---

PRENATAL / ANTENATAL CARE AND DIAGNOSTIC METHODS

---

PART I: ANTENATAL CARE

Definition

• Park's Textbook of Preventive and Social Medicine

---

Objectives of Antenatal Care

1. Promote, protect and maintain the health of the mother during pregnancy
2. Detect "high-risk" cases and give them special attention
3. Foresee complications and prevent them
4. Remove anxiety and dread associated with delivery
5. Reduce maternal and infant mortality and morbidity
6. Teach the mother elements of child care, nutrition, personal hygiene, and environmental sanitation
7. Sensitize the mother to the need for family planning
8. Attend to under-fives accompanying the mother

---

Schedule of Antenatal Visits

Note: WHO updated guidelines (2016) recommend a minimum of 8 antenatal contacts for positive pregnancy experience, emphasizing "contacts" rather than "visits."

---

Clinical Assessment at Each Visit

• Pallor - indicates anaemia; correlate with Hb estimation
• Pulse - normal 60-90 bpm
• Respiratory rate - normal 18-20 breaths/min
• Oedema - evening oedema that disappears by morning may be normal; facial, hand, vulval oedema is abnormal
• Blood pressure - measured every visit; HTN diagnosed at ≥140/90 mmHg on two readings ≥4 hours apart
• Weight - normal gain 9-11 kg total; ~2 kg/month after first trimester

• Fundal height - correlates with gestational age (uterus at umbilicus = 20 weeks, at xiphisternum = 36 weeks)
• Leopold's maneuvers - to determine fetal lie, presentation, position, and engagement
• Fetal heart sounds - auscultated with Pinard fetoscope or Doppler; normal 120-160 bpm

---

Prenatal Advice (Key Components)

• Diet: Extra 300 kcal/day during pregnancy; adequate protein, iron, calcium, folate
• Iron and Folic Acid supplementation: 100 mg elemental iron + 500 mcg folic acid daily from first trimester
• Tetanus toxoid immunization (2 doses, or 1 booster in previously immunized)
• Rest and exercise: 8 hours sleep, avoid strenuous work, light exercise acceptable
• Avoidance: Alcohol, smoking, certain medications (teratogens), X-rays in first trimester
• Danger signs counselling: bleeding, severe headache, visual changes, reduced fetal movements, rupture of membranes

---

High-Risk Factors in Pregnancy

---

PART II: DIAGNOSTIC METHODS IN OBSTETRICS

---

1. ULTRASONOGRAPHY (USG)

Principles

Types of Obstetric Ultrasound Examinations

• Creasy & Resnik's Maternal-Fetal Medicine

---

First Trimester Ultrasound (6-14 weeks)

• Crown-rump length (CRL) - most accurate measurement for gestational age dating (accurate to ±5-7 days)
• Yolk sac - confirms intrauterine pregnancy (seen at ~5.5 weeks transvaginal)
• Fetal cardiac activity - seen from ~6 weeks
• Nuchal translucency (NT) - measured 11-13+6 weeks (CRL 45-84 mm); normal <3 mm; increased NT associated with Down syndrome (trisomy 21) and other aneuploidies
• Nasal bone - present in 99% of normal fetuses at 11-13 weeks; absent/hypoplastic in ~60-70% of Down syndrome
• Ductus venosus flow - reversed A-wave associated with aneuploidy and cardiac defects

---

Second Trimester Anatomy Scan (18-20 weeks)

• BPD - Biparietal diameter
• HC - Head circumference
• AC - Abdominal circumference
• FL - Femur length
• These four measurements together generate Estimated Fetal Weight (EFW)

• Head: Lateral ventricles, choroid plexus, cisterna magna, cerebellum, cavum septi pellucidi, posterior fossa
• Face: Lips (for cleft), orbits
• Heart: Four-chamber view, outflow tracts (LVOT, RVOT), three-vessel view
• Spine: Longitudinal and transverse views
• Abdomen: Stomach, intestines, kidneys, bladder, umbilical cord insertion
• Extremities: Upper and lower long bones, hand/foot anatomy and posture
• Genitalia

• Placental location (rule out placenta praevia)
• Placental appearance (cysts, lucencies, accessory lobe)
• Umbilical cord vessels (normally 2 arteries + 1 vein)
• Amniotic Fluid Index (AFI) or Maximum Vertical Pocket (MVP)
  • Normal AFI: 8-24 cm; Oligohydramnios: <5 cm; Polyhydramnios: >25 cm
  • Normal MVP: 2-8 cm

---

Third Trimester Ultrasound (28+ weeks)

• Growth surveillance - serial EFW, AC measurements; plot on growth curves
• Presentation and position confirmation
• Placental location - especially important if low-lying on 20-week scan
• Doppler assessment (see below)
• Biophysical Profile (BPP)

---

Doppler Ultrasound in Obstetrics

• Most commonly used Doppler assessment
• Reflects downstream placental vascular resistance
• Normal: resistance falls progressively through pregnancy
• Abnormal findings (in order of severity):
  • Elevated S/D ratio (systolic/diastolic)
  • Absent End-Diastolic Velocity (AEDV) - ominous; associated with FGR
  • Reversed End-Diastolic Velocity (REDV) - most severe; high perinatal mortality

A meta-analysis of 31 studies showed OR for fetal death of 3.59 with AEDV and 7.27 with REDV in FGR fetuses <34 weeks.

• Creasy & Resnik's Maternal-Fetal Medicine

• Used to assess fetal anaemia and brain-sparing redistribution in FGR
• MCA Peak Systolic Velocity (MCA-PSV): >1.5 MoM (multiples of median) indicates significant fetal anaemia (sensitivity ~88%)
• Brain-sparing: decreased MCA resistance (low PI/RI) with elevated UA resistance

• Reflects cardiac preload and venous pressure
• Reversed A-wave: severe fetal compromise, indication for urgent delivery consideration

• Used in pre-eclampsia risk assessment (first trimester combined screening)
• Persistent bilateral notching + elevated RI in second trimester = high risk for pre-eclampsia and FGR

• Beneficial in high-risk pregnancies (FGR, hypertension, chronic illness)
• Routine use in low-risk pregnancies has not been shown to be beneficial

---

2. CARDIOTOCOGRAPHY (CTG)

Principle

1. Fetal Heart Rate (FHR) - via Doppler ultrasound (external) or fetal scalp electrode (internal)
2. Uterine contractions - via tocodynamometer (external) or intrauterine pressure catheter (internal)

Technical Aspects

• Fetal scalp electrode (FSE): Spiral stainless steel wire attached to fetal scalp; measures true beat-to-beat variability from fetal ECG R-wave; most accurate
• Intrauterine pressure catheter (IUPC): Measures true contraction intensity in mmHg

• Doppler ultrasound transducer (cardiotachometer): Emits ~2.5 MHz signal; reflected from fetal cardiac structures; interval between signals calculates FHR; recorded at 3 cm/min paper speed; uses autocorrelation technology
• Tocodynamometer: Detects contraction frequency and duration but not true intensity
• Creasy & Resnik's Maternal-Fetal Medicine

---

Antenatal CTG: Non-Stress Test (NST)

• ≥2 FHR accelerations within 20-30 minutes
• Each acceleration: rises ≥15 bpm above baseline, lasts ≥15 seconds
• For fetuses <32 weeks: modified criteria of 10 bpm rise lasting 10 seconds acceptable

• Fetal sleep cycle (most common - resolve with vibroacoustic stimulation)
• Prematurity
• FGR
• Maternal medications (narcotics, magnesium sulfate)
• Fetal acidosis/hypoxia

---

Contraction Stress Test (CST)

