Douglas
- Serum β-hCG: when indeterminate on USS — a "discriminatory level" of ~1500–2000 IU/L is used (above this level, an intrauterine pregnancy should be visible on TVS; if not → suspect ectopic)
- "Positive pregnancy test strongly suggests presence of an ectopic pregnancy if an intrauterine pregnancy cannot be visualized" [2]
2. Investigation Modalities — Systematic Approach
I'll present investigations in the order you would logically request them: bedside → blood → microbiology → imaging → invasive/definitive.
| Investigation | What It Tests | Key Findings / Interpretation | When to Use |
|---|---|---|---|
| Urine β-hCG | Pregnancy | Positive → pregnancy-related cause (intrauterine, ectopic, miscarriage, GTD). Must do first in ALL reproductive-age women [12][13] | Every woman of reproductive age with abnormal bleeding, pelvic pain, or amenorrhoea |
| pH paper (range 4–6) [1] | Vaginal pH | < 4.5: normal, candidiasis. > 4.5: BV, trichomoniasis, atrophic vaginitis, cervicitis. Take from vaginal wall, NOT cervix (cervical mucus is alkaline and gives a false high reading) | Vaginal discharge |
| Amine ("whiff") test [1] | Volatile amines | Fishy odour when KOH added to discharge → positive in BV (amines from anaerobes volatilised by alkali) | Vaginal discharge |
| Saline wet mount | Clue cells, trichomonads, WBCs | Clue cells → BV. Motile flagellated organisms → trichomoniasis. ↑WBCs → inflammatory (candidiasis, cervicitis, trichomoniasis). WBCs with no organisms → consider Chlamydia | Vaginal discharge |
| KOH (10%) preparation | Fungal elements | Pseudohyphae / budding yeast → candidiasis. KOH dissolves epithelial cells, making fungi easier to see | Suspected candidiasis |
| Urinalysis (dipstick + microscopy) [1][13] | UTI, haematuria, proteinuria | Nitrites + leucocytes → UTI. RBCs → consider urological cause or contamination. Repeat after menstruation if haematuria found during period [11] | Dysuria, frequency, haematuria, pelvic pain |
| Urine MC&S (midstream) | Urinary infection | ≥ 10⁵ CFU/mL → significant bacteriuria. Common organisms: E. coli (80%), Klebsiella, Proteus | Suspected UTI |
pH Testing Pitfall
Do NOT take the pH from the cervical os or from pooled discharge mixed with cervical mucus — cervical mucus is alkaline (pH ~7) and will give a falsely elevated reading. Swab the lateral vaginal wall for accurate pH assessment.
| Investigation | What It Tests | Key Findings / Interpretation | When to Use |
|---|---|---|---|
| FBE (Full Blood Examination / CBC) [1] | Haemoglobin, MCV, platelets, WCC | ↓Hb + ↓MCV + ↓ferritin → iron deficiency anaemia (from chronic HMB). ↑WCC → infection (PID, TOA). ↓Platelets → thrombocytopenia causing HMB | All abnormal bleeding, suspected infection |
| ESR / CRP [1] | Inflammatory markers | ↑ in PID, TOA, endometritis, malignancy. CRP more specific for acute infection | Suspected PID, chronic pelvic pain |
| Iron studies (ferritin, serum iron, TIBC, transferrin sat) | Iron status | ↓Ferritin (< 30 μg/L) is the single best test for iron deficiency. ↓Serum iron + ↑TIBC → IDA | HMB, anaemia |
| Coagulation screen (PT, APTT, fibrinogen) | Clotting pathway | Isolated ↑APTT → consider vWD (APTT can be normal in mild vWD). Normal PT + ↑APTT → intrinsic pathway defect | HMB since menarche, easy bruising, family history of bleeding [3] |
| vWF panel (vWF:Ag, vWF:Act/RiCof, Factor VIII activity) | von Willebrand disease | vWF:Ag < 30 IU/dL + ↓vWF:Act + ↓Factor VIII → consistent with vWD. aPTT can be normal in: (1) mild deficiency (2) stress-induced ↑vWF/F8 during phlebotomy (3) hormonal factors (menstrual cycle, pregnancy, OCP) [3] | HMB since menarche, bleeding history |
| Hormonal profile | HPO axis assessment | See dedicated table below | Amenorrhoea, oligomenorrhoea, suspected PCOS, perimenopause |
| Serum β-hCG (quantitative) | Pregnancy viability / ectopic monitoring | Doubling time ~48h in normal early pregnancy. Suboptimal rise or plateau → ectopic or failing pregnancy. Above discriminatory level (~1500–2000 IU/L) with empty uterus on TVS → ectopic | Suspected ectopic, pregnancy of unknown location |
| TFTs (TSH, free T4) | Thyroid function | ↑TSH → hypothyroidism (→ anovulation, HMB). ↓TSH → hyperthyroidism (→ oligomenorrhoea) | Menstrual irregularity, amenorrhoea |
| Prolactin | Hyperprolactinaemia | ↑Prolactin → suppresses GnRH → anovulation. Causes: prolactinoma, drugs (antipsychotics, metoclopramide) | Amenorrhoea, galactorrhoea, oligomenorrhoea |
Hormonal Profile Interpretation:
| Test | Timing | Interpretation |
|---|---|---|
| FSH | Day 2–5 (early follicular) | ↑↑FSH (> 25–40 IU/L) → ovarian failure (premature ovarian insufficiency if < 40y, menopause if > 40y). Normal/low FSH with anovulation → hypothalamic/pituitary cause |
| LH | Day 2–5 | LH:FSH ratio ≥ 2:1 suggests PCOS (though not required for Rotterdam criteria). ↓LH → hypothalamic cause |
| Oestradiol (E2) | Day 2–5 | ↓E2 + ↑FSH → ovarian failure. ↓E2 + low/normal FSH → hypothalamic/pituitary |
| Day 21 progesterone | Day 21 (or 7 days before expected period) | > 16 nmol/L (some use > 30 nmol/L) → confirms ovulation. Low → anovulatory cycle |
| Testosterone, DHEA-S | Any day | ↑ → hyperandrogenism (PCOS, adrenal, tumour). Markedly ↑testosterone (> 5 nmol/L) → suspect androgen-secreting tumour |
| 17-OH progesterone | Early morning, follicular phase | ↑ → non-classical congenital adrenal hyperplasia (21-hydroxylase deficiency) |
| AMH (anti-Müllerian hormone) | Any day | Reflects ovarian reserve. ↑AMH → PCOS (> 35 pmol/L). ↓AMH → diminished ovarian reserve |
| Investigation | Specimen | Key Findings | When to Use |
|---|---|---|---|
| Chlamydia PCR (NAAT) [1] | Endocervical swab or first-void urine | Positive → C. trachomatis infection. Gold standard — sensitivity > 95%, specificity > 99% | Suspected cervicitis, PID, routine STI screening, abnormal discharge |
| Gonorrhoea NAAT | Endocervical swab or first-void urine | Positive → N. gonorrhoeae. Always test alongside Chlamydia (co-infection common) | Same as above |
| Gonorrhoea culture | Endocervical swab (special transport medium — must be plated quickly) [14] | Gram-negative intracellular diplococci. Culture allows antibiotic sensitivity testing — critical given rising resistance | Suspected gonorrhoea (always do culture in addition to NAAT for resistance testing) |
| High vaginal swab (HVS) | Posterior fornix | Culture for BV, Candida, Trichomonas, Group B Strep. Gram stain for Nugent scoring | Vaginal discharge, recurrent infections |
| Endocervical swab — Gram stain | Endocervix | ≥ 30 PMN/HPF → cervicitis. Intracellular Gram-negative diplococci → gonorrhoea [14] | Purulent cervical discharge |
| Urethral swab — Gram stain | Urethra | Urethritis diagnosed when ≥ 5 PMN per HPF ± intracellular G- diplococci (diagnostic of gonorrhoea) [14] | Urethral discharge |
| Herpes PCR / viral culture | Vesicle fluid or ulcer swab | Positive → HSV-1 or HSV-2. PCR preferred (more sensitive than culture) | Vulval vesicles/ulcers |
| Syphilis serology (RPR/VDRL + TPHA/FTA-Abs) | Blood | Screening + confirmatory tests | Genital ulcers, STI screen |
| HPV testing | Cervical sample (co-test with cytology) | High-risk HPV (16, 18, others) detected → ↑risk cervical dysplasia/cancer | Women ≥ 30 as primary screening or reflex test for ASCUS cytology |
| Modality | What It Shows | Key Findings | When to Use |
|---|---|---|---|
| Transvaginal ultrasound (TVS) | Uterus, endometrium, ovaries, adnexa, Pouch of Douglas | Endometrial thickness: ≤ 4 mm postmenopausal → cancer very unlikely (NPV > 99%). > 4 mm → needs biopsy. Fibroids: well-circumscribed hypoechoic masses ± calcification. Adenomyosis: heterogeneous myometrium, asymmetric wall thickening, myometrial cysts. Ovarian cyst: simple (thin-walled, anechoic) vs complex (septations, solid components, irregular). Ectopic: empty uterus + adnexal mass ± free fluid. PCOS morphology: ≥ 20 follicles/ovary or volume > 10 mL | First-line imaging for virtually all menstrual/vaginal complaints. TVS is most appropriate for left adnexal mass detected on PV [15] |
| Transabdominal ultrasound (TAS) | Pelvic structures (less resolution than TVS) | Large masses better visualised (extends beyond TVS range). Useful when TVS not tolerated (virgo intacta, severe tenderness) | Large pelvic masses, young patients, adjunct to TVS |
| Saline infusion sonography (SIS / sonohysterography) | Endometrial cavity detail | Fluid distends cavity → polyps and submucosal fibroids seen as filling defects. Distinguishes diffuse endometrial thickening (hyperplasia) from focal lesion (polyp, fibroid) | AUB with thickened endometrium on TVS — to determine if focal or diffuse before deciding on biopsy vs hysteroscopy |
| MRI pelvis | Soft tissue detail of uterus, ovaries, parametrium | Best for adenomyosis (junctional zone thickening > 12 mm is diagnostic), fibroid mapping pre-surgery, endometriosis (deep infiltrating), staging of cervical/endometrial cancer | Indeterminate TVS findings, pre-surgical planning, suspected deep endometriosis, cancer staging |
| CT abdomen-pelvis | Broad overview; less soft tissue detail than MRI | Useful in acute abdomen (appendicitis, diverticulitis, ovarian torsion — "whirlpool sign"). Can show adnexal masses but poor endometrial detail | Acute abdomen, suspected non-gynaecological cause, emergency setting |
| Hysterosalpingography (HSG) | Uterine cavity + tubal patency (contrast injected via cervix under fluoroscopy) | Filling defects → polyps, submucosal fibroids, adhesions (Asherman). Tubal blockage → PID sequelae, for infertility workup | Infertility workup, suspected Asherman syndrome |
TVS vs TAS: When to Use Which
TVS (transvaginal) gives superior resolution of endometrium, ovaries, and adnexa because the probe is closer to the structures. It is first-line for almost all gynaecological imaging. TAS (transabdominal) is used when the mass is too large for TVS field, or when TVS is contraindicated/not tolerated. For a left adnexal mass detected on PV examination, TVS (transvaginal US) is the most appropriate investigation [15].
