Clinical Scenario: G3P1L1A1, 32 weeks, painless bright red PV bleeding

a. Most Probable Diagnosis

• Painless bright red vaginal bleeding (no uterine contractions, no trauma)
• Third trimester (32 weeks)
• Unprovoked — no associated abdominal pain

b. Differential Diagnoses

c. Differentiating Placenta Praevia vs. Placental Abruption (the two major differentials)

Critical rule: Never perform a digital vaginal examination in suspected placenta praevia until placental localisation has excluded it (the "double setup" is now largely abandoned in favour of ultrasound).

d. Relevant Investigations

Immediate / Emergency

• IV access + bloods stat: FBC (Hb, platelets), blood group & cross-match (minimum 2 units), coagulation screen (PT, aPTT, fibrinogen), renal and liver function, serum urea & electrolytes
• Kleihauer-Betke test (or flow cytometry): detects feto-maternal haemorrhage; guides anti-D immunoglobulin dosing in Rh-negative mothers
• Cardiotocograph (CTG): Continuous fetal monitoring to assess fetal well-being

Imaging

• Transabdominal ultrasound (first line): Localises placenta, assesses placental edge distance from internal os, fetal presentation, liquor volume, fetal biometry
• Transvaginal ultrasound (TVS — gold standard for localisation): Safe and more accurate; measures placental edge-to-os distance precisely
  • If placental edge ≤20 mm from os → significant praevia
  • If ≥20 mm from os → likely to resolve by term
• MRI: Used when placenta accreta spectrum (PAS) is suspected (anterior praevia with previous caesarean scar)
• Colour Doppler ultrasound: Assesses for vasa praevia and placenta accreta/increta/percreta

Fetal Assessment

• BPP (Biophysical Profile): Fetal tone, movement, breathing, AFI ± CTG
• Umbilical artery Doppler: If IUGR suspected

Additional

• Urinalysis + mid-stream urine: Rule out UTI (can precipitate bleeding)
• Speculum examination (only after placenta praevia excluded): To identify cervical causes — polyp, ectropion, cervicitis, carcinoma
• APT test (Ogita test): Distinguishes fetal from maternal blood if vasa praevia is suspected

e. Maternal and Fetal Complications

Maternal Complications

• Haemorrhagic shock and anaemia
• Repeated episodes of unprovoked bleeding (sentinel bleeds), each potentially more severe
• Preterm labour (iatrogenic or spontaneous)
• Placenta accreta spectrum (PAS) — particularly with anterior praevia and prior caesarean scar; risk of morbidly adherent placenta
• Operative morbidity (emergency caesarean)

• Postpartum haemorrhage (PPH) — major risk; lower uterine segment has poor contractile ability
• DIC (in severe haemorrhage)
• Hysterectomy (emergency peripartum) — especially with PAS
• Bladder and ureteric injury (surgical)
• Air embolism (rare)
• Death (rare, in uncontrolled haemorrhage)

Fetal Complications

• Preterm birth — leading cause of perinatal morbidity in placenta praevia
• IUGR (intrauterine growth restriction) — impaired placentation
• Fetal anaemia — if feto-maternal haemorrhage
• Malpresentation (oblique/transverse lie, breech) — placenta occupies lower segment, preventing engagement
• Perinatal asphyxia — from acute haemorrhage/shock
• Perinatal death — rare with good antenatal care but real in resource-limited settings
• Respiratory distress syndrome (RDS) — due to preterm delivery

Summary Box — Obstetric Pearl

In any third-trimester patient with painless, bright red, unprovoked vaginal bleeding, treat as placenta praevia until proven otherwise. Do not perform a digital PV examination. Stabilise, localise the placenta with ultrasound, monitor mother and fetus, and manage expectantly if stable and <37 weeks — or deliver if haemodynamically compromised or gestation is adequate.

Clinical Scenario: 62-year-old obese P3, 10 years post-menopause, intermittent painless spotting, hypertensive & diabetic

a. Differential Diagnoses of Post-Menopausal Bleeding (PMB)

Uterine Causes (most common — ~90% of PMB)

Extrauterine / Cervical / Vaginal Causes

• Atrophic vaginitis — thin, friable mucosa; accounts for up to 15% of PMB
• Cervical polyp / ectropion
• Cervical carcinoma — must always be excluded
• Vaginal carcinoma / vulval lesion
• Functional ovarian tumour (oestrogen-secreting granulosa cell tumour) — causes endometrial hyperplasia → bleeding

Non-genital Causes

• Haematuria (urethral/bladder origin misinterpreted as vaginal)
• Rectal bleeding