• Evaluates FHR response to uterine contractions
• Contractions provoked by oxytocin infusion or nipple stimulation
• Negative (normal): No late decelerations with adequate contractions (3 in 10 min)
• Positive (abnormal): Persistent late decelerations with 50% or more of contractions

---

Intrapartum CTG Classification

• Early decelerations: Mirror contractions; uniform shape; due to fetal head compression (vagal reflex); benign
• Late decelerations: Begin after contraction peak; uniform; due to uteroplacental insufficiency; pathological
• Variable decelerations: Abrupt onset, variable shape and timing; due to cord compression; may be benign or pathological
• Prolonged deceleration: >2 minutes

• Category I (Normal): Baseline 110-160, moderate variability, no late/variable decelerations, accelerations present/absent
• Category II (Indeterminate): All traces not in Category I or III
• Category III (Abnormal): Sinusoidal pattern, or absent variability + recurrent late/variable decelerations or bradycardia; requires prompt evaluation and delivery

---

Biophysical Profile (BPP)

---

3. HYSTEROSALPINGOGRAPHY (HSG)

Definition

Indications

• Primary investigation for infertility (tubal patency assessment)
• Recurrent miscarriage (uterine cavity assessment)
• Suspected congenital uterine anomalies (septum, bicornuate uterus, unicornuate)
• Suspected intrauterine adhesions (Asherman's syndrome)
• Follow-up after tubal surgery or sterilization reversal
• Suspected tubal occlusion

Timing

• Day 7-10 of menstrual cycle (post-menstrual, pre-ovulatory phase)
• Avoid in active pelvic infection

Procedure

1. Cervix cannulated with Foley catheter or Leech-Wilkinson cannula
2. Water-soluble contrast injected under fluoroscopy
3. Images taken in AP and oblique views

Normal Findings

• Uterine cavity: triangular/pear-shaped outline, smooth margins
• Tubes: fill bilaterally, free peritoneal spill confirms patency

Abnormal Findings

Limitations

• Ionizing radiation (avoid in pregnancy)
• Does not assess ovaries or peritubal adhesions
• Cannot visualize pelvic endometriosis
• 10-20% false-positive rate for tubal block (due to spasm)

---

4. AMNIOCENTESIS

Definition

Timing

• Second trimester amniocentesis: 15-20 weeks (standard)
• Early amniocentesis: <15 weeks (higher complication rate - not recommended)

Indications

1. Fetal chromosomal abnormality suspected (abnormal screening: NT, serum screening, cfDNA)
2. Previous child with chromosomal aneuploidy or genomic imbalance
3. Parental balanced chromosomal rearrangement (translocation, inversion)
4. Advanced maternal age (AMA) - though ACOG now offers to all women regardless of age
5. Both parents carriers of autosomal recessive disorder (e.g., cystic fibrosis, thalassaemia, SMA)
6. Mother carrier of X-linked disorder (e.g., haemophilia, Duchenne MD)
7. Family history of neural tube defect (amniotic AFP measurement)
8. Suspected fetal infection (CMV, toxoplasma, rubella by PCR)
9. Fetal lung maturity assessment (L/S ratio, PG - rarely done now)
10. In-utero treatment (e.g., decompression of severe polyhydramnios)

Procedure

• Performed under continuous real-time ultrasound guidance
• 22-gauge spinal needle
• 15-20 mL amniotic fluid withdrawn
• Sample sent for: karyotype (takes 10-14 days), QF-PCR (rapid; results in 48h), chromosomal microarray (CMA), FISH, metabolic studies, PCR

Complications

• Procedure-related pregnancy loss: 0.1-0.3% (previously quoted as ~0.5-1%; modern series show lower rates)
• Transient leakage of amniotic fluid
• Chorioamnionitis (<0.1%)
• Feto-maternal haemorrhage (anti-D prophylaxis for Rh-negative mothers)
• Failed/dry tap

---

5. CHORIONIC VILLUS SAMPLING (CVS)

Definition

Timing

• Transabdominal or transcervical: 10-13 weeks (earlier results than amniocentesis)

Advantages over Amniocentesis

• Earlier result (first trimester)
• Earlier decision-making if termination needed

Disadvantages

• Cannot detect NTDs (no amniotic fluid for AFP)
• Higher complication rate than mid-trimester amniocentesis
• Confined placental mosaicism (discrepancy between placenta and fetus): 1-2% of cases
• Transcervical route: higher infection risk

Karyotyping from CVS

• Long-term culture (10-14 days): From mesenchymal core of villus - more closely represents fetal karyotype
• Short-term rapid metaphase (48-72h): From cytotrophoblast - higher mosaicism rate, lower resolution

---

6. CELL-FREE DNA (cfDNA) / NON-INVASIVE PRENATAL TESTING (NIPT)

Principle

What NIPT Screens For

• Trisomy 21 (Down syndrome) - DR >99%, FPR <0.1%
• Trisomy 18 (Edwards syndrome) - DR ~97%
• Trisomy 13 (Patau syndrome) - DR ~92%
• Sex chromosome aneuploidies (XXX, XXY, XYY, monosomy X)
• Microdeletion syndromes (22q11 deletion - variable performance)
• Fetal sex determination

Important Points

• Screening test, NOT diagnostic - positive NIPT must be confirmed by amniocentesis or CVS
• ACOG recommends offering to all women (not just high-risk), regardless of age
• False-positive rate much lower than serum screening
• Failure rate: ~2-5% (low fetal fraction, usually in obese patients)

---

7. MATERNAL SERUM SCREENING

First Trimester Combined Screen (11-13+6 weeks)

• NT ultrasound + free β-hCG + PAPP-A
• Detection rate for trisomy 21: ~85-90%, FPR 5%

Second Trimester "Quad Screen" (15-20 weeks)

• Down syndrome detection rate: ~80% with FPR 5%
• AFP elevation: Suspect open NTD, abdominal wall defect, or fetal demise

Integrated/Sequential/Contingency Screening

• Combines first and second trimester markers for highest detection rates (>90%)

---

8. FETAL ECHOCARDIOGRAPHY

Indications

• Family history of congenital heart disease (CHD)
• Maternal diabetes, SLE, anti-Ro/La antibodies (risk of heart block)
• Maternal phenylketonuria
• Teratogen exposure (lithium, alcohol, isotretinoin)
• Abnormal 4-chamber view on routine scan
• Increased NT or abnormal cfDNA
• Fetal hydrops or arrhythmia

Timing

• 18-22 weeks (ideally 20-22 weeks for optimal visualization)
• Can be repeated later if needed

Views Assessed

• 4-chamber view
• Left and right ventricular outflow tracts (LVOT, RVOT)
• 3-vessel view and 3-vessel trachea view
• Aortic arch, ductal arch
• Superior and inferior vena cava

---

9. ADDITIONAL INVASIVE PROCEDURES

Cordocentesis (Percutaneous Umbilical Blood Sampling - PUBS)

• Aspiration of fetal blood from umbilical cord under ultrasound guidance
• Used for: rapid karyotype (24-48h), fetal blood group, Hb, coagulation, IgM for infection, intrauterine transfusion for severe fetal anaemia
• Procedure-related loss rate: ~1-2% (higher than amniocentesis)

Fetoscopy

• Direct endoscopic visualization of fetus
• Now largely replaced by high-resolution ultrasound
• Used for: fetal skin biopsy, fetal blood sampling, laser therapy in TTTS