| Investigation | What It Does | Key Findings / Interpretation | When to Use |
|---|---|---|---|
| Speculum examination | Direct visualisation of vagina and cervix | Look for discharge, polyps, warts, ectropion, prolapses, fistulas [1]. Cervix: well-visualised with no gross lesions / polyp / ectropion / discharge / bleeding / irregular shape / flush to vaginal wall [7]. Mucopurulent discharge from cervical os → cervicitis (PID). Irregular friable mass → cervical carcinoma | All women with vaginal complaints [1][7] |
| Bimanual pelvic examination | Assess uterine size/shape/tenderness, adnexal masses, cervical excitation | Bulky irregular uterus → fibroids. Boggy tender uterus → adenomyosis. Cervical excitation + adnexal tenderness → PID/ectopic. Fixed retroverted uterus → endometriosis/adhesions | All women with menstrual complaints or pelvic pain |
| Endometrial biopsy (Pipelle) | Outpatient sampling of endometrium | Histology: normal secretory/proliferative endometrium, disordered proliferation, hyperplasia (± atypia), endometrial carcinoma, chronic endometritis (plasma cells in stroma) | PMB (after TVS shows ET > 4 mm or persistent symptoms despite thin endometrium), AUB in women ≥ 45, AUB + risk factors for endometrial hyperplasia/cancer at any age, failed medical therapy |
| Hysteroscopy (+ directed biopsy) | Direct visualisation of endometrial cavity via camera | Gold standard for intracavitary pathology: polyps (pedunculated glistening mass), submucosal fibroids (smooth bulge covered by endometrium), adhesions (Asherman — white bands bridging cavity), endometrial cancer (irregular friable mass) | Abnormal endometrial findings on TVS/SIS, inconclusive Pipelle biopsy, removal of polyps/submucosal fibroids (operative hysteroscopy), persistent AUB despite normal initial investigations |
| Cervical cytology (Pap smear / liquid-based cytology) | Screening for cervical dysplasia | Normal, ASCUS (atypical squamous cells of undetermined significance), LSIL, HSIL, AGC, malignant cells. Taking the smear: Cervex brush rotated clockwise ×5 at transformation zone [7] | Routine screening (age 25–64 per HK guidelines), PCB, suspicious cervix |
| Colposcopy + cervical biopsy | Magnified examination of cervix after acetic acid/Lugol's iodine application | Acetowhite areas → dysplasia (acetic acid denatures excess nuclear protein in dysplastic cells → white). Lugol's-negative areas → abnormal epithelium (normal squamous cells take up iodine → brown; dysplastic cells don't). Punch biopsy → histological grading (CIN 1/2/3 or carcinoma) | Abnormal Pap smear, suspicious cervical appearance, PCB with normal cytology |
| Laparoscopy | Direct visualisation of pelvic organs | Gold standard for endometriosis (powder-burn spots, chocolate cysts, adhesions), PID (tubal erythema, purulent exudate), ovarian pathology. Also therapeutic (excision/ablation of endometriosis, cystectomy, salpingectomy for ectopic) | Chronic pelvic pain not explained by non-invasive tests, suspected endometriosis, suspected ectopic (when USS indeterminate and clinical concern), PID with uncertain diagnosis |
| Culdocentesis | Aspiration from Pouch of Douglas via posterior fornix | Non-clotting blood → haemoperitoneum (ruptured ectopic, ruptured cyst). Pus → pelvic abscess. Largely replaced by TVS but may be useful in resource-limited settings | Suspected ruptured ectopic (now largely replaced by TVS + serial β-hCG) |
| Urodynamic studies | Detailed assessment of bladder function (filling cystometry, pressure-flow studies, leak point pressure) | Detrusor overactivity → urge incontinence. Low leak point pressure → stress incontinence. Gold standard, only if complicated [16] | Urinary incontinence not responding to initial management, pre-surgical assessment |
4. Specific Diagnostic Algorithms by Complaint
This is the highest-yield algorithm because it is a potential cancer pathway.
| Step | Action | Rationale |
|---|---|---|
| 1 | History + examination (speculum + bimanual) | Identify obvious cervical/vaginal pathology (polyp, atrophic vaginitis, cancer) |
| 2 | TVS — measure endometrial thickness | Screening test to stratify risk. ET ≤ 4 mm → NPV > 99% for endometrial cancer |
| 3a | If ET ≤ 4 mm AND single episode → reassure + safety-net | Likely atrophy; recurrence warrants re-investigation |
| 3b | If ET > 4 mm OR recurrent PMB → endometrial sampling (Pipelle biopsy or hysteroscopy-guided biopsy) | To obtain histological diagnosis |
| 4 | Hysteroscopy if Pipelle is inadequate/insufficient, or if focal lesion suspected on SIS/TVS | Direct visualisation + targeted biopsy; allows removal of polyps |
| 5 | If cervical pathology suspected → cervical cytology + colposcopy + biopsy | R/O cervical cancer |
The 4mm Rule
An endometrial thickness of ≤ 4 mm on TVS in a postmenopausal woman has a negative predictive value > 99% for endometrial cancer. This is the cornerstone of the PMB investigation pathway. However, if bleeding recurs or persists despite thin endometrium, biopsy is still indicated — rare cancers (especially Type II serous carcinoma) can occur with a thin endometrium.
Key investigations: pH test with paper of range 4–6, Amine or "whiff" test [1]
| Step | Action | Interpretation |
|---|---|---|
| 1 | Speculum examination — observe character of discharge, cervix | Look for discharge, polyps, warts, ectropion, prolapses, fistulas [1] |
| 2 | pH paper (lateral vaginal wall) | < 4.5 → Candida/physiological. > 4.5 → BV/Trichomonas/atrophic/cervicitis |
| 3 | Whiff test (KOH to discharge) | Positive → BV (or Trichomoniasis) |
| 4 | Wet mount (saline) | Clue cells → BV. Motile organisms → Trichomoniasis. ↑WBCs → inflammatory |
| 5 | KOH prep | Pseudohyphae → Candidiasis |
| 6 | Endocervical swab for NAAT (Chlamydia + Gonorrhoea) | If mucopurulent cervical discharge, STI risk factors, or PID suspected |
| 7 | Culture if recurrent/resistant | Sabouraud's for Candida species; GC culture for antibiotic sensitivity |
Diagnostic tips: Urethritis causes pain at the onset of micturition and cystitis at the end. Suprapubic discomfort is a feature of bladder infection (cystitis). Unexplained dysuria could be a pointer to chlamydia urethritis. [17]
| Feature | UTI (Cystitis) | Vaginitis | Urethritis (STD) |
|---|---|---|---|
| Dysuria location | "Internal" — burning felt inside urethra, especially at end of micturition | "External" — burning felt when urine contacts inflamed vulva | "Internal" — pain at onset of micturition [17] |
| Associated symptoms | Frequency, urgency, nocturia, suprapubic pain, cloudy/foul urine | Vaginal discharge, pruritus, dyspareunia | Urethral discharge (especially morning void), +ve sexual Hx [7][14] |
| Vaginal discharge | Absent (vaginal discharge is incompatible with simple cystitis [9]) | Present | May be present (urethral) |
| Key test | Dipstick testing of urine; Microscopy or culture (MSU) [17] | pH, whiff test, wet mount, KOH | Urethral swab or first-pass urine for STIs [17], Chlamydia/GC NAAT |
| Scenario | First-Line Investigations | Second-Line / Definitive |
|---|---|---|
| HMB (reproductive age) | FBE + iron studies, TFTs, coag screen (if since menarche), TVS | Hysteroscopy ± endometrial biopsy, vWF panel, SIS |
| IMB / PCB | Speculum (cervical assessment), Chlamydia/GC NAAT, cervical cytology, TVS | Colposcopy + cervical biopsy, hysteroscopy |
| PMB | TVS (endometrial thickness), speculum | Pipelle biopsy, hysteroscopy ± directed biopsy, cervical cytology |
| Amenorrhoea / Oligomenorrhoea | β-hCG, FSH, LH, oestradiol, prolactin, TSH, testosterone, TVS | MRI pituitary (if ↑prolactin), karyotype (if primary amenorrhoea + ↑FSH), Day 21 progesterone, 17-OH progesterone, DHEA-S |
| Vaginal discharge | pH, whiff test, wet mount, KOH prep, Chlamydia/GC NAAT | HVS C&S, herpes PCR, cervical cytology if PCB |
| Acute pelvic pain | β-hCG, FBE, CRP, urine MC&S, TVS | CT (if non-gynae suspected), laparoscopy (if diagnosis uncertain), serial β-hCG (ectopic pathway) |
| Dysuria | Urinalysis (dipstick + microscopy), MSU C&S, urethral swabs or first-pass urine for STIs [17] | Chlamydia/GC NAAT, cystoscopy (if refractory → r/o interstitial cystitis) |
| Vulval symptoms | Inspection, biopsy if suspicious lesion | Patch testing (if contact dermatitis), vulval biopsy (if lichen sclerosus, VIN suspected) |
Endometrial biopsy (Pipelle): Quick outpatient procedure — a thin plastic suction catheter is passed through the cervix and a strip of endometrium is aspirated. Sensitivity for endometrial cancer ~90–99% when adequate tissue obtained. However, it is a "blind" procedure — can miss focal lesions (polyps, small cancers). If inadequate or discordant with clinical picture → proceed to hysteroscopy.
Speculum examination preparation: Cusco's bivalve speculum of appropriate size according to gravidity. Lubricate with sterile saline to minimise risk of contamination of Pap smear. If liquid-based cytology is used, KY jelly can be used. [7]
Pap smear technique: Cervex brush rotated clockwise × 5 times at transformation zone → put into liquid-based medium and pushed into bottom of vial for 10 times → brush bent and broken with tip left inside vial → label immediately. [7]
Urinalysis in the context of menstrual complaints: Contamination with menstrual blood should be ruled out by repeating urinalysis after the menstruation has ceased. Cyclic haematuria during and shortly after menstruation suggests endometriosis of the urinary tract [11].
High Yield Summary — Diagnostics
-
Always urine β-hCG first in reproductive-age women — before any other investigation.
-
Vaginal discharge bedside workup: pH paper (range 4–6) + amine/whiff test [1] + wet mount + KOH prep + NAAT for Chlamydia/GC. pH < 4.5 → Candida; pH > 4.5 → BV/Trichomonas/atrophic/cervicitis.
-
BV is diagnosed by Amsel criteria (≥ 3 of 4): discharge character, pH > 4.5, positive whiff test, clue cells.
-
PID is a clinical diagnosis (CDC minimum criteria): lower abdominal tenderness + adnexal tenderness + cervical excitation tenderness. Low threshold to treat.
-
PMB investigation: TVS → endometrial thickness ≤ 4 mm → NPV > 99% for cancer. > 4 mm or recurrent → endometrial biopsy.
-
PCOS: Rotterdam criteria — ≥ 2 of 3: oligo/anovulation, clinical/biochemical hyperandrogenism, polycystic ovaries on USS (after excluding other causes).
-
Ectopic pregnancy: positive β-hCG + empty uterus on TVS + adnexal mass. Serial β-hCG with suboptimal rise confirms non-viable pregnancy.
-
vWD screening in HMB since menarche: APTT (may be normal!), vWF:Ag, vWF:Act, Factor VIII activity.
-
Dysuria tip: urethritis = pain at onset of micturition; cystitis = pain at end. Suprapubic discomfort → cystitis. Unexplained dysuria → Chlamydia urethritis [17].
-
Speculum + bimanual examination is essential for ALL menstrual/vaginal complaints — it is both diagnostic and guides further investigation [1][7].