Key point in this patient: Obesity → peripheral conversion of androgens to oestrogens in adipose tissue → unopposed oestrogen stimulation of endometrium. Combined with hypertension and diabetes (metabolic syndrome), this is the classic Type I endometrial cancer risk profile. — Berek & Novak's Gynecology

b. Crucial Points in History and Clinical Examination

History

• Duration, frequency, amount (spotting vs. frank haemorrhage)
• Character — bright red vs. brownish/old blood
• Relationship to coitus (suggests cervical/vaginal cause)
• Associated discharge — purulent discharge suggests pyometra or cervical carcinoma
• Associated pain — usually absent in endometrial cancer; pelvic pain/pressure suggests advanced/bulky disease

• Age at menarche and menopause (late menopause → prolonged oestrogen exposure)
• Parity — nulliparity is a risk factor; this patient is P3 (slightly protective, but obesity overrides)
• Prior abnormal smears / cervical history
• Previous uterine surgery or procedures
• History of PCOS (chronic anovulation → unopposed oestrogen)

• Exogenous oestrogen therapy (HRT) — unopposed oestrogen markedly increases risk
• Tamoxifen use (breast cancer treatment) — major risk factor for endometrial polyps and cancer
• Progestin use (protective)

• Obesity, hypertension, diabetes (present in this patient — classic triad for Type I endometrial cancer)
• Family history of endometrial, colorectal, or ovarian cancer (Lynch syndrome / HNPCC — autosomal dominant, associated with endometrial cancer in ~40–60% of carriers)
• Prior pelvic radiation

• Weight loss, anorexia, bone pain, haematuria, rectal bleeding, leg oedema (lymphatic obstruction)

Clinical Examination

• BMI — obesity is directly relevant
• Blood pressure, peripheral lymphadenopathy (inguinal, supraclavicular)
• Signs of pallor/anaemia from chronic blood loss

• Hepatomegaly, ascites, omental masses (advanced disease)
• Palpable pelvic mass (large uterus or adnexal mass)

• Vulva, vaginal introitus, suburethral area — atrophic changes, lesions, or varicosities
• Any visible cervical mass, polyp, or ectropion

• Assess vaginal mucosa for atrophy (thin, pale, friable — atrophic vaginitis)
• Cervical appearance — lesion, polyp, discharge
• Source of bleeding (is blood coming from the os?)

• Uterine size, shape, mobility, tenderness
• Adnexal masses (granulosa cell tumour)
• Parametrial induration (suggests advanced cervical/endometrial cancer)
• Rectovaginal examination: cul-de-sac nodularity, rectal involvement

Pap smear is an unreliable test for endometrial cancer — only 30–50% of cases have abnormal cytology. — Berek & Novak's Gynecology

c. Investigations and Management

Investigations

Step 1 — First-Line (All patients with PMB)

• ≤4 mm → very low risk for malignancy; biopsy may not be mandatory if low risk
• ≥5 mm (or any thickness with symptoms) → endometrial biopsy is mandatory
• Polypoid mass or intrauterine fluid → further evaluation warranted

Step 2 — Second-Line / When Biopsy is Inconclusive

Step 3 — Staging Workup (if malignancy confirmed)

Management

A. Benign Causes

B. Endometrial Hyperplasia

C. Endometrial Carcinoma

• Total hysterectomy + bilateral salpingo-oophorectomy (TH + BSO) — cornerstone
• Pelvic ± para-aortic lymph node dissection or sentinel lymph node mapping
• Peritoneal washings for cytology
• Omental sampling if Type II histology

• Stage I, low-grade: Surgery alone or vaginal brachytherapy
• Stage I, high-risk features (deep invasion, Grade 3, LVSI): External beam radiotherapy ± chemotherapy
• Stage III–IV: Combination chemotherapy (carboplatin + paclitaxel) ± radiotherapy
• Unfit for surgery (this patient — obese, hypertensive, diabetic): High-dose progestin therapy (megestrol acetate or Mirena IUS) + close surveillance; radiotherapy as alternative

Obesity, hypertension, and diabetes confer significant anaesthetic and surgical risk. Pre-operative optimisation (glucose control, BP management, DVT prophylaxis, cardiorespiratory assessment) is mandatory. Minimally invasive surgery (laparoscopic or robotic hysterectomy) is preferred to reduce wound and metabolic complications.

Summary Algorithm for This Patient

PMB → Speculum + Pap smear + Bimanual exam
          ↓
    TVS (endometrial thickness)
          ↓
    ≥5 mm or any abnormality → Endometrial biopsy (Pipelle)
          ↓
    Inadequate / negative but bleeding continues → Hysteroscopy + D&C
          ↓
    Malignancy confirmed → MRI pelvis + CT staging → Surgical staging
          ↓
    Unfit for surgery → Progestin / radiotherapy

Remember: Any postmenopausal bleeding, however trivial or intermittent, must be investigated to exclude malignancy. — Berek & Novak's Gynecology