---

SUMMARY TABLE: Antenatal Diagnostic Methods

---

• Creasy & Resnik's Maternal-Fetal Medicine: Principles and Practice (Chapters on Obstetric Imaging, Fetal Heart Rate Monitoring, Prenatal Diagnosis)
• Park's Textbook of Preventive and Social Medicine (Antenatal Care chapter)
• Thompson & Thompson Genetics and Genomics in Medicine, 9th ed. (Prenatal Diagnosis chapter)
• Williams Obstetrics knowledge base (standard obstetric reference; not separately available in this library, but content above aligns with Williams Obstetrics 25th/26th edition standards)
• DC Dutta's Textbook of Obstetrics content reflected in ANC sections above (not separately indexed in this library; the notes above cover equivalent material)

Note: Williams Obstetrics and DC Dutta's Textbook of Obstetrics were not separately present as standalone texts in this textbook library; the most equivalent resources (Creasy & Resnik's Maternal-Fetal Medicine) were used, which covers the same material with greater depth.---

1. USG - Types (first trimester, anatomy scan, Level II), key measurements (CRL, BPD, HC, AC, FL, AFI), anomaly detection rates
2. Doppler USG - Umbilical artery (AEDV/REDV in FGR), MCA-PSV (fetal anaemia), ductus venosus, uterine artery
3. CTG - Technical aspects (internal vs external), NST criteria (reactive = 2 accels ≥15 bpm), BPP scoring, ACOG 3-tier intrapartum classification
4. HSG - Indications, timing, findings for tubal patency and uterine cavity
5. Amniocentesis - Indications, timing (15-20 wks), complications (0.1-0.3% loss)
6. CVS - First trimester (10-13 wks), advantages/limitations vs amniocentesis
7. cfDNA/NIPT - Detection rates (>99% for T21), screening vs diagnostic distinction
8. Serum screening - First trimester combined, Quad screen markers
9. Cordocentesis - PUBS for fetal blood sampling and intrauterine transfusion

---

PRACTICAL SKILLS IN OBSTETRICS

A Complete Clinical Reference

---

SECTION 1: PELVIMETRY

Definition

"A particularly important measurement is the true conjugate of the pelvic inlet (the obstetric conjugate), which is the smallest anteroposterior dimension of the lesser pelvis. With pelvimetry, a method of measuring pelvic dimensions, potential obstructions to labor can be identified prior to delivery."

• General Anatomy and Musculoskeletal System, THIEME Atlas

---

Anatomy of the Bony Pelvis

1. Pelvic Inlet (Brim) - bounded by sacral promontory posteriorly, linea terminalis laterally, pubic symphysis anteriorly
2. Mid-pelvis (Cavity) - bounded by ischial spines (narrowest part)
3. Pelvic Outlet - bounded by coccyx posteriorly, ischial tuberosities laterally, subpubic arch anteriorly

---

CONJUGATE DIAMETERS - All Types

---

1. TRUE CONJUGATE (Conjugata Vera Anatomica)

---

2. OBSTETRIC CONJUGATE (True Conjugate / Conjugata Vera Obstetrica)

Obstetric Conjugate = Diagonal Conjugate − 1.5 cm

---

3. DIAGONAL CONJUGATE

True (Obstetric) Conjugate = Diagonal Conjugate − 1.5 cm

• If DC = 12.5 cm → Obstetric Conjugate ≈ 11 cm (adequate)
• If DC < 11.5 cm → Obstetric Conjugate < 10 cm → suspect contracted pelvis

1. Patient in dorsal lithotomy position, bladder empty
2. Two fingers (index + middle) inserted into vagina, with palm facing upward
3. The middle finger reaches toward the sacral promontory
4. The examiner's other hand marks where the index finger touches the lower border of the symphysis pubis
5. The distance from the tip of the middle finger to the mark = diagonal conjugate
6. Measured with a ruler or pelvimeter
7. If the fingers cannot reach the sacral promontory - pelvis is adequate (DC >12.5 cm)
8. If sacral promontory is easily palpable - pelvis may be contracted

• THIEME Atlas of Anatomy - General Anatomy and Musculoskeletal System

---

4. EXTERNAL CONJUGATE (Baudelocque's Diameter)

True Conjugate ≈ External Conjugate − 9 cm (Subtract 8-10 cm depending on soft tissue thickness)

---

5. CONJUGATE OF PELVIC OUTLET

---

Summary Table: All Conjugates

---

Other Pelvic Diameters

Transverse Diameters

Oblique Diameters (of inlet)

External Pelvic Measurements (Obstetric Conjugate Estimation)

• A diamond-shaped area on the lower back
• Upper angle = depression below L5
• Lower angle = tip of sacrum
• Side angles = posterior superior iliac spines
• Normal dimensions: vertical ≈ 11 cm, horizontal ≈ 10 cm
• A flat, asymmetric, or malformed rhomboid suggests pelvic contraction

---

Types of Pelves (Caldwell-Moloy Classification)

---

Contracted Pelvis - Definitions

---

SECTION 2: LEOPOLD'S MANEUVERS

Definition

• Bladder empty
• Patient supine, knees slightly flexed (semi-recumbent)
• Examiner stands to the patient's right side (for maneuvers 1-3), then facing feet (maneuver 4)
• Warm hands; palpate gently

---

MANEUVER 1 - Fundal Grip (Fundal Palpation)

• Examiner faces the patient's head
• Both hands placed on the fundus, fingers pointing downward and inward
• Palpate the mass in the fundus

---

MANEUVER 2 - Lateral (Umbilical) Grip (Lateral Palpation)

• Examiner faces the patient's head
• Both hands placed on the lateral sides of the uterus at umbilical level
• One hand steadies the uterus; the other palpates the opposite side, then vice versa

---

MANEUVER 3 - Pawlik's Grip (Lower Pole Palpation)

• Examiner faces the patient's head
• One hand only - right hand
• Thumb and fingers grasp the lower uterine segment just above the symphysis pubis
• Gently move the presenting part side to side

---

MANEUVER 4 - Pelvic (Bi-manual) Grip

• Examiner turns and faces the patient's feet
• Both hands placed on the lower abdomen, fingers pointing downward toward the pelvic inlet
• Fingers slide down toward the pelvic brim on both sides of the presenting part
• Press inward and downward

• On the same side as the back → head extended (face/brow presentation)
• On the opposite side from the back → head flexed (normal vertex - occiput is cephalic prominence)

---

Engagement Assessment (Fifths Rule)

---

Determining Fetal Lie, Presentation, Position

• Longitudinal (99%)
• Transverse
• Oblique

• Vertex (cephalic - occiput leading): most common (95%)
• Face, Brow (cephalic - deflexed)
• Breech (frank, complete, footling)
• Shoulder (transverse lie)

• LOA (Left Occiput Anterior) - most common
• ROA (Right Occiput Anterior)
• LOT, ROT (transverse)
• LOP, ROP (posterior)
• OA (direct anterior), OP (direct posterior)

---

SECTION 3: AUSCULTATION OF FETAL HEART SOUNDS

Instruments

1. Pinard fetoscope (wooden/metal stethoscope) - from 20-24 weeks
2. Sonicaid / handheld Doppler (CTG) - from 12-14 weeks
3. Electronic CTG monitor - from 28 weeks

Technique with Pinard Fetoscope

1. Patient supine, abdomen exposed
2. Identify fetal back (from Leopold's maneuver 2)
3. Place Pinard fetoscope over the fetal back - sounds are transmitted through fetal chest wall
4. Apply ear (not hand-held stethoscope style) firmly to the fetoscope opening - use head contact, not holding
5. Listen for 1 full minute

Normal Fetal Heart Rate

110-160 beats per minute

• Tachycardia: >160 bpm (sustained) - may indicate fetal distress, maternal fever, drugs
• Bradycardia: <110 bpm - may indicate cord compression, fetal hypoxia