Active Recall - Diagnostic Criteria, Algorithm and Investigations
References
[1] Lecture slides: murtagh merge.pdf (p103–104 — Vaginal discharge: key investigations including pH test, amine test, key examination) [2] Senior notes: felixlai.md (section on appendicitis differential diagnosis — ectopic pregnancy) [3] Senior notes: Ryan Ho Haemtology.pdf (p128 — von Willebrand disease, aPTT caveats) [5] Senior notes: Ryan Ho GI.pdf (p99, p151 — PID clinical features, appendicitis differential in females) [7] Senior notes: Ryan Ho Fundamentals.pdf (p196 — Pelvic examination, speculum technique, Pap smear technique) [9] Senior notes: Ryan Ho Urogenital.pdf (p125 — Acute cystitis differential, vaginal discharge incompatible with cystitis) [11] Senior notes: felixlai.md (section on haematuria — menstrual contamination, cyclic haematuria and endometriosis) [12] Senior notes: Ryan Ho Fundamentals.pdf (p273 — PID clinical features and diagnosis) [13] Senior notes: Ryan Ho Fundamentals.pdf (p279 — Investigations for acute abdomen including urine pregnancy test, urinalysis) [14] Senior notes: Ryan Ho Urogenital.pdf (p248 — Urethritis approach, Gram stain criteria, NAAT) [15] Senior notes: Ryan Ho Radiology.pdf (p40 — TVS for adnexal mass) [16] Senior notes: Ryan Ho Urogenital.pdf (p161 — Urodynamic studies, investigations for incontinence) [17] Lecture slides: murtagh merge.pdf (p42 — Dysuria: key investigations, diagnostic tips)
Management of Menstrual / Vaginal Complaints
Management follows directly from diagnosis. The overarching principle is: treat the underlying cause, not just the symptom. But in practice you often need to provide symptomatic relief while working up the cause — and for many conditions (e.g. primary dysmenorrhoea, BV, candidiasis) the management IS the treatment. I'll organise this by clinical scenario, explain the pharmacology from first principles, and give you clear indications and contraindications for every modality.
Every patient with menstrual/vaginal complaints needs management structured across four tiers:
- Emergency stabilisation (if haemodynamically unstable — e.g. ruptured ectopic, massive HMB with shock)
- Treat the underlying cause (definitive — e.g. excise polyp, treat PID with antibiotics, remove fibroid)
- Symptomatic / medical management (hormonal therapy for AUB, analgesia for dysmenorrhoea, antifungals for candidiasis)
- Prevention and follow-up (safe sex education, cervical screening, iron supplementation, contact tracing)
Before anything else: if a woman presents with haemodynamic instability (tachycardia, hypotension, pallor, cold peripheries) from a gynaecological cause, you must resuscitate.
Causes of haemorrhagic hypovolaemic shock include ruptured ectopic pregnancy, post-partum haemorrhage, uterine or vaginal haemorrhage [18]
Management of hypovolaemic shock: [18]
- High flow O₂ with BVM with reservoir
- Volume resuscitation:
- Obtain large bore IV access (14/16G at antecubital vein)
- Take blood for CBC, RFT, clotting, T/S
- Give rapid fluid challenge over 5–10 min (500 mL or 1000 mL crystalloid)
- Reassess BP/P every 5 min → repeat if not responding
- Consider Foley's catheter for UO monitoring
- Consider RBC transfusion depending on Hb if haemorrhagic shock
- Treat underlying cause: may need urgent transferral to OT
- Vasopressors and inotropes are generally unhelpful and are reserved as last resort
For ruptured ectopic pregnancy specifically: immediate surgical management (laparoscopic salpingectomy preferred) once stabilised. This is a surgical emergency — do not delay for further investigations if the clinical picture is clear.
4. Management of Abnormal Uterine Bleeding (AUB)
This is the largest section because AUB is so common and encompasses many conditions.
The key principle: medical therapy is first-line for HMB without structural pathology (or with small intramural fibroids that don't distort the cavity). Choose based on whether the patient desires contraception.
| Agent | Mechanism of Action | Indication | Contraindications | Key Points |
|---|---|---|---|---|
| LNG-IUS (Mirena) — levonorgestrel-releasing intrauterine system | Releases levonorgestrel locally → profound endometrial suppression (thin, decidualised, atrophic endometrium) → markedly ↓menstrual blood loss (~96% reduction by 12 months). Also provides contraception. | First-line for HMB (NICE). Suitable whether or not contraception desired. Effective for 5 years (8 years per updated licence). | Distorted uterine cavity (submucosal fibroids distorting cavity, Müllerian anomalies), current PID, unexplained PV bleeding (until investigated), pregnancy, cervical/endometrial cancer. | Why it's first-line: most effective medical treatment, avoids systemic side effects, provides contraception, reduces dysmenorrhoea. Breakthrough bleeding is common in first 3–6 months → counsel patient. |
| Tranexamic acid | Antifibrinolytic — inhibits plasminogen activation → ↓fibrinolysis at the endometrial surface → allows clots to persist → ↓bleeding. Remember: HMB partly results from excess endometrial fibrinolysis (tissue plasminogen activator). Tranexamic acid counteracts this. | HMB (acute and chronic). Taken only during menstruation (1g TDS–QDS for up to 4 days). Can be combined with other agents. | Active thromboembolic disease, history of VTE (relative — use with caution), renal impairment (dose adjust). Commonly stated but evidence for VTE risk is weak. | Non-hormonal → good for women wanting to conceive. Reduces blood loss by ~40–50%. |
| NSAIDs (mefenamic acid, ibuprofen, naproxen) | Inhibit cyclooxygenase → ↓prostaglandin synthesis (especially PGF₂α and PGE₂). In the endometrium, prostaglandins mediate vasoconstriction, myometrial contraction, and inflammation. Excess PGE₂ promotes vasodilation → ↑bleeding; NSAIDs shift the balance towards vasoconstriction → ↓bleeding. Also ↓dysmenorrhoea. | HMB + dysmenorrhoea. Taken during menstruation. Particularly useful when dysmenorrhoea coexists. | PUD, aspirin-sensitive asthma, renal impairment, anticoagulant use, 3rd trimester pregnancy. | Reduces blood loss by ~20–30%. Mefenamic acid (Ponstan) 500 mg TDS is commonly used. Less effective than LNG-IUS or tranexamic acid but dual benefit for pain. |
| Combined oral contraceptive pill (COCP) | Exogenous oestrogen + progesterone → suppresses HPO axis → thin, stable endometrium → regular, lighter withdrawal bleeds. Downregulates HPG axis → ↓ovarian androgen secretion [19]. | HMB, especially in younger women desiring contraception. Also used for dysmenorrhoea, endometriosis, PCOS (cycle regulation + anti-androgen effect). | Must be balanced against risks: ↑CVS risk, ↑VTE, ↑CA breast, ↑CA cervix [19]. Absolute C/I: active/past VTE, known thrombophilia, migraine with aura, uncontrolled HTN, breast cancer, smoker > 35y, hepatic disease. | Reduces blood loss by ~40%. Extended or continuous cycling (skipping placebo week) can be used to ↓frequency of withdrawal bleeds. |
| Oral progestogens (norethisterone, medroxyprogesterone acetate) | Progesterone stabilises the endometrium → prevents irregular shedding in anovulatory cycles. In luteal-phase dosing: supports secretory transformation. In long-course dosing (day 5–26): suppresses endometrium. | Anovulatory HMB (e.g. perimenopause, PCOS). Acute HMB (norethisterone 5 mg TDS to stop acute bleeding, then taper). Also for endometrial hyperplasia without atypia. | Liver disease, active VTE, breast cancer, undiagnosed PV bleeding. | Short luteal-phase dosing (day 15–26 only) is LESS effective than LNG-IUS or tranexamic acid. Long-course (day 5–26) is more effective but more side effects (bloating, mood changes, breakthrough bleeding). |
| Injectable progestogen (DMPA — depot medroxyprogesterone acetate) | IM injection Q12 weeks → suppresses ovulation + thins endometrium → many women become amenorrhoeic. | HMB, contraception, endometriosis. | Same as oral progestogens. Additional concern: reversible ↓bone mineral density with prolonged use (> 2 years — review need). | Often used when compliance with oral medications is difficult. |
| GnRH agonists (goserelin, leuprolide) | Initially stimulate, then downregulate GnRH receptors → pituitary desensitisation → ↓FSH/LH → "medical menopause" → ↓oestrogen → endometrial atrophy. | Pre-operative shrinkage of fibroids, severe HMB as bridge to surgery, endometriosis. Usually max 6 months without add-back HRT. | Osteoporosis (prolonged use), pregnancy. | Not for long-term use alone (bone loss, menopausal symptoms). Add-back therapy (low-dose oestrogen + progestogen) required if used > 6 months to protect bone. |
| GnRH antagonists (elagolix, relugolix, linzagolix) | Competitively block GnRH receptors → immediate dose-dependent suppression of FSH/LH → ↓oestrogen. Oral administration. Partial suppression possible (avoids full menopausal state). | Fibroids (relugolix combination tablet approved), endometriosis (elagolix). Newer agents — increasingly used. | Osteoporosis risk with full-dose long-term use, pregnancy. | Advantage over GnRH agonists: no initial flare, oral route, dose-titratable partial suppression. |
Unopposed oestrogen is dangerous in women without hysterectomy as it can ↑risk of CA endometrium [20]. This is why we ALWAYS give progesterone alongside oestrogen in HRT or hormonal management of AUB in women with an intact uterus.
Why LNG-IUS First and Not COCP?
The LNG-IUS delivers progesterone locally to the endometrium with minimal systemic absorption → fewer systemic side effects (no VTE risk increase, no effect on BP). It reduces menstrual blood loss by ~96% vs ~40% for COCP. It also provides highly effective contraception (> 99%). The only downside: initial irregular bleeding for 3–6 months, and it requires insertion. But overall it outperforms every other medical option for HMB.
When a patient presents with acute, heavy ongoing menstrual bleeding (soaking through pads, Hb dropping):
| Step | Action | Rationale |
|---|---|---|
| 1 | Assess haemodynamic stability | If shocked → resuscitate as per hypovolaemic shock protocol [18] |
| 2 | IV tranexamic acid (1g IV slowly) if severe | Immediate antifibrinolytic effect |
| 3 | High-dose oral norethisterone (5 mg TDS) OR high-dose IV conjugated oestrogen (25 mg IV Q4–6H for 24h, then switch to oral progestogen) | Progestogen stabilises the endometrium. IV oestrogen rapidly promotes endometrial proliferation and stabilisation in severely denuded endometrium |
| 4 | COCP (monophasic pill, one tablet TDS for 7 days, then taper to one daily) | Alternative to norethisterone — "medical curettage" effect |
| 5 | Iron replacement + check coagulation | Treat/prevent IDA. Exclude coagulopathy (vWD, thrombocytopenia) |
| 6 | If unresponsive to medical therapy → surgical intervention (intrauterine balloon tamponade, D&C, emergency hysteroscopy, or hysterectomy if life-threatening) | Mechanical haemostasis or definitive surgery |
| Condition | Surgical Options | Indications | Key Points |
|---|---|---|---|
| Endometrial polyp | Hysteroscopic polypectomy (first-line) | Symptomatic polyps (AUB, IMB), large polyps, postmenopausal polyps (↑cancer risk) | Outpatient or day-case procedure. Send specimen for histology always. |
| Submucosal fibroid | Hysteroscopic myomectomy (FIGO types 0–2) | Symptomatic submucosal fibroids causing HMB or infertility | Can be done via resectoscope. Fibroid must protrude ≥ 50% into cavity for hysteroscopic approach. |
| Intramural / subserosal fibroid | Laparoscopic / open myomectomy | HMB, pressure symptoms, infertility. Wants to preserve uterus | Uterine scar → risk of uterine rupture in future pregnancy if myometrium breached |
| Uterine artery embolisation (UAE) | Interventional radiology — particulate embolisation of uterine arteries → fibroid ischaemia → shrinkage | Clinical indication for transcatheter embolisation: uterine fibroid embolisation [21] | Not suitable if future pregnancy desired (↑miscarriage risk). Also used for post-partum haemorrhage [21]. Advantage: uterus-sparing, minimally invasive. |
| Endometrial ablation | Destruction of endometrial lining (thermal balloon, radiofrequency, microwave, laser, resectoscopic) | HMB refractory to medical therapy, completed family, no desire for hysterectomy | Must ensure no endometrial cancer before performing. Contraception still required (pregnancy after ablation is dangerous). Not suitable if uterus > 10-week size. |
| Hysterectomy | Removal of uterus (total = including cervix; subtotal = retaining cervix). Routes: vaginal, laparoscopic, abdominal | Definitive treatment for HMB refractory to all other Mx, large fibroids, adenomyosis, endometrial hyperplasia with atypia (if childbearing complete), endometrial cancer | Only treatment that guarantees amenorrhoea. Major surgery with risks: VTE, infection, bladder/bowel injury, vaginal vault prolapse. Ovaries can be conserved in premenopausal women if no ovarian pathology. |
| Adenomyosis | LNG-IUS (first-line medical), GnRH agonists/antagonists (bridge). Hysterectomy is definitive. Conservative surgery (adenomyomectomy) is technically difficult. | Symptomatic adenomyosis | Adenomyosis is diffuse → you can't "excise" it like a fibroid. Hysterectomy is the only cure. |
| Scenario | Management |
|---|---|
| ET ≤ 4 mm, single episode | Reassure, safety-net ("return if recurrent"). Consider topical vaginal oestrogen if atrophic vaginitis. |
| ET > 4 mm or recurrent PMB | Endometrial biopsy (Pipelle or hysteroscopy-guided). If hyperplasia without atypia → oral progestogen (medroxyprogesterone acetate or LNG-IUS) + surveillance. If hyperplasia WITH atypia → hysterectomy (risk of concurrent/progression to cancer ~30%). If endometrial cancer → refer to gynaecological oncology (staging, surgery ± adjuvant therapy). |
| Cervical cause found on speculum | Cervical polyp → polypectomy + histology. Cervical cancer → refer to oncology. |
| Atrophic vaginitis | Topical vaginal oestrogen (estriol cream or pessary). Very effective, minimal systemic absorption. |
5. Management of Dysmenorrhoea
Remember: primary dysmenorrhoea is caused by excess prostaglandins (PGF₂α) from secretory endometrium → myometrial hypercontractility → ischaemia → pain. Treatment targets this mechanism directly.
| Line | Treatment | Mechanism | Notes |
|---|---|---|---|
| 1st line | NSAIDs (ibuprofen 400 mg TDS, mefenamic acid 500 mg TDS, naproxen 250–500 mg BD) | Inhibit COX → ↓PGF₂α + PGE₂ synthesis → ↓myometrial contraction + ↓ischaemia | Start at onset of menses (or 1–2 days before if predictable). Take for 2–3 days. Most effective if started early. |
| 2nd line | COCP (any combined pill) or LNG-IUS | Suppresses ovulation → thin endometrium → ↓prostaglandin production. Also ↓amount of endometrium available to produce prostaglandins. | Good for women who also want contraception. Extended cycling (continuous COCP without breaks) can eliminate menstruation entirely. |
| Adjuncts | Heat therapy (hot water bottle), exercise, TENS, dietary supplements (vitamin B1, magnesium, omega-3) | Heat → local vasodilation + muscle relaxation. Exercise → ↑endorphins. TENS → gate control theory of pain modulation. | Evidence moderate but low risk. |
Treat the underlying cause:
| Cause | Management |
|---|---|
| Endometriosis | Medical: COCP (continuous cycling), progestogens (norethisterone, dienogest, DMPA), LNG-IUS, GnRH agonists/antagonists. Surgical: laparoscopic excision/ablation of endometriotic implants, cystectomy for endometriomas. Pain management: NSAIDs + neuropathic pain agents (amitriptyline, gabapentin) for chronic pain. |
| Adenomyosis | LNG-IUS (first-line), GnRH agonists (short-term). Hysterectomy if refractory and family complete. |
| PID | Antibiotics (see Section 6). |
| Cervical stenosis | Cervical dilatation. |
| Fibroids | As per Section 4C. |
6. Management of Vaginal Discharge / Vulvovaginitis / Cervicitis
| Aspect | Detail |
|---|---|
| 1st line | Metronidazole 400 mg BD × 5–7 days (oral) OR Metronidazole 0.75% gel intravaginally × 5 days |
| Alternative | Clindamycin 300 mg BD × 7 days (oral) OR Clindamycin 2% cream intravaginally × 7 days |
| Partner treatment | NOT required (BV is not an STI) |
| Pregnancy | Oral metronidazole preferred (avoid high single-dose regimen). Intravaginal clindamycin in first trimester as alternative. |
| Recurrent BV | Maintenance: metronidazole gel twice weekly × 4–6 months. Consider vaginal probiotics (Lactobacillus). |
| Why metronidazole? | "Metro" = metra (uterus) is a coincidence — actually named after its nitro-imidazole structure. It is selectively toxic to anaerobes: anaerobic bacteria reduce the nitro group → cytotoxic intermediates that damage DNA. Aerobic organisms cannot reduce it → spared. BV is an anaerobic overgrowth → metronidazole is targeted therapy. |
| C/I | Avoid alcohol during treatment and for 48h after (disulfiram-like reaction: inhibits aldehyde dehydrogenase → acetaldehyde accumulates → nausea, flushing, vomiting). |
| Aspect | Detail |
|---|---|
| Uncomplicated (occasional, mild-moderate, C. albicans, immunocompetent) | Topical intravaginal azole: clotrimazole 500 mg pessary stat (or 200 mg × 3 nights, or 1% cream × 7 days). OR Oral fluconazole 150 mg PO stat. Both equally effective. |
| Complicated (recurrent ≥ 4/year, severe, non-albicans, immunocompromised, pregnancy) | Longer course: fluconazole 150 mg day 1 and day 4 (or topical × 7–14 days). For recurrent: fluconazole 150 mg weekly × 6 months (maintenance). Non-albicans (C. glabrata): intravaginal boric acid 600 mg daily × 14 days or topical nystatin. |
| Pregnancy | Topical azoles only (clotrimazole, miconazole). Oral fluconazole is CONTRAINDICATED in pregnancy (teratogenic — craniofacial and cardiac defects in high-dose animal studies, FDA Category D). |
| Partner treatment | Usually NOT required unless male partner has symptomatic balanitis. |
| Why azoles work | Azoles ("conazoles") inhibit lanosterol 14α-demethylase (CYP51), a fungal cytochrome P450 enzyme → blocks synthesis of ergosterol (the fungal equivalent of cholesterol in cell membranes) → membrane integrity compromised → fungal cell death. Human cell membranes use cholesterol, not ergosterol → selectivity. |
| Aspect | Detail |
|---|---|
| 1st line | Metronidazole 400 mg BD × 5–7 days (oral) OR Metronidazole 2 g PO stat (single dose — lower cure rate ~85% vs ~95% for 7-day course) |
| Alternative | Tinidazole 2 g PO stat |
| Partner treatment | MANDATORY — T. vaginalis is a sexually transmitted pathogen. Treat all sexual partners simultaneously to prevent "ping-pong infection" (infected partner remains asymptomatic, especially female, and untreated → re-infect the patient after recovery [22]). |
| Pregnancy | Metronidazole is considered safe in pregnancy (no evidence of teratogenicity despite old concerns). Treat symptomatic trichomoniasis. |
| Test of cure | Not routinely required unless symptoms persist. If persistent → consider metronidazole resistance → higher-dose or longer-course metronidazole, or tinidazole. |
| Aspect | Detail |
|---|---|
| 1st line | Doxycycline 100 mg BD × 7 days [22] |
| Alternative | Azithromycin 1 g PO stat [22] (previously first-line; now demoted because studies show doxycycline is more effective, especially for rectal Chlamydia) |
| Pregnancy | Azithromycin 1 g PO stat (doxycycline is CONTRAINDICATED in pregnancy — tetracyclines deposit in developing teeth and bones → dental discolouration and impaired bone growth) |
| Partner treatment / contact tracing | Essential. Test and treat all partners from preceding 60 days. Principles of STI management: secure follow-up for test of cure (treatment failure can be due to non-compliance or re-infection), health education on safe sex, advise cervical cancer screening for females, contact tracing [22] |
| Follow-up | Test of cure at 3–4 weeks (NAAT may remain positive for weeks post-treatment due to dead organisms → re-test by NAAT ≥ 3 weeks post-treatment). Re-test for re-infection at 3 months. |
| Aspect | Detail |
|---|---|
| 1st line | IM ceftriaxone 500 mg stat (updated from 250 mg in older guidelines, reflecting rising MIC values) [22]. Plus doxycycline 100 mg BD × 7 days (to cover likely co-infection with Chlamydia). |
| Alternative | Spectinomycin 2 g IM stat [22] (if cephalosporin allergy — but not effective for pharyngeal gonorrhoea). Gentamicin 240 mg IM + azithromycin 2 g PO as another alternative. |
| Why ceftriaxone? | N. gonorrhoeae has developed resistance to virtually every antibiotic ever used — penicillin, tetracycline, fluoroquinolones. Third-generation cephalosporins (ceftriaxone) are one of the last reliable agents. IM route ensures adequate single-dose bactericidal levels. |
| Partner treatment | Mandatory — as per Chlamydia principles. |
| Test of cure | Recommended at 2 weeks post-treatment (culture, or NAAT ≥ 2 weeks post-Rx). |
| Complications of untreated gonorrhoea in females: | PID, Fitz-Hugh-Curtis syndrome, peritonitis, bartholinitis, infertility, ectopic pregnancy, prematurity, PROM, chorioamnionitis, septic abortion, post-abortal PID [22] |
Always Treat Both!
When you find one STI, always test for the other common STIs (Chlamydia, gonorrhoea, syphilis, HIV, hepatitis B). Co-infection is common. The standard practice when treating gonorrhoea is to add doxycycline to cover presumptive Chlamydia co-infection even before results return [22].
Treatment: [23]
- Topical acyclovir is NOT effective!