Point of Maximum Intensity (PMI) of Fetal Heart

Differentiating from Maternal Pulse

• Simultaneously palpate maternal radial pulse
• If rate same as auscultated rate → maternal aortic pulsation (not fetal)
• True FHR differs from maternal pulse

Souffle (Murmurs)

• Uterine souffle (funic souffle): Soft blowing sound, synchronous with FHR - from umbilical arteries
• Placental souffle: Soft blowing sound, synchronous with maternal pulse - from uteroplacental vessels

---

SECTION 4: ESTIMATION OF FETAL WEIGHT

A. Clinical Estimation (Abdominal Palpation)

EFW (grams) = (Fundal Height in cm − n) × 155

• n = 12 if presenting part is above the ischial spines (not engaged)
• n = 11 if presenting part is at or below the ischial spines (engaged)

• Fundal height = 36 cm, head not engaged
• EFW = (36 - 12) × 155 = 24 × 155 = 3720 g

---

B. Dawson's / McDonald's Rule (Fundal Height for Gestational Age)

Gestational age (weeks) ≈ SFH (cm) in cm measured from symphysis pubis to uterine fundus

"Measurement of the symphysis-fundal height is helpful in screening for abnormal fetal growth and documenting continued growth if performed repeatedly by the same observer." - Creasy & Resnik's Maternal-Fetal Medicine

---

C. Ultrasound Fetal Weight Estimation

Log10(EFW) = 1.326 - 0.00326(AC × FL) + 0.0107(HC) + 0.0438(AC) + 0.158(FL)

Log10(EFW) = 1.304 + 0.05281(AC) + 0.1938(FL) - 0.004(AC × FL)

Log10(EFW) = -1.7492 + 0.166(BPD) + 0.046(AC) - 2.646(AC × BPD)/1000

---

D. Additional Clinical Estimation Methods

EFW (grams) = Fundal height (cm) × Abdominal girth (cm)

---

SECTION 5: EXPECTED DATE OF DELIVERY (EDD)

Naegele's Rule (Standard Method)

EDD = LMP + 9 months + 7 days OR equivalently: EDD = LMP − 3 months + 7 days + 1 year

1. Take the first day of the Last Menstrual Period (LMP)
2. Add 9 calendar months (or subtract 3 months)
3. Add 7 days

• LMP: 1st May 2025
• Add 9 months → 1st February 2026
• Add 7 days → EDD: 8th February 2026

• LMP: 1st May 2025
• Subtract 3 months → 1st February 2025
• Add 7 days + 1 year → 8th February 2026 ✓

• Regular 28-day cycle
• Ovulation on day 14
• Normal duration of pregnancy = 280 days (40 weeks) from LMP = 266 days from conception

---

Adjustments to EDD

Adjusted EDD = Naegele's EDD ± (actual cycle length − 28 days)

---

Other Methods to Estimate Gestational Age

---

SECTION 6: STRESS TESTS

A. NON-STRESS TEST (NST)

• Post-dates pregnancy
• Gestational diabetes
• Hypertensive disorders
• FGR, decreased fetal movements
• IUGR, multiple pregnancy
• Oligohydramnios

1. Patient semi-recumbent, left lateral tilt preferred
2. External CTG applied: Doppler transducer (FHR) + tocodynamometer (uterine activity)
3. Monitor for minimum 20-30 minutes
4. Patient presses button when fetal movement felt (event marker)
5. If non-reactive at 20 min: extend to 40-60 min, use vibroacoustic stimulation (VAS)

REACTIVE (Normal) NST:

• ≥2 accelerations in 20-30 minutes
• Each acceleration: peaks ≥15 bpm above baseline and lasts ≥15 seconds
• For <32 weeks gestation: ≥10 bpm rise lasting ≥10 seconds (modified criteria)

NON-REACTIVE NST:

• Does not meet above criteria within 40-60 minutes

• Creasy & Resnik's Maternal-Fetal Medicine

• Fetal sleep (most common; 20-40 min sleep cycles)
• Prematurity (<32 weeks)
• FGR / fetal hypoxia
• Maternal sedatives, narcotics, magnesium sulfate
• Neurological anomaly

• Apply acoustic stimulator (artificial larynx) to maternal abdomen over fetal head for 1-3 seconds
• Should produce FHR acceleration
• If reactive after VAS → reactive NST

---

B. CONTRACTION STRESS TEST (CST) / OXYTOCIN CHALLENGE TEST (OCT)

"The CST uses spontaneously occurring contractions or contractions induced by maternal nipple stimulation. The OCT uses intravenous oxytocin to cause repetitive uterine activity." - Creasy & Resnik's Maternal-Fetal Medicine

• Placenta praevia
• Previous classical (vertical) caesarean scar
• Preterm labour or risk of preterm labour
• Incompetent cervix
• Premature rupture of membranes
• Multiple pregnancy (relative)

1. IV oxytocin by infusion pump: start at 0.5-1 mU/min, increase every 15-20 min
2. Goal: 3 contractions of ≥40 seconds duration in 10 minutes
3. Monitor FHR and uterine activity throughout
4. Perform in hospital with emergency backup

1. Patient stimulates nipple through clothing intermittently
2. Releases endogenous oxytocin
3. Same FHR assessment applied

"Although these test results are good indicators of fetal well-being when negative (negative predictive values exceeding 99.8%), a positive test result alone is not sufficiently predictive to form the basis for clinical action." - Creasy & Resnik's Maternal-Fetal Medicine

---

C. BIOPHYSICAL PROFILE (BPP)

---

D. VIBROACOUSTIC STIMULATION TEST (VAST)

• Fetal acoustic stimulation using an artificial larynx (EAL) at 82-95 dB placed on maternal abdomen
• Applied for 1-3 seconds
• Normal response: FHR acceleration ≥15 bpm for ≥15 seconds within 15 seconds of stimulus
• Can convert non-reactive NST to reactive
• Considered part of routine NST protocol

---

SECTION 7: VAGINAL EXAMINATION IN LABOUR (Internal Examination)

Findings to Assess

• Dilatation (0-10 cm): measured as finger-breadths (1 finger = ~2 cm) or in cm with both fingers spread
• Effacement (%): shortening/thinning of cervical canal; 0% = 3-4 cm long; 100% = completely thinned
• Consistency: firm (unripe), medium, soft/ripe
• Position: posterior, mid, anterior
• Bishop Score combines all above + station (see below)

• Nature (vertex, breech, face)
• Station (level relative to ischial spines)
  • -3 to +3 scale (ACOG) or -5 to +5 (older)
  • 0 = at level of ischial spines (= engaged in ACOG scale)
  • Negative = above spines; positive = below spines

• Intact / ruptured
• If intact: can feel membranes bulging through cervix
• Confirm rupture: pooling in posterior fornix, ferning on glass slide, Amnisure (AFP/IGFBP-1 test)

• Diagonal conjugate (if not done)
• Ischial spines prominence (prominent = narrowed mid-pelvis)
• Subpubic angle (normal >90° in females)
• Sacral curve
• Convergence/divergence of side walls

---

Bishop Score

---

SECTION 8: PARTOGRAPH (Labour Monitoring Tool)

• FHR (every 30 min)
• Membranes and liquor (colour)
• Moulding of fetal skull

• Cervicograph (cervical dilatation plotted over time)
  • Alert line: Starts at 4 cm dilatation, progresses at 1 cm/hour
  • Action line: 4 hours to the right of alert line
• Descent of presenting part (in fifths palpable abdominally)
• Uterine contractions (frequency, duration, strength per 10 min)

• BP, pulse, temperature
• Urine (volume, protein, acetone)
• Drugs / IV fluids

---

QUICK REFERENCE FORMULA SHEET

---

• Creasy & Resnik's Maternal-Fetal Medicine: Principles and Practice - CST/OCT, NST, BPP, Doppler, Fundal height
• THIEME Atlas of Anatomy - General Anatomy and Musculoskeletal System - Pelvimetry, conjugate diameters
• Berek & Novak's Gynecology - Pelvic anatomy, ischial spines, pelvic articulations
• Park's Textbook of Preventive and Social Medicine - ANC, fundal height landmarks, clinical examination
• Williams Obstetrics and DC Dutta standard knowledge (Leopold's maneuvers, Johnson's formula, Naegele's rule, Bishop score)

---

ACUTE ABDOMINAL SYNDROME IN GYNAECOLOGY

A Comprehensive Chapter

Including: Acute Pelvic Pain | Myoma Uteri | Endometriosis | PCOS

---

PART I: ACUTE ABDOMINAL SYNDROME IN GYNAECOLOGY

---

Definition

• Sudden or rapid onset
• Often associated with unstable vital signs
• Obvious abnormalities on physical examination and laboratory assessment
• Improper diagnosis can result in significant morbidity and even mortality

"Acute pain is intense and characterized by sudden onset, sharp rise, and short course... Timely and thorough assessment, guided by organ system (reproductive, gastrointestinal, urinary) and category of pathology, will ensure effective diagnosis and management of infection, obstruction, ischaemia (torsion), leakage of irritating substance (viscus or cyst rupture), or pregnancy-related pain."

• Berek & Novak's Gynecology

---

Classification of Gynaecological Acute Abdomen

1. Adnexal torsion
2. Ovarian cyst accident (rupture)
3. Pelvic Inflammatory Disease (PID)
4. Endometriosis
5. Appendicitis
6. Bowel obstruction

• Bailey & Love's Short Practice of Surgery, 28th Edition

---

General Approach to the Patient

• Berek & Novak's Gynecology

1. Genital - abnormal vaginal bleeding/discharge, dysmenorrhea, dyspareunia, subfertility
2. Enterocoelic - constipation, diarrhea, flatulence, hematochezia
3. Musculoskeletal/neuropathic - trauma, postural exacerbation, weakness
4. Urologic - urgency, frequency, dysuria, hematuria
5. Psychological - anxiety, depression, prior physical or sexual trauma

---

Physical Examination

• Distension, guarding, rigidity
• Site and character of tenderness
• Rebound tenderness (peritoneal irritation)
• Bowel sounds (absent = ileus/peritonitis)
• Shifting dullness (haemoperitoneum)

• Cervical motion tenderness (PID, ectopic)
• Adnexal tenderness and mass
• Uterine size and tenderness
• Rectovaginal examination for nodules (endometriosis), mass in cul-de-sac (TOA)

---

Key Investigations

"Diagnostic laparoscopy is reserved for establishing the diagnosis in patients who have acute abdomen of uncertain cause, for elucidating the nature of an ambiguous adnexal mass, or for delineating whether a pregnancy is intrauterine or extrauterine." - Berek & Novak's Gynecology

---

ACUTE GYNAECOLOGICAL CONDITIONS

---

1. ECTOPIC PREGNANCY

• Classic triad: Amenorrhoea + lower abdominal pain + vaginal bleeding
• Sudden severe pain if ruptured - shoulder tip pain (diaphragmatic irritation from haemoperitoneum)
• Fainting/syncope (haemodynamic compromise)

• Tachycardia, hypotension (if ruptured and significant haemorrhage)
• Abdominal guarding, rigidity, rebound tenderness
• Cervical excitation (cervical motion tenderness)
• Unilateral adnexal mass ± tenderness
• Fullness/tenderness in posterior fornix

• Serum β-hCG: Positive; discriminatory zone = β-hCG 1500-2000 mIU/mL (TVS should show IUP above this level; if not - suspect ectopic)
• TVS: Empty uterus ± adnexal mass ± free fluid in POD
• Culdocentesis (historic): Non-clotting blood in cul-de-sac = haemoperitoneum

• Haemodynamically unstable → Emergency laparotomy/laparoscopy + salpingectomy
• Stable, unruptured → Laparoscopy ± salpingotomy (fertility-preserving) or salpingectomy
• Medical: Methotrexate - single dose (50 mg/m²) or multi-dose - criteria: unruptured, β-hCG <5000 mIU/mL, no cardiac activity, tube <4 cm

---

2. RUPTURED OVARIAN CYST / HAEMORRHAGIC CYST

• Follicular cyst (ruptures at ovulation → Mittelschmerz)
• Corpus luteum cyst (most common to rupture and bleed)
• Endometrioma rupture (chemical peritonitis)
• Dermoid cyst rupture (sebaceous material → chemical peritonitis)

• Follicle rupture: midcycle mild to moderate pain, self-limited
• Corpus luteum rupture: sudden severe pain in luteal phase, similar to ectopic
• Delayed menses (persistently functioning corpus luteum)
• Dizziness/syncope with significant haemoperitoneum
• Endometrioma rupture: pain without significant hypovolemia

• Orthostasis only when intravascular volume depletion
• Fever rare
• Significant abdominal tenderness, rebound
• Adnexal mass may be palpable if leaking (not fully ruptured)
• Hematocrit decreased if active bleeding

• β-hCG negative (rules out ectopic)
• TVS: Free fluid in pelvis ± collapsed cyst ± echogenic blood
• If haemodynamically unstable: type and crossmatch, laparoscopy/laparotomy

• Haemodynamically stable + minimal bleeding: Conservative (observation, analgesia)
• Significant haemoperitoneum or chemical peritonitis: Surgical (laparoscopy/laparotomy) - cystectomy, haemostasis

"Surgical exploration is indicated if the rupture leads to significant hemoperitoneum (corpus luteum) or chemical peritonitis (endometrioma or dermoid), which could impair future fertility, or an acute abdomen (abscess), which is life-threatening." - Berek & Novak's Gynecology

---

3. ADNEXAL TORSION

• Enlarged ovary (cyst, benign cystic teratoma/dermoid - most common neoplasm to tort)
• Para-ovarian cyst
• Hydrosalpinx
• Previous torsion
• Pregnancy (corpus luteum enlargement)
• Ovarian hyperstimulation syndrome (OHSS)
• Polycystic ovary

"Diagnosis of adnexal torsion is challenging. The clinician must base the diagnosis on history, clinical examination, and additional investigations such as pelvic ultrasound. There is no specific size criteria for ovarian torsion, but one study found that 83% of torsion occurred in ovaries that were 5 cm or larger." - Berek & Novak's Gynecology

• Pain: Severe and constant if complete; waxing and waning if partial/intermittent
• Onset often coincides with activity (lifting, exercise, intercourse)
• Nausea, vomiting (autonomic reflex)
• Tachycardia, apprehension
• Diarrhea

• Mild temperature elevation, tachycardia, leukocytosis
• Pregnancy test usually negative
• Localized lower quadrant direct and rebound tenderness
• Unilateral adnexal mass on bimanual examination

• Unilateral ovarian enlargement and oedema with less defined borders
• Peripheral displacement of follicles - "follicular ring sign"
• Twisted pedicle appearing as "whirlpool sign" on colour Doppler
• Abnormal Doppler: coiling of vessels (early), absent perfusion (late)
• Free fluid in pelvis

Important: "The presence of Doppler blood flow to the ovary on ultrasound does not definitely rule out torsion." - Berek & Novak's Gynecology

• Surgical emergency - laparoscopy or laparotomy
• Detorsion (unwinding) + cystectomy at same or delayed setting
• Even when necrosis appears present, detorsion can preserve function - oophorectomy not always necessary
• Oophoropexy (fixation) on both sides after torsion in pediatric patients
• Bailey & Love's Short Practice of Surgery / Berek & Novak's Gynecology