- Primary infection:
- Acyclovir 200 mg orally 5 times daily (or 400 mg TID) for 7–10 days; or
- Famciclovir 250 mg orally TID for 7–10 days; or
- Valaciclovir 1 g orally BID for 7–10 days
- Episodic treatment:
- Acyclovir 800 mg TID for 2 days / 400 mg TID for 5 days
- Famciclovir 1000 mg BID for 1 day / 125 mg BID for 5 days
- Valaciclovir 500 mg BID for 3 days / 500 mg BID for 5 days
- Prophylaxis for recurrence if > 6 significant relapses per year
- Acyclovir 400 mg BID
- Famciclovir 250 mg BID
- Valaciclovir 0.5–1 g orally once daily
Why acyclovir? Acyclovir is a guanosine analogue. It requires viral thymidine kinase (found in HSV-infected cells but not uninfected human cells) to be phosphorylated to its active triphosphate form → then incorporated into viral DNA by viral DNA polymerase → chain termination. This selectivity for virally-infected cells gives it a high therapeutic index.
| Aspect | Detail |
|---|---|
| 1st line | Topical vaginal oestrogen: estriol cream (Ovestin) or oestradiol pessary/ring. Applied nightly for 2 weeks then twice weekly maintenance. |
| Why topical oestrogen works | Restores oestrogen to vaginal epithelium → ↑glycogen → ↑Lactobacilli → ↓pH → restores natural defence. Also ↑epithelial thickness, ↑vascularity, ↑lubrication. |
| Systemic absorption | Minimal with low-dose topical preparations → generally safe even in breast cancer survivors (controversial — discuss with oncologist). No need for endometrial protection with progestogen if using low-dose topical vaginal oestrogen. |
| Non-hormonal alternatives | Vaginal moisturisers (e.g. Replens) applied regularly, lubricants during intercourse. Ospemifene (selective oestrogen receptor modulator) orally — alternative if topical not tolerated. |
| Additional role | Topical oestrogen for postmenopausal women: ↓75% incidence of recurrent cystitis in RCTs [24] — relevant when recurrent UTI coexists with atrophic vaginitis. |
| Condition | Management |
|---|---|
| Cervical polyp [1] | Avulsion (twisting off at base) in clinic or hysteroscopic polypectomy. Always send for histology. |
| Bartholin's cyst / abscess | Cyst: observation if small and asymptomatic. Abscess: incision and drainage + Word catheter insertion (keeps tract open for 4–6 weeks to allow marsupialisation). Recurrent: marsupialisation (surgical creation of permanent opening). |
| Cervical ectropion | Reassurance (physiological). If symptomatic (persistent discharge, PCB): cryotherapy, electrocautery, or silver nitrate ablation. |
| Foreign body (retained tampon) | Remove under direct vision during speculum examination. Course of metronidazole if secondary infection. |
| Chemical / contact vaginitis | Remove irritant (soaps, deodorants, pessaries, douches) [1]. Emollient, barrier cream. Consider latex allergy (e.g. condoms) [1] → switch to non-latex alternatives. |
| Threadworms | Mebendazole 100 mg stat (repeat in 2 weeks). Treat entire household. Hygiene measures. |
Treat the underlying cause:
| Cause | Management |
|---|---|
| PCOS | Lifestyle (weight loss ↓insulin resistance → can restore ovulation), COCP (cycle regulation + anti-androgen), metformin (↓insulin resistance → may restore ovulation). If fertility desired: letrozole (first-line ovulation induction) or clomifene. Spironolactone: potent anti-androgen activity (↓testosterone production, AR antagonist) — limited to female due to risk of gynaecomastia in males; S/E: diuresis, menstrual irregularities, hyperK [19] |
| Hypothalamic amenorrhoea | Address underlying cause (restore weight, ↓exercise, stress management). If prolonged hypo-oestrogenism → HRT to protect bone. If fertility desired: pulsatile GnRH or gonadotropin therapy. |
| Hyperprolactinaemia | If drug-induced: switch/stop causative drug. If prolactinoma: dopamine agonist (cabergoline or bromocriptine) — shrinks tumour + normalises prolactin → restores ovulation. |
| Premature ovarian insufficiency (POI) | HRT (oestrogen + progesterone) until average age of menopause (~51y) — essential to protect bone, cardiovascular health, and neurocognition. Gonadotropin deficiency in F: oestrogen ± progestogen in the form of COCP. Gonadotropins for ovulation induction (HMG, hCG, recombinant FSH/LH) [20] |
| Thyroid disease | Levothyroxine for hypothyroidism, antithyroid drugs / RAI / surgery for hyperthyroidism. |
| Asherman syndrome | Hysteroscopic adhesiolysis (lysis of intrauterine adhesions) + post-operative oestrogen therapy to promote endometrial regrowth + IUD placement to prevent re-adhesion. |
| Condition | Management |
|---|---|
| Ectopic pregnancy | Expectant: if β-hCG < 1500, declining, asymptomatic, able to follow up closely. Medical: methotrexate IM (single or multi-dose) — inhibits dihydrofolate reductase → ↓DNA synthesis → destroys rapidly dividing trophoblast. Criteria: haemodynamically stable, β-hCG < 5000 (ideally < 3000), unruptured ectopic < 3.5 cm, no fetal heartbeat. Surgical: laparoscopic salpingectomy (preferred if completed family or tubal damage) or salpingotomy (if wants to preserve tube). Emergency laparotomy if ruptured + haemodynamic instability. |
| Ovarian torsion | Surgical emergency — laparoscopic detorsion (untwist the ovary). Ovarian viability often recovers even if cyanotic. Oophorectomy only if clearly necrotic or postmenopausal. |
| Ruptured ovarian cyst | Usually self-limiting — supportive care (analgesia, observation, serial Hb). Surgery if haemodynamically unstable or ongoing bleeding. |
| PID | Key investigations: FBE/ESR/CRP, Urine MC, Chlamydia PCR [1]. Empirical antibiotics — must cover Chlamydia, gonorrhoea, AND anaerobes. Outpatient (mild-moderate): IM ceftriaxone 500 mg stat + doxycycline 100 mg BD × 14 days + metronidazole 400 mg BD × 14 days. Inpatient (severe, TOA, pregnancy, failed outpatient): IV ceftriaxone + IV metronidazole → switch to oral when improved. TOA not responding to antibiotics: ultrasound-guided drainage or surgical drainage. |
| Miscarriage (incomplete) | Expectant (if stable, can wait for spontaneous passage), medical (misoprostol PV/PO to promote uterine evacuation), surgical (suction evacuation / D&C) — especially if heavy bleeding, infection, or failed expectant/medical management. |
Management of recurrent cystitis: [24]
- Behavioural changes:
- Avoid use of spermicides and diaphragms → use alternative methods
- Observe personal hygiene → wipe from front to back after voiding
- Post-coital voiding
- Hydration to maintain adequate urine output → aim 2–3 L/day fluid intake
- Topical oestrogen for postmenopausal women: ↓75% incidence of recurrent cystitis in RCTs
- Antimicrobial prophylaxis in selected cases:
- Indication: recurrent UTI-specific symptoms persisting despite non-Rx measures
- Continuous prophylaxis if no temporal relation to sexual activity
- Postcoital prophylaxis if temporally related to sexual activity
- Regimen: usually co-trimoxazole or nitrofurantoin
General principles (FEST): [22]
- Secure Follow-up — for test of cure, re-testing at 90 days for syphilis and HIV serology
- Health Education on safe sex — proper and consistent condom use, prompt consultation after unsafe sex
- Advise cervical cancer Screening for females
- Contact Tracing — arrange screening and management for partner
- Ping-pong infection: infected partner remains asymptomatic (especially female) and untreated → re-infect the patient after recovery
- Epidemiological treatment of contacts: patient can pass a slip with a code to the partner, who can visit SHC to receive treatment [22]
Two management approaches: [22]
- Syndromic management approach → treatment based on presenting syndrome (preferred as patients are often too symptomatic to wait)
- Etiological management approach → treatment based on diagnostic tests
| Drug | Key Contraindications | Why |
|---|---|---|
| COCP | Active/past VTE, thrombophilia, migraine with aura, smoker > 35y, uncontrolled HTN, breast cancer, hepatic disease | Oestrogen → ↑hepatic clotting factor synthesis → ↑VTE risk. Oestrogen → ↑stroke risk in migraine with aura. |
| Oral fluconazole | Pregnancy (especially 1st trimester) | Teratogenic (craniofacial, cardiac defects) |
| Doxycycline | Pregnancy, children < 8y | Deposits in developing teeth/bones → permanent yellow-brown discolouration, enamel hypoplasia |
| Metronidazole | Relative: avoid alcohol during + 48h after | Disulfiram-like reaction (inhibits aldehyde dehydrogenase) |
| Methotrexate | Pregnancy (except therapeutic for ectopic), breastfeeding, immunodeficiency, hepatic/renal impairment, blood dyscrasias | Folic acid antagonist → teratogenic (neural tube defects, limb defects). Myelosuppressive. |
| Isotretinoin | MUST use contraception for female of childbearing potential. C/I in pregnancy [19] | Highly teratogenic (craniofacial, cardiac, CNS defects) |
| GnRH agonists (prolonged) | Osteoporosis, pregnancy | Hypo-oestrogenism → ↓bone mineral density |
| Spironolactone | Limited to female (gynaecomastia in males), pregnancy (anti-androgen → feminisation of male fetus) [19] | Anti-androgen effects |
| Tamoxifen | Pregnancy, concurrent anticoagulation (relative) | Oestrogenic on endometrium → ↑polyps, hyperplasia, cancer |
High Yield Summary — Management
-
LNG-IUS (Mirena) is first-line for HMB — 96% reduction in blood loss, provides contraception, ↓dysmenorrhoea. Main limitation: initial irregular bleeding for 3–6 months.
-
Tranexamic acid (antifibrinolytic) is first-line non-hormonal option for HMB — taken only during menses.
-
NSAIDs are first-line for primary dysmenorrhoea — directly target excess PGF₂α production.
-
BV: metronidazole 400 mg BD × 5–7 days. No partner treatment needed.
-
Candidiasis: topical azole or fluconazole 150 mg stat. Oral fluconazole CONTRAINDICATED in pregnancy.
-
Trichomoniasis: metronidazole + mandatory partner treatment.
-
Chlamydia: doxycycline 100 mg BD × 7 days (1st line). Gonorrhoea: IM ceftriaxone 500 mg stat + doxycycline [22].
-
PID: low threshold to treat empirically. IM ceftriaxone + doxycycline + metronidazole × 14 days.
-
Genital herpes: oral acyclovir / valaciclovir / famciclovir. Topical acyclovir is NOT effective [23].
-
PMB with ET > 4 mm → endometrial biopsy to exclude cancer.
-
Unopposed oestrogen is dangerous in women without hysterectomy [20] — always add progesterone.
-
STI management principles: Follow-up, Education, Screening (cervical), Contact Tracing [22].
-
Ruptured ectopic → resuscitate + emergency surgery. Unruptured ectopic → methotrexate (if criteria met) or surgical salpingectomy/salpingotomy.
Active Recall - Management of Menstrual/Vaginal Complaints
References
[1] Lecture slides: murtagh merge.pdf (p2 — Abdominal pain in women: key investigations; p104 — Vaginal discharge: key examination, pitfalls, masquerades) [18] Senior notes: Ryan Ho Critical Care.pdf (p21 — Management of hypovolaemic shock, causes including ruptured ectopic pregnancy) [19] Senior notes: Ryan Ho Rheumatology.pdf (p128 — COCP mechanism, risks, spironolactone anti-androgen therapy, isotretinoin C/I in pregnancy) [20] Senior notes: Ryan Ho Endocrine.pdf (p113 — Gonadotropin deficiency management, unopposed oestrogen danger, ovulation induction agents) [21] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p85 — Uterine fibroid embolisation, uterine artery embolisation for PPH) [22] Senior notes: Ryan Ho Urogenital.pdf (p243, p249 — STI management principles, gonorrhoea treatment, Chlamydia treatment, contact tracing, ping-pong infection) [23] Senior notes: Ryan Ho Urogenital.pdf (p247 — Genital herpes treatment: acyclovir, valaciclovir, famciclovir regimens, topical acyclovir ineffective) [24] Senior notes: Ryan Ho Urogenital.pdf (p126 — Recurrent cystitis management, behavioural changes, topical oestrogen, antimicrobial prophylaxis)
Complications of Menstrual and Vaginal Complaints
Complications arise either from the underlying condition itself (e.g. PID → tubal damage → infertility) or from treatment (e.g. hysterectomy → surgical complications). I'll systematically cover both, grouped by clinical scenario, always linking back to pathophysiology so you understand why each complication occurs rather than just memorising lists.
1. Complications of Abnormal Uterine Bleeding
This is the single most common systemic complication of chronic heavy menstrual bleeding.
| Aspect | Detail |
|---|---|
| Pathophysiology | Chronic menstrual blood loss → ongoing loss of iron (each mL of blood contains ~0.5 mg iron). When loss exceeds dietary absorption (~1–2 mg/day), iron stores deplete → ferritin falls → serum iron falls → transferrin rises (body "reaches" for more iron) → insufficient iron for haem synthesis → microcytic hypochromic anaemia |
| Prevalence | IDA is present in ~20% of females, especially at childbearing age [3]. HMB is the commonest cause of IDA in premenopausal women. |
| Clinical features | Fatigue, pallor, exertional dyspnoea, palpitations, dizziness, pica (craving ice or soil), koilonychia (spoon nails), glossitis, angular cheilitis |
| Diagnosis | ↓Hb, ↓MCV, ↓ferritin (< 30 μg/L is diagnostic; < 15 confirms depletion), ↓serum iron, ↑TIBC, ↓transferrin saturation |
| Management | Oral iron (ferrous sulphate 200 mg BD–TDS, contains ~65 mg elemental iron per tablet) for ≥ 3 months beyond normalisation of Hb to replenish stores. IV iron (ferric carboxymaltose) if oral intolerant, severe anaemia, or rapid correction needed. Crucially: treat the underlying cause of HMB simultaneously. |
| Why it matters | Anaemia impairs quality of life, work productivity, exercise tolerance, and cognition. Severe anaemia can precipitate high-output cardiac failure. In pregnancy, untreated IDA ↑risk of preterm delivery and low birth weight. |
Exam Pearl
Menorrhagia (HMB) is the commonest cause of iron deficiency anaemia in premenopausal women. Conversely, if a premenopausal woman presents with IDA, always ask about her periods — HMB is the answer until proven otherwise [3].
| Aspect | Detail |
|---|---|
| Pathophysiology | Chronic anovulation → unopposed oestrogen → continuous endometrial proliferation without progesterone-induced secretory transformation or shedding → progressive endometrial hyperplasia → if undetected, can progress to atypical hyperplasia → endometrial carcinoma (risk ~30% for atypical hyperplasia). |
| At-risk populations | PCOS, obesity (peripheral aromatisation), perimenopausal anovulation, tamoxifen use, oestrogen-secreting tumours |
| Prevention | Regular progestogen opposition (LNG-IUS, cyclical progestogens, COCP) in any woman with chronic anovulation to prevent endometrial hyperplasia |
| Why this complication is important | Endometrial cancer incidence is rising in HK and globally, driven largely by the obesity epidemic and metabolic syndrome [4] |
This is under-recognised but extremely real:
- Chronic HMB or unpredictable bleeding → social embarrassment, activity restriction, missed work/school
- Chronic pelvic pain (endometriosis, adenomyosis) → depression, anxiety, relationship strain
- Masquerades checklist: Depression [1] — always consider depression as a coexisting condition (and sometimes a masquerading cause for the complaint itself)
- "Is the patient trying to tell me something?" — Can be very relevant. Consider various problems and sexual dysfunction [1]
- Rare but life-threatening, especially with ruptured ectopic pregnancy, massive fibroid haemorrhage, or coagulopathy
- Causes of haemorrhagic hypovolaemic shock include ruptured ectopic pregnancy, post-partum haemorrhage, uterine or vaginal haemorrhage, spontaneous haemorrhage due to bleeding diathesis [18]
- Clinical features: ↑sympathetic outflow → vasoconstriction → pallor, peripheral cyanosis, cold extremities, delayed capillary refill, empty peripheral veins, tachycardia, sweating [18]
2. Complications of Specific Menstrual Conditions
| Complication | Pathophysiology | Clinical Presentation |
|---|---|---|
| Anaemia (from chronic HMB) | Submucosal fibroids → ↑endometrial surface area + fragile vasculature → chronic blood loss | Fatigue, pallor, microcytic anaemia |
| Pressure effects | Large fibroids compress adjacent organs | Urinary frequency/retention (anterior fibroid compresses bladder), constipation (posterior fibroid compresses rectum), ureteric obstruction → hydronephrosis (lateral cervical fibroids) |
| Degeneration | Fibroid outgrows blood supply → ischaemic necrosis. Types: hyaline (commonest, asymptomatic), red/carneous (pregnancy — acute pain), cystic, calcific (postmenopausal) | Acute pelvic pain, tenderness over fibroid, low-grade fever |
| Torsion | Pedunculated subserosal fibroid twists on its stalk → vascular compromise | Acute abdominal pain, mimics ovarian torsion |
| Infertility | Submucosal fibroids distort cavity → impaired implantation. Large intramural fibroids may compress tubal ostia | Subfertility, recurrent miscarriage |
| Pregnancy complications | Fibroids are oestrogen/progesterone-responsive → grow during pregnancy | Miscarriage, preterm labour, malpresentation (fibroid occupies pelvis → breech), obstructed labour, postpartum haemorrhage (impaired myometrial contraction) |
| Malignant transformation | Leiomyosarcoma — extremely rare (< 0.5% of fibroids). Controversial whether it arises from pre-existing fibroids or de novo | Rapid growth (especially postmenopausal), pain. Suspect if fibroid grows after menopause. |
| Complication | Pathophysiology |
|---|---|
| Infertility | Adhesions distort tubal-ovarian anatomy → impaired ovum pick-up. Endometriomas damage ovarian tissue. Peritoneal inflammation creates hostile environment for sperm/embryo. Altered endometrial receptivity. Present in 25–50% of infertile women. |
| Chronic pelvic pain | Cyclical inflammation, fibrosis, nerve infiltration by deep endometriotic nodules → central sensitisation → pain becomes chronic and neuropathic |
| Ovarian endometrioma ("chocolate cyst") | Ectopic endometrial tissue on ovary → cyclical bleeding within cyst → accumulation of old blood (dark brown = "chocolate") → progressive enlargement. Risk of rupture (chemical peritonitis from spillage of cyst contents). Risk of malignant transformation (endometrioid or clear cell ovarian carcinoma — rare but recognised, ~1%) |
| Adhesions | Chronic inflammation → fibrosis → organs become adherent (e.g. ovary stuck to pelvic sidewall, bowel adherent to uterus, obliterated Pouch of Douglas) → pain, bowel/ureteric obstruction |
| Fistula formation | Deep infiltrating endometriosis can penetrate bowel wall, bladder, or vagina. Enterovaginal fistula → passage of gas or faeces through vagina [25]. Rare but documented. |
| Bladder/ureteric involvement | Endometriotic implants on bladder → cyclical haematuria (catamenial haematuria). Ureteric involvement → obstruction → hydronephrosis |
| Complication | Pathophysiology |
|---|---|
| Progressive dysmenorrhoea | Intramyometrial endometrial tissue swells cyclically → worsening pain with each cycle |
| HMB + IDA | Enlarged uterus + impaired myometrial contraction → chronic heavy bleeding |
| Infertility | Altered junctional zone contractility → impaired implantation. Often coexists with endometriosis. |
PCOS is far more than a menstrual complaint — its complications are metabolic, reproductive, and psychological:
| Complication | Pathophysiology |
|---|---|
| Endometrial hyperplasia / carcinoma | Chronic anovulation → unopposed oestrogen (as above). Risk 2–6× increased. |
| Type 2 diabetes mellitus | Insulin resistance → hyperinsulinaemia → eventual β-cell failure → T2DM. PCOS is a manifestation of metabolic syndrome [4] |
| Dyslipidaemia | Insulin resistance → ↑hepatic VLDL production → ↑TG, ↓HDL-C, ↑LDL-C [4] |
| Cardiovascular disease | Clustering of risk factors: obesity, HTN, dyslipidaemia, insulin resistance, chronic inflammation |
| Non-alcoholic fatty liver disease | Manifestation of metabolic syndrome [4] |
| Infertility | Anovulation → inability to conceive. PCOS is the commonest cause of anovulatory infertility. |
| Obstructive sleep apnoea | Obesity + possible androgen effects on upper airway → OSA. Prevalence markedly ↑ in PCOS. |
| Psychological | Depression, anxiety, poor self-esteem (related to hirsutism, acne, obesity, infertility) |
| Pregnancy complications | If conception achieved (often with ovulation induction): ↑risk of gestational DM, pre-eclampsia, preterm delivery, C-section |
3. Complications of Vaginal/Cervical Infections
PID is the single most important complication of untreated cervicitis (Chlamydia, gonorrhoea). Its complications are devastating and often irreversible.
| Complication | Pathophysiology | Clinical Significance |
|---|---|---|
| Tubal factor infertility | Salpingitis → tubal mucosal damage → fibrosis → tubal occlusion or impaired ciliary function → ova cannot be transported → infertility. Risk: ~10% after 1 episode, ~25% after 2, ~50% after 3 episodes. | Most feared long-term complication. Often "silent" PID (subclinical Chlamydia) causes damage without the patient ever knowing she had PID. |
| Ectopic pregnancy | Tubal damage impairs transport of fertilised ovum → implantation occurs in damaged tube → ectopic pregnancy. Risk ↑6–10× after PID. | Ectopic pregnancy remains a potentially lethal condition so always be "ectopic minded" [1] |
| Tubo-ovarian abscess (TOA) | Extension of infection → walled-off collection of pus involving tube, ovary, and adjacent structures | Persistent fever despite antibiotics, palpable tender mass. May require drainage (USS-guided or surgical). Rupture → generalised peritonitis → sepsis → life-threatening emergency. |
| Fitz-Hugh-Curtis syndrome | Perihepatitis — infection spreads along paracolic gutters or via lymphatics/haematogenous route → inflammation of liver capsule (Glisson's capsule) → "violin string" adhesions between liver surface and anterior abdominal wall [22] | RUQ pain mimicking cholecystitis or biliary colic. Can be missed if PID not considered. Elevated LFTs sometimes present. |
| Chronic pelvic pain | Post-inflammatory adhesions → traction on pelvic organs → chronic intermittent pain. Altered pain processing (central sensitisation). | Present in ~18% of women post-PID |
| Peritonitis | Spread of infection beyond adnexa [22] | Generalised abdominal tenderness, guarding, rigidity — surgical emergency |
| Obstetric complications | Ectopic pregnancy, prematurity, premature rupture of membranes, chorioamnionitis, septic abortion, post-abortal PID [22] | Underscores the importance of pre-conception STI screening |
Why Chlamydia Screening Matters So Much
Chlamydia is often completely asymptomatic (up to 70% of women) yet causes "silent" salpingitis → tubal damage → infertility and ectopic pregnancy. By the time the patient presents with infertility, the damage is done and irreversible. This is why opportunistic screening of sexually active young women is so important — Chlamydia PCR [1] catches the infection before it ascends.