---

4. PELVIC INFLAMMATORY DISEASE (PID) AND TUBO-OVARIAN ABSCESS (TOA)

• Acute onset pelvic pain (increases with movement)
• Fever (>38.3°C)
• Purulent vaginal discharge
• Nausea, vomiting
• Dyspareunia

• Tachycardia, elevated temperature
• Direct and rebound lower abdominal tenderness
• Cervical motion tenderness (CMT) - most important sign
• Bilateral adnexal tenderness
• Fitz-Hugh-Curtis Syndrome: Right upper quadrant pain from perihepatitis (PID-related inflammation of liver capsule and peritoneal surfaces)

• Minimum criteria (treat empirically): uterine/cervical motion/adnexal tenderness without other cause
• Additional supporting: fever, elevated WBC, elevated ESR/CRP, positive GC/chlamydia, mucopurulent discharge, WBCs on wet mount
• Definitive: laparoscopic evidence of salpingitis/oophoritis OR thickened fluid-filled tubes on USS

• Complication of acute salpingo-oophoritis
• Usually bilateral, can be unilateral
• Ruptured TOA = life-threatening surgical emergency (gram-negative endotoxic shock)
• Signs: fever, tachycardia, bilateral fixed tender adnexal masses, pointing in cul-de-sac
• 90% have abdominal/pelvic pain, 60-80% have fever/leukocytosis
• ESR >19.5 mm/hr and CRP >11.5 mg/L predict TOA over simple PID
• Management: IV antibiotics (cefoxitin + doxycycline, or clindamycin + gentamicin); surgical drainage if rupture or no response
• Berek & Novak's Gynecology

---

PART II: MYOMA UTERI (UTERINE LEIOMYOMA / FIBROID)

---

Definition

Epidemiology

• Most common benign tumour of the uterus and female reproductive system
• Prevalence: 20-40% of women over 35 years
• Higher incidence in Black women (2-3× more than White women)
• Risk factors: early menarche, nulliparity, obesity, family history, Black race

---

Classification by Location

• SM0: Entirely submucosal
• SM1: <50% intramural
• SM2: ≥50% intramural
• Types 3-8 for intramural and subserosal variants

---

Aetiology and Pathogenesis

• Monoclonal tumours arising from a single myometrial cell
• Oestrogen-dependent: grow during reproductive years, regress after menopause
• Progesterone also plays a role in growth stimulation
• Molecular: chromosomal rearrangements (6p21, 7q, 12q14-15, 14q24), MED12 mutations (most common, ~70%)
• Aromatase activity within fibroids converts androgens to oestrogen locally

---

Pathological Changes (Types of Degeneration)

RED DEGENERATION (Carneous Degeneration) - ACUTE ABDOMEN

• Rapid growth during pregnancy due to oestrogen stimulation
• Outstrips blood supply
• Venous occlusion at periphery → haemorrhagic infarction
• Gross appearance: beefy red, fish flesh-like cut surface

• Sudden onset severe abdominal pain
• Localised to the fibroid (point tenderness over fibroid)
• Fever (low-grade)
• Nausea, vomiting
• Uterine tenderness

• Conservative - bed rest, hydration, NSAIDs/analgesics (paracetamol in pregnancy)
• Majority resolve with 7-10 days
• Premature labour may be precipitated
• Surgery rarely needed; myomectomy in pregnancy has high morbidity

---

Symptoms of Uterine Fibroids

• Menorrhagia (heavy menstrual bleeding) - most common symptom (submucous fibroids)
• Dysmenorrhea
• Irregular bleeding
• Postcoital bleeding (if pedunculated submucous)

• Pelvic discomfort, heaviness
• Urinary frequency, urgency, retention (anterior fibroids compressing bladder)
• Constipation (posterior fibroids compressing rectum)
• Backache
• Varicosities (large fibroids)

"Rarely, women may present acutely with pain arising from torsion of a pedunculated fibroid or red degeneration, especially in pregnancy." - Bailey & Love's Short Practice of Surgery

• Infertility (submucosal fibroids most significant)
• Recurrent miscarriage
• Preterm labour
• Malpresentation (in pregnancy)
• Postpartum haemorrhage

"When a submucous leiomyoma becomes pedunculated within the endometrial cavity, the uterus contracts forcefully as if to expel a foreign body and the resulting pain is similar to that of labour." - Berek & Novak's Gynecology

---

Signs

• Enlarged, irregular (lobulated), firm, non-tender uterus on bimanual examination
• Mobile (unless adhesions present)
• Cervical os deviated or displaced
• Large fibroids: palpable abdominally as hard, irregular midline/lateral mass

---

Investigations

---

Differential Diagnosis

• Ovarian tumour (felt separately from uterus on vaginal examination - key differentiating sign)
• Adenomyosis (uterus uniformly enlarged, softer, tender)
• Pregnancy
• Endometrial carcinoma
• Uterine sarcoma (rapid growth, particularly postmenopausally)

---

Management

• Asymptomatic fibroids, approaching menopause
• Annual surveillance ultrasound

"Emergency surgical treatment is only required if there is substantial menstrual bleeding or uncontrollable pain; these are rare events." - Bailey & Love's Short Practice of Surgery

Morcellation risk: Laparoscopic morcellation carries risk of disseminating undiagnosed leiomyosarcoma. Risk increases with age (perimenopausal/postmenopausal), BRCA mutations, Lynch syndrome, and rapidly growing fibroids. - Bailey & Love's Short Practice of Surgery

---

PART III: ENDOMETRIOSIS

---

Definition

"Endometriosis is defined by the presence of endometrial glands and stroma in a location outside the uterus." - Robbins & Kumar Basic Pathology

---

Sites of Involvement

1. Ovaries (most common site) - endometrioma / "chocolate cyst"
2. Pouch of Douglas / rectovaginal septum
3. Uterosacral ligaments
4. Fallopian tubes
5. Bladder and vesico-uterine pouch
6. Bowel (rectosigmoid, appendix)
7. Cervix, vagina, vulva
8. Surgical scars (episiotomy, laparotomy)
9. Distant sites: pleura (catamenial pneumothorax), umbilicus, lungs, bone (rare)

---

Pathogenesis Theories

1. Sampson's Regurgitation / Retrograde Menstruation Theory (most accepted)
   • Endometrial tissue implants at ectopic sites via retrograde flow of menstrual endometrium through the fallopian tube
   • Explains pelvic distribution
2. Benign Metastasis Theory
   • Endometrial tissue spreads to distant sites via blood vessels and lymphatic channels
   • Explains extra-pelvic endometriosis (bone, lung)
3. Coelomic Metaplasia (Meyer's Theory)
   • Endometrium arises directly from coelomic epithelium (pelvic/abdominal mesothelium)
   • Müllerian ducts and ultimately the endometrium originate from coelomic epithelium during embryogenesis
4. Extrauterine Stem/Progenitor Cell Theory
   • Stem/progenitor cells from bone marrow differentiate into endometrial tissue

• Increased prostaglandin E2 (PGE2)
• Elevated VEGF (angiogenesis)
• Matrix metalloproteinases (MMPs) from activated macrophages
• High aromatase activity in endometriotic cells → local oestrogen production from androgens
• Resistance to progesterone action (progesterone resistance)
• Inflammatory microenvironment maintained by recruited macrophages

---

Classification (revised ASRM Classification)

• Superficial peritoneal endometriosis - red/blue/black/white lesions
• Ovarian endometriosis (endometrioma)
• Deep infiltrating endometriosis (DIE) - invades >5 mm; rectovaginal septum, bowel, bladder; highest malignant potential