Complications of untreated gonorrhoea in females: [22]
- Pelvic inflammatory disease
- Fitz-Hugh-Curtis syndrome
- Peritonitis
- Bartholinitis
- Infertility
- Obstetric complications: ectopic pregnancy, prematurity, PROM, chorioamnionitis, septic abortion, post-abortal PID
In children: [22]
- Vulvovaginitis
- Ophthalmia neonatorum (gonococcal conjunctivitis of the newborn — acquired during passage through infected birth canal → purulent discharge within days of birth → corneal ulceration → blindness if untreated. Prevented by prophylactic eye drops at birth.)
Disseminated gonococcal infection (0.5–3%): [22]
- Purulent arthritis or triad of tenosynovitis, dermatitis, polyarthralgia
- Can affect endocardium and meninges
| Complication | Pathophysiology |
|---|---|
| Recurrent episodes | HSV establishes latency in sacral dorsal root ganglia (S2–S4) → periodic reactivation triggered by stress, illness, immunosuppression, menses, UV exposure → recurrent vesicular eruptions |
| Neonatal herpes | Transmission during vaginal delivery when active lesions present → devastating neonatal infection (disseminated disease, encephalitis, skin-eye-mouth disease). Mortality up to 30% for disseminated disease. This is why patients must be educated to report HSV history to obstetricians [23]. Active primary genital herpes at time of delivery → Caesarean section recommended. |
| Urinary retention | Sacral radiculitis (HSV-induced inflammation of sacral nerve roots) → neurogenic bladder → acute urinary retention |
| Meningitis | HSV meningitis (Mollaret's meningitis if recurrent) — usually benign and self-limiting but distressing |
| Psychological impact | Significant anxiety, shame, relationship difficulties — often disproportionate to the actual clinical severity |
| Complication | Pathophysiology |
|---|---|
| Pregnancy complications | Untreated trichomoniasis associated with preterm delivery, premature rupture of membranes, low birth weight |
| HIV acquisition | Trichomoniasis causes mucosal inflammation → breaks in epithelial barrier + recruitment of CD4+ T cells to inflamed mucosa → ↑susceptibility to HIV acquisition (estimated 1.5–2× increased risk) |
| Recurrent/persistent infection | "Ping-pong infection" if partner not treated [22] |
| Complication | Pathophysiology |
|---|---|
| Pregnancy complications | BV associated with preterm labour, PPROM, chorioamnionitis, postpartum endometritis. Anaerobic bacteria ascend → decidual inflammation → prostaglandin release → preterm contractions |
| Post-surgical infection | BV prior to gynaecological surgery (hysterectomy, D&C, termination) → ↑risk of post-operative pelvic infection. This is why some centres screen and treat BV before planned procedures |
| ↑STI acquisition | Disrupted vaginal flora → ↓protective lactobacilli → ↑susceptibility to Chlamydia, gonorrhoea, HIV |
4. Complications of Specific Treatments
| Treatment | Complications | Pathophysiology |
|---|---|---|
| COCP | VTE (DVT, PE), arterial thromboembolism (stroke, MI — especially in migraine with aura), breast cancer (small ↑risk), cervical cancer (modest ↑risk with prolonged use), hepatic adenoma (rare) | Oestrogen → ↑hepatic synthesis of clotting factors (fibrinogen, II, VII, X) → prothrombotic state. ↓antithrombin III. |
| Progestogen-only methods (DMPA) | Irregular bleeding, weight gain, ↓bone mineral density (reversible after cessation), delayed return of fertility (DMPA) | DMPA suppresses ovulation → hypo-oestrogenic state → ↓osteoblast activity → bone loss |
| GnRH agonists | Menopausal symptoms (hot flushes, night sweats, vaginal dryness, mood changes), osteoporosis (if used > 6 months without add-back therapy) | Pituitary desensitisation → ↓FSH/LH → ↓oestrogen → "medical menopause" |
| LNG-IUS | Irregular bleeding/spotting (first 3–6 months), hormonal side effects (acne, breast tenderness, mood changes — usually mild), perforation (rare, ~1/1000 insertions), expulsion (~5%) | Local progestogenic effects; mechanical complications during insertion |
| Tamoxifen | Endometrial polyps, endometrial hyperplasia, endometrial cancer (↑2–7×), VTE | Tamoxifen is anti-oestrogenic on breast but pro-oestrogenic on endometrium (partial agonist) |
| Procedure | Complications |
|---|---|
| Hysterectomy | Early: haemorrhage, infection (wound, vault, UTI), VTE, anaesthetic complications, bladder/ureteric/bowel injury (0.5–1%). Late: vaginal vault prolapse (loss of uterosacral ligament support), premature menopause (if ovaries removed — "surgical menopause" → need HRT), sexual dysfunction, psychological impact |
| Myomectomy | Haemorrhage (may require blood transfusion), infection, uterine scar → risk of uterine rupture in future pregnancy (especially if myometrium breached deeply), adhesion formation → future infertility or pain, recurrence of fibroids (~15–30% over 5 years) |
| Endometrial ablation | Failure (return of bleeding), haematometra (blood trapped behind cervical stenosis or tubal obstruction), uterine perforation (rare), pregnancy after ablation (dangerous — abnormal placentation, ectopic, miscarriage) → must use contraception |
| Hysteroscopy | Uterine perforation (0.1–1%), fluid overload (from distension media — can cause hyponatraemia, pulmonary oedema), infection, cervical laceration |
| Laparoscopy (for endometriosis, ectopic, torsion) | Port-site bleeding/hernia, visceral injury (bowel, bladder, vascular), gas embolism (very rare), shoulder-tip pain (diaphragmatic irritation from CO₂), adhesion formation |
| Uterine artery embolisation (UAE) | Post-embolisation syndrome (pain, fever, nausea — self-limiting), fibroid expulsion (if submucosal → may pass per vagina), premature ovarian failure (non-target embolisation of ovarian blood supply — ↑risk in women > 45), infection, very rarely uterine necrosis |
| Complication | Pathophysiology |
|---|---|
| Treatment failure | ~10–15% of single-dose methotrexate fails → β-hCG does not decline adequately → requires repeat dose or surgical intervention |
| Tubal rupture | Can occur even after starting methotrexate (particularly in first week as trophoblastic tissue initially swells before regressing) → patients must be counselled to present immediately with severe pain/haemodynamic instability |
| Bone marrow suppression | Methotrexate inhibits dihydrofolate reductase → ↓DNA synthesis in all rapidly dividing cells → ↓WBC, platelets, RBCs. Usually mild at doses used for ectopic. |
| Hepatotoxicity | Direct hepatotoxic effect → monitor LFTs |
| Stomatitis, GI upset | Mucositis from inhibition of rapidly dividing GI epithelial cells |
This is specifically highlighted in the lecture slides as a serious disorder not to be missed [1].
Staphylococcal toxic shock syndrome: [26]
- Cause: various exotoxins from S. aureus → acts as superantigens to activate large numbers of T cells → systemic inflammation ensues
- Classically associated with use of tampons and nasal packing for epistaxis, but ≥ 1/2 are non-menstrual related
- Clinical features develop rapidly (≤ 48h):
- Hypotension: sBP ≤ 90 mmHg due to widespread 3rd-spacing
- Skin: widespread erythematous, macular desquamating rash (sunburn-like) involving palms and soles ± mucosal involvement (eye, vaginal, oropharynx)
- Multiorgan failure
| Feature | Pathophysiology |
|---|---|
| Why tampons? | Prolonged retention of absorbent tampon → creates warm, moist, protein-rich environment ideal for S. aureus proliferation → if toxin-producing strain (TSST-1), superantigen is absorbed through vaginal mucosa → massive non-specific T-cell activation (~20% of T cells, vs < 0.01% in conventional antigen response) → cytokine storm → capillary leak, hypotension, multiorgan failure |
| Management | Remove tampon immediately. IV antistaphylococcal antibiotics (flucloxacillin/clindamycin — clindamycin specifically inhibits toxin production). Aggressive IV fluid resuscitation. ICU for organ support. |
| Prevention | Use lowest-absorbency tampon needed, change regularly (every 4–8 hours), alternate with pads |
6. Complications Relating to Vulvovaginal Conditions
While SJS/TEN is primarily a dermatological emergency, its vulvovaginal complications are frequently overlooked and highly relevant to this topic:
Vulvovaginal complications of SJS/TEN: [27]
- Acute phase: erosive/ulcerative vaginitis, vulvar bullae, urethritis (up to 2/3) ± urinary retention and genital erosions
- Long-term sequelae: labial agglutination, introital stenosis, vaginal dryness, dyspareunia, urinary retention, haematocolpos [27]
These complications occur because the vulvovaginal epithelium (mucosal surface) is involved in the same full-thickness epidermal necrosis that affects the skin → healing by secondary intention → scarring → adhesion formation → stenosis.
Sexual dysfunction is very common in women with menstrual/vaginal complaints: [28]
- Lack of sexual interest (40% prevalence in women at 6-month assessment)
- Inability of orgasm (14%)
- Pain during coitus (12%)
- Anxiety on performance (7%)
| Cause | Mechanism of Sexual Dysfunction |
|---|---|
| Chronic dyspareunia (endometriosis, atrophic vaginitis, PID sequelae) | Pain during intercourse → avoidance behaviour → ↓desire → relationship strain |
| Vaginismus | Involuntary spasm of pelvic floor muscles (often psychogenic or post-traumatic) → inability to achieve penetration |
| Vulvodynia | Chronic vulval pain syndrome of unknown aetiology → pain with touch/intercourse |
| Post-hysterectomy | Some women report altered sexual sensation (loss of uterine contractions during orgasm, cervical stimulation). Evidence mixed — many women report improved sexual function after resolution of HMB/pain. |
| Psychological | Depression, anxiety, body image issues (PCOS — hirsutism, obesity), relationship difficulties, history of sexual abuse |
"Is the patient trying to tell me something? — Needs careful consideration; possible sexual dysfunction" [1]
| Source Condition | Key Complications |
|---|---|
| Chronic HMB | Iron deficiency anaemia, ↓QoL, haemorrhagic shock (acute severe HMB) |
| Chronic anovulation | Endometrial hyperplasia, endometrial carcinoma, infertility |
| Fibroids | Anaemia, pressure symptoms, degeneration, torsion, infertility, pregnancy complications |
| Endometriosis | Infertility, chronic pain, endometrioma (rupture, malignant transformation), adhesions, fistulae |
| PCOS | T2DM, CVD, dyslipidaemia, NAFLD, endometrial cancer, infertility, OSA, depression |
| PID | Tubal infertility, ectopic pregnancy, TOA, Fitz-Hugh-Curtis, chronic pain, peritonitis |
| Gonorrhoea | PID + all its complications, disseminated infection, neonatal ophthalmia |
| Chlamydia | "Silent" PID → infertility, ectopic pregnancy |
| Genital herpes | Recurrence, neonatal herpes, urinary retention, meningitis |
| BV | Preterm labour, post-surgical infection, ↑STI susceptibility |
| Trichomoniasis | Preterm delivery, ↑HIV acquisition |
| Tampon use | Toxic shock syndrome |
| COCP | VTE, arterial thromboembolism, breast cancer, cervical cancer |
| Hysterectomy | Haemorrhage, infection, organ injury, vault prolapse, surgical menopause |
| Methotrexate (ectopic) | Treatment failure, tubal rupture, bone marrow suppression |
High Yield Summary — Complications
-
IDA is the commonest complication of chronic HMB — present in ~20% of reproductive-age women [3]. Always check Hb and ferritin.
-
Chronic anovulation → unopposed oestrogen → endometrial hyperplasia → carcinoma. This sequence is preventable with progestogen opposition.
-
PID complications are devastating and often irreversible: tubal infertility (~10% per episode), ectopic pregnancy (6–10× risk), chronic pelvic pain, TOA. Fitz-Hugh-Curtis syndrome (perihepatitis) can mimic biliary disease [22].
-
Chlamydia is the "silent" destroyer — up to 70% asymptomatic, yet causes tubal damage → infertility. Chlamydia PCR screening is essential [1].
-
Ectopic pregnancy remains a potentially lethal condition — always be "ectopic minded" [1].
-
Tampon toxic shock syndrome is a serious, life-threatening complication caused by staphylococcal superantigens [1][26].
-
Gonorrhoea complications in females: PID, Fitz-Hugh-Curtis, peritonitis, bartholinitis, infertility, obstetric complications. In children: ophthalmia neonatorum [22].
-
PCOS is a metabolic syndrome — complications extend far beyond menstrual irregularity to include T2DM, CVD, NAFLD, and endometrial cancer [4].
-
Surgical complications of hysterectomy include bladder/ureteric injury (0.5–1%), VTE, vault prolapse, and surgical menopause if ovaries removed.
-
SJS/TEN vulvovaginal sequelae: labial agglutination, introital stenosis, vaginal dryness, dyspareunia — often overlooked but cause significant long-term morbidity [27].
Active Recall - Complications of Menstrual/Vaginal Complaints
References
[1] Lecture slides: murtagh merge.pdf (p2 — Abdominal pain in women: masquerades checklist, diagnostic tips; p3 — ectopic pregnancy; p103 — Vaginal discharge: serious disorders not to be missed including TSS; p104 — masquerades checklist, sexual dysfunction) [3] Senior notes: Ryan Ho Haemtology.pdf (p17 — Iron deficiency anaemia, epidemiology in females at childbearing age) [4] Senior notes: Ryan Ho Endocrine.pdf (p77 — PCOS and metabolic syndrome; p117 — Complications of obesity including PCOS, T2DM, NAFLD) [18] Senior notes: Ryan Ho Critical Care.pdf (p21 — Management and causes of hypovolaemic shock including ruptured ectopic, uterine/vaginal haemorrhage) [22] Senior notes: Ryan Ho Urogenital.pdf (p249 — Gonorrhoea complications in females and children, Fitz-Hugh-Curtis syndrome, obstetric complications; p243 — STI management principles, ping-pong infection) [23] Senior notes: Ryan Ho Urogenital.pdf (p247 — Genital herpes complications, educate to report HSV to obstetricians) [25] Senior notes: felixlai.md (section on Crohn's disease complications — enterovaginal fistula) [26] Senior notes: Ryan Ho Rheumatology.pdf (p133 — Staphylococcal toxic shock syndrome: cause, superantigen mechanism, clinical features) [27] Senior notes: Ryan Ho Rheumatology.pdf (p149, p151 — SJS/TEN urogenital complications and long-term vulvovaginal sequelae) [28] Senior notes: Ryan Ho Psychiatry.pdf (p232 — Sexual dysfunction epidemiology and 4-phase sexual response cycle)
High Yield Summary
Menstrual/Vaginal Complaints — Key Takeaways:
-
Always exclude pregnancy (urine β-hCG) in any reproductive-age woman with abnormal bleeding or pelvic pain.
-
PALM-COEIN is the FIGO classification for AUB: Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia (structural) + Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not classified (non-structural).
-
Anovulatory bleeding = no ovulation → no progesterone → unopposed oestrogen → irregular endometrial shedding. Most common at extremes of reproductive life and in PCOS.
-
Menstruation is a progesterone-withdrawal bleed. Primary dysmenorrhoea is caused by excess PGF₂α → myometrial ischaemia → NSAIDs are first-line.
-
von Willebrand disease is present in 10–15% of women with HMB — always consider in HMB since menarche or with bleeding history.
-
Vaginal discharge: pH < 4.5 → think Candida; pH > 4.5 → think BV or Trichomoniasis. The amine/whiff test is positive in BV.
-
Normal vaginal defence depends on oestrogen → glycogen → Lactobacilli → lactic acid → low pH. Disruption at any step predisposes to infection.
-
Postmenopausal bleeding = endometrial cancer until proven otherwise (~10% of PMB is malignant).
-
Key examination: speculum (bivalve) + bimanual palpation. Key investigations: FBE/ESR/CRP, Urine MC, Chlamydia PCR, pH test, amine test.
-
Always ask: "Is the patient trying to tell me something?" — consider sexual dysfunction, domestic violence, psychosocial factors.
High Yield Summary — Differential Diagnosis
-
Probability diagnoses for vaginal discharge: physiological, BV (40–50%), candidiasis (20–30%), trichomoniasis (10–20%) [1].
-
Probability diagnoses for abdominal/pelvic pain in women: primary dysmenorrhoea, Mittelschmerz, adhesions, endometriosis [1].
-
Must-not-miss: ectopic pregnancy, cervical/endometrial cancer, PID/TOA, ovarian torsion, toxic shock syndrome [1], sexual abuse in children [1].
-
Pitfalls often missed: chemical vaginitis, retained foreign body, endometriosis (brownish discharge), ectopic pregnancy ("prune juice" discharge), pelvic congestion syndrome, misplaced IUCD, constipation [1].
-
Masquerades: diabetes, drugs, UTI, depression, spinal dysfunction (referred pain) [1].
-
Always exclude pregnancy (β-hCG) first in any reproductive-age woman.
-
pH paper is your bedside friend: < 4.5 → Candida/physiological; > 4.5 → BV/Trichomonas/atrophic/cervicitis.
-
For PID: classically sexually active female < 40y, lower abdominal pain, vaginal discharge, cervical excitation ("chandelier sign"), fever [5].
-
For appendicitis ddx in adult females: always take full gynaecological history, especially menstrual cycle, vaginal discharge and possible pregnancy [5].
-
For secondary amenorrhoea: think anatomical level — hypothalamus → pituitary → ovary → uterus/outflow — and investigate accordingly [4].
High Yield Summary — Diagnostics
-
Always urine β-hCG first in reproductive-age women — before any other investigation.
-
Vaginal discharge bedside workup: pH paper (range 4–6) + amine/whiff test [1] + wet mount + KOH prep + NAAT for Chlamydia/GC. pH < 4.5 → Candida; pH > 4.5 → BV/Trichomonas/atrophic/cervicitis.
-
BV is diagnosed by Amsel criteria (≥ 3 of 4): discharge character, pH > 4.5, positive whiff test, clue cells.
-
PID is a clinical diagnosis (CDC minimum criteria): lower abdominal tenderness + adnexal tenderness + cervical excitation tenderness. Low threshold to treat.
-
PMB investigation: TVS → endometrial thickness ≤ 4 mm → NPV > 99% for cancer. > 4 mm or recurrent → endometrial biopsy.
-
PCOS: Rotterdam criteria — ≥ 2 of 3: oligo/anovulation, clinical/biochemical hyperandrogenism, polycystic ovaries on USS (after excluding other causes).
-
Ectopic pregnancy: positive β-hCG + empty uterus on TVS + adnexal mass. Serial β-hCG with suboptimal rise confirms non-viable pregnancy.
-
vWD screening in HMB since menarche: APTT (may be normal!), vWF:Ag, vWF:Act, Factor VIII activity.
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Dysuria tip: urethritis = pain at onset of micturition; cystitis = pain at end. Suprapubic discomfort → cystitis. Unexplained dysuria → Chlamydia urethritis [17].
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Speculum + bimanual examination is essential for ALL menstrual/vaginal complaints — it is both diagnostic and guides further investigation [1][7].
High Yield Summary — Management
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LNG-IUS (Mirena) is first-line for HMB — 96% reduction in blood loss, provides contraception, ↓dysmenorrhoea. Main limitation: initial irregular bleeding for 3–6 months.
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Tranexamic acid (antifibrinolytic) is first-line non-hormonal option for HMB — taken only during menses.
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NSAIDs are first-line for primary dysmenorrhoea — directly target excess PGF₂α production.
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BV: metronidazole 400 mg BD × 5–7 days. No partner treatment needed.
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Candidiasis: topical azole or fluconazole 150 mg stat. Oral fluconazole CONTRAINDICATED in pregnancy.
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Trichomoniasis: metronidazole + mandatory partner treatment.
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Chlamydia: doxycycline 100 mg BD × 7 days (1st line). Gonorrhoea: IM ceftriaxone 500 mg stat + doxycycline [22].
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PID: low threshold to treat empirically. IM ceftriaxone + doxycycline + metronidazole × 14 days.
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Genital herpes: oral acyclovir / valaciclovir / famciclovir. Topical acyclovir is NOT effective [23].
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PMB with ET > 4 mm → endometrial biopsy to exclude cancer.
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Unopposed oestrogen is dangerous in women without hysterectomy [20] — always add progesterone.
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STI management principles: Follow-up, Education, Screening (cervical), Contact Tracing [22].
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Ruptured ectopic → resuscitate + emergency surgery. Unruptured ectopic → methotrexate (if criteria met) or surgical salpingectomy/salpingotomy.
High Yield Summary — Complications
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IDA is the commonest complication of chronic HMB — present in ~20% of reproductive-age women [3]. Always check Hb and ferritin.
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Chronic anovulation → unopposed oestrogen → endometrial hyperplasia → carcinoma. This sequence is preventable with progestogen opposition.
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PID complications are devastating and often irreversible: tubal infertility (~10% per episode), ectopic pregnancy (6–10× risk), chronic pelvic pain, TOA. Fitz-Hugh-Curtis syndrome (perihepatitis) can mimic biliary disease [22].
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Chlamydia is the "silent" destroyer — up to 70% asymptomatic, yet causes tubal damage → infertility. Chlamydia PCR screening is essential [1].
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Ectopic pregnancy remains a potentially lethal condition — always be "ectopic minded" [1].
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Tampon toxic shock syndrome is a serious, life-threatening complication caused by staphylococcal superantigens [1][26].
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Gonorrhoea complications in females: PID, Fitz-Hugh-Curtis, peritonitis, bartholinitis, infertility, obstetric complications. In children: ophthalmia neonatorum [22].
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PCOS is a metabolic syndrome — complications extend far beyond menstrual irregularity to include T2DM, CVD, NAFLD, and endometrial cancer [4].
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Surgical complications of hysterectomy include bladder/ureteric injury (0.5–1%), VTE, vault prolapse, and surgical menopause if ovaries removed.
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SJS/TEN vulvovaginal sequelae: labial agglutination, introital stenosis, vaginal dryness, dyspareunia — often overlooked but cause significant long-term morbidity [27].
Localized Lump
A localized lump is a discrete, palpable mass confined to a specific anatomical area, arising from abnormal growth or swelling of tissue such as a cyst, abscess, lipoma, or neoplasm.
Nasal Congestion, Runny Nose
Nasal congestion and runny nose (rhinorrhea) are symptoms resulting from inflammation and increased mucus production of the nasal mucosa, commonly caused by infections, allergies, or irritants.