---

Morphology (Gross Pathology)

"Endometriosis typically consists of functioning endometrium, which undergoes cyclic bleeding. Because blood collects in these aberrant foci, they appear grossly as red-brown nodules or implants, ranging in size from microscopic to 1 to 2 cm in diameter, that lie on or just under the affected serosal surface. When lesions are widespread, organizing hemorrhage can cause extensive fibrous adhesions... The ovaries may become markedly distorted by large cystic masses (3 to 5 cm in diameter) filled with brown fluid resulting from previous hemorrhage; these are referred to as chocolate cysts or endometriomas." - Robbins & Kumar Basic Pathology

---

Symptoms

1. Dysmenorrhoea (secondary, progressive) - begins before menses, peaks at menstruation
2. Dyspareunia (deep dyspareunia - worse in certain positions)
3. Chronic pelvic pain

• Infertility (30-40% of patients)
• Dysuria, haematuria (bladder involvement)
• Dyschezia - painful defaecation (rectovaginal/bowel involvement)
• Rectal bleeding (cyclic haematochezia) - bowel endometriosis
• Catamenial pneumothorax - cyclic chest pain/dyspnoea (pleural endometriosis)
• Fatigue

"Clinical signs and symptoms usually include severe dysmenorrhea, dyspareunia, and pelvic pain due to intrapelvic bleeding and periuterine adhesions. Menstrual irregularities are common, and infertility is the presenting issue for 30% to 40% of patients." - Robbins & Kumar Basic Pathology

---

Signs

• Fixed retroverted uterus (from adhesions obliterating POD)
• Nodularity of uterosacral ligaments and rectovaginal septum (on rectovaginal examination)
• Adnexal mass (endometrioma)
• Restricted uterine mobility
• Tender nodules in posterior fornix/POD
• Normal examination in early/superficial disease

---

Investigations

---

Endometriosis and Acute Abdomen

---

Treatment

"Effective treatments include COX-2 inhibitors and aromatase inhibitors." - Robbins & Kumar Basic Pathology

---

Malignant Transformation

"Although uncommon, malignancies can develop within endometriotic tissue. Risk of malignant transformation is mainly confined to deep infiltrating endometriosis." - Robbins & Kumar Basic Pathology

• Endometriosis-associated ovarian cancer: mainly clear cell carcinoma and endometrioid carcinoma
• Lifetime risk of malignant transformation: ~1%

---

PART IV: POLYCYSTIC OVARY SYNDROME (PCOS)

---

Definition

"PCOS is one of the most common endocrine disorders affecting women with a prevalence between 6% and 10%. The syndrome is characterized by hyperandrogenism, ovulatory dysfunction, and polycystic-appearing ovaries." - Berek & Novak's Gynecology

---

Diagnostic Criteria

"The presence of two of the three criteria is sufficient to diagnose PCOS: menstrual cycle anomalies (amenorrhea, oligomenorrhea), clinical and/or biochemical HA, and/or the ultrasound appearance of polycystic ovaries after all other diagnoses are ruled out." - Berek & Novak's Gynecology

1. HA + ovarian dysfunction + PCO morphology (classic - most severe metabolic risk)
2. HA + ovarian dysfunction (without PCO morphology)
3. HA + PCO morphology (without ovarian dysfunction)
4. Ovarian dysfunction + PCO morphology (without HA - mild phenotype)

---

Polycystic Ovary Morphology on Ultrasound

• ≥12 follicles in each ovary measuring 2-9 mm in diameter
• AND/OR ovarian volume >10 mL (in either ovary)

• ≥20 follicles in each ovary measuring 2-9 mm
• AND/OR ovarian volume >10 mL

---

Pathophysiology

1. Elevated LH → stimulates theca cells → excess androgen (testosterone, androstenedione) production
2. Relative FSH deficiency → impaired follicle development → anovulation → no ovulation → no corpus luteum → no progesterone
3. Peripheral conversion of androgens to oestrone (E1) in adipose tissue → unopposed oestrogen → endometrial stimulation

• Present in 50-70% of PCOS women (obese and non-obese)
• Insulin + LH synergistically stimulate theca cell androgen production
• Insulin inhibits hepatic SHBG synthesis → more free (bioavailable) testosterone
• Compensatory hyperinsulinemia drives excess androgen production

Hyperinsulinism → ↑ androgens → ↑ aromatization in fat → ↑ oestrone → abnormal LH:FSH ratio → ↑ LH → more androgens

• Fasting insulin >25 μIU/mL, total testosterone >150 ng/dL, maximal serum insulin response >300 μIU/mL at 2 hours post-glucose load

---

Clinical Features

• Oligomenorrhoea (cycles >35 days) - most common
• Amenorrhoea (secondary)
• Irregular/unpredictable cycles
• From puberty in most cases

• Hirsutism (~70% in USA; modified Ferriman-Gallwey score ≥8)
• Acne (persistent, adult-onset)
• Male-pattern alopecia (androgenic alopecia)
• Virilisation (clitoromegaly, voice change) - rare; suggests tumour

• Obesity (BMI >30) - 50-60% of PCOS women
• Acanthosis nigricans - thickened, pigmented, velvety skin at nape, axilla, vulva, inner thigh - marker of insulin resistance
• Central (android) fat distribution

• Anovulatory infertility
• Recurrent miscarriage
• Increased risk of complications in pregnancy (GDM, pre-eclampsia)

---

Investigations

• Bilateral polycystic ovary morphology (as above)
• Thickened endometrium (from unopposed oestrogen)

---

Exclusion Diagnoses (Must Rule Out)

---

Long-Term Complications

"In chronic anovulatory patients with PCOS, persistently elevated estrogen levels, which are uninterrupted by progesterone, increase the risk of endometrial carcinoma... Endometrial biopsy should be considered in PCOS patients, because they may occasionally harbor these cancers as early as the second decade of life." - Berek & Novak's Gynecology

---

Management of PCOS

• Weight loss 5-10% → improves all features (menstrual regularity, hyperandrogenism, insulin resistance, fertility)
• Exercise, dietary caloric restriction
• Even in non-obese, lifestyle optimisation improves outcomes

• Combined OCP - first-line; lowers LH, reduces androgens, regulates periods, protects endometrium
• Cyclic progestins (medroxyprogesterone 10 mg × 10-14 days every 1-3 months) - induces withdrawal bleed, protects endometrium
• Levonorgestrel IUS - for menorrhagia and endometrial protection

• Metformin 500-2000 mg/day - improves IR, lowers androgens, restores ovulation
• Screening for T2DM: OGTT (75g) for all obese PCOS and non-obese with risk factors
• Vitamin D supplementation (often deficient in PCOS)
• Statin therapy if dyslipidaemia

---

COMPARISON TABLE: Key Gynaecological Causes of Acute/Chronic Pelvic Pain

---

• Berek & Novak's Gynecology - Acute pelvic pain (Chapter 12), PID/TOA (Chapter 15), Uterine Leiomyomas, PCOS (Chapter 35)
• Robbins & Kumar Basic Pathology - Endometriosis pathogenesis and morphology
• Bailey & Love's Short Practice of Surgery, 28th Edition - Acute abdomen in gynaecology, uterine fibroids, endometriosis
• Creasy & Resnik's Maternal-Fetal Medicine - Clinical management protocols
• Williams Obstetrics and DC Dutta's Textbook of Obstetrics knowledge base - Classification, management principlesThe chapter is complete. Here's what was covered across the four major sections:

---

• Ectopic pregnancy - classic triad, discriminatory zone, methotrexate criteria, surgical options
• Ruptured ovarian cyst - corpus luteum (most common), dermoid/endometrioma (chemical peritonitis), conservative vs surgical management
• Adnexal torsion - "follicular ring sign," whirlpool sign, Doppler flow can be present despite torsion, detorsion preferred over oophorectomy
• PID / TOA - CDC criteria, Fitz-Hugh-Curtis syndrome, ESR/CRP cutoffs for TOA, ruptured TOA as life-threatening emergency

---

NORMAL AND ABNORMAL MENSTRUAL CYCLE

PRIMARY AND SECONDARY AMENORRHEA | MENOPAUSE

A Comprehensive Chapter

---

PART I: THE NORMAL MENSTRUAL CYCLE

---

Definition and Normal Parameters

"A normal menstrual cycle lasts from 21 to 35 days, with 2 to 6 days of flow and an average blood loss of 20 to 60 mL. However, studies of large numbers of women with normal menstrual cycles showed that approximately two-thirds of adult women have cycles lasting 21 to 35 days." - Berek & Novak's Gynecology

"The mean time between menstrual periods is 28 days (±7 days), with menstruation generally lasting for 5 days. It is considered abnormal to bleed for more than 7 days. The average blood loss per menstruation is 35 mL; a loss of more than 80 mL is abnormal." - Rosen's Emergency Medicine

---

The Hypothalamo-Pituitary-Ovarian (HPO) Axis

• Secretes Gonadotropin-Releasing Hormone (GnRH) in a pulsatile fashion
• Pulse frequency: every 60-90 minutes (varies by phase)
• Two feedback centres:
  • Tonic negative feedback centre (basal medial hypothalamus): suppressed by low E2 (follicular phase)
  • Cyclic positive feedback centre (anterior hypothalamus): stimulated by high E2 (pre-ovulatory surge)
• GnRH has a self-priming effect - first dose potentiates subsequent doses

• GnRH stimulates release of FSH and LH (gonadotropins) from gonadotroph cells
• LH response to GnRH increases through the follicular phase, peaks at the preovulatory surge

• FSH drives follicular development → granulosa cells secrete oestradiol (E2) and inhibin B
• LH acts on theca cells → androgen synthesis → aromatised to oestrogen in granulosa cells
• Post-ovulation corpus luteum secretes progesterone, oestradiol, and inhibin A

---

Phases of the Menstrual Cycle

• Ovarian cycle: Follicular phase → Ovulation → Luteal phase
• Endometrial cycle: Menstrual → Proliferative → Secretory (± Premenstrual) phase

---

A. THE FOLLICULAR PHASE (Days 1-14)

1. At the start of the cycle, oestrogen and progesterone are at nadir (corpus luteum from prior cycle has regressed)
2. FSH begins to rise (released from negative feedback) → recruits a cohort of antral follicles
3. Selected follicles secrete increasing E2 as they grow → endometrial proliferation
4. Rising E2 → negative feedback on FSH (FSH begins to fall by mid-follicular phase)
5. Growing follicles also secrete inhibin B → further suppresses FSH
6. LH initially decreases with rising E2, then late in follicular phase shows biphasic response (rises dramatically - positive feedback)
7. One dominant follicle (Graafian follicle) emerges; others undergo atresia
8. FSH-induced LH receptors appear on granulosa cells of dominant follicle → progesterone begins to be secreted (responsible for FSH midcycle surge)

• Triggered when E2 rises above threshold (~200 pg/mL sustained for ≥50 hours)
• Onset of LH surge occurs 16-58 hours before ovulation
• Peak of LH surge: 3-36 hours before ovulation
• LH surge duration: 48-60 hours
• Tietz Textbook of Laboratory Medicine / Berek & Novak's Gynecology

B. OVULATION (Day ~14 in 28-day cycle)

• Triggered by LH surge → resumption of meiosis, follicular rupture
• Ovum (secondary oocyte) released from dominant Graafian follicle
• Occurs 24-36 hours after onset of LH surge
• Prostaglandins facilitate follicular wall rupture
• Heralds transition to luteal-secretory phase

C. THE LUTEAL PHASE (Days 14-28)

• Duration: Fixed at ~14 days (variation in total cycle length is due to variation in follicular phase)
• Ruptured follicle → corpus luteum (granulosa-lutein and theca-lutein cells)
• Corpus luteum secretes:
  • Progesterone (peaks ~Day 21, ~8 days after ovulation) - main product
  • Oestradiol (rises again after initial post-ovulatory dip)
  • Inhibin A
• Progesterone + oestrogen + inhibin A → suppress FSH and LH → prevent new follicular development
• If no pregnancy: corpus luteum degenerates (~Day 24-26) → progesterone and oestrogen fall → endometrial breakdown → menstruation
• If pregnancy occurs: embryonic hCG maintains corpus luteum → sustained progesterone

---

Endometrial Changes During the Cycle

"The endometrium undergoes dynamic physiologic and morphologic changes during the menstrual cycle in response to sex steroid hormones... The histologic appearance of the endometrium may be used to assess hormonal status, document ovulation, and determine causes of endometrial bleeding and infertility." - Robbins, Cotran & Kumar Pathologic Basis of Disease

• Day 17 - Subnuclear vacuoles (earliest sign of secretory change; confirms ovulation)
• Day 22 - Stromal oedema maximum
• Day 23-24 - Spiral arteriole prominence; predecidual change begins
• Day 28 - Maximum predecidual change; menstruation imminent

"At ovulation, endometrial proliferation ceases, and differentiation commences in response to the effects of progesterone made by the corpus luteum... With the dissolution of the corpus luteum and the subsequent drop in progesterone levels, the functionalis layer degenerates and bleeding into the stroma occurs, followed by stromal breakdown and onset of the next menstrual cycle." - Robbins, Cotran & Kumar Pathologic Basis of Disease

---

Mechanism of Menstruation

1. Corpus luteum degenerates → fall in progesterone and oestrogen
2. Endometrial spiral arterioles vasoconstrict (prostaglandin F2α-mediated) → ischaemia of functionalis
3. Prostaglandin E2 then causes vasodilation → blood escapes into stroma
4. Lysosomal enzymes (phospholipases) digest the functionalis
5. Menstrual blood contains: blood, endometrial debris, prostaglandins, tissue enzymes
6. Menstrual blood does not clot (fibrinolytic enzymes in endometrium dissolve clots); large clots suggest excessive bleeding

---

Hormonal Profile Through the Cycle (Summary)

---

PART II: ABNORMAL UTERINE BLEEDING (AUB)

---

Terminology

"The use of the term dysfunctional uterine bleeding is no longer recommended, and the term abnormal uterine bleeding is preferred." - Rosen's Emergency Medicine

---

PALM-COEIN Classification (FIGO 2011)

"Approximately 50% of cases of excessive menstruation fall under the nonstructural PALM-COEIN category of ovulatory dysfunction, which includes anovulatory bleeding. If a woman does not ovulate, there is no corpus luteum to produce progesterone, which results in estrogen being unopposed. Unopposed estrogen causes the endometrium to proliferate to the point at which it becomes unstable and begins to break down, causing irregular and unpredictable bleeding to occur." - Rosen's Emergency Medicine

---

Approach to AUB - Investigations

• Serum β-hCG (exclude pregnancy first)
• FBC (anaemia, thrombocytopenia)
• Coagulation screen + vWF assay if adolescent or history of easy bruising
• Thyroid function (TSH)
• Prolactin
• Pelvic ultrasound (transvaginal preferred)

• Endometrial biopsy (Pipelle) - all postmenopausal AUB, age >45, risk factors for endometrial cancer
• Hysteroscopy + directed biopsy - focal lesions suspected
• MRI pelvis - adenomyosis, fibroids
• SIS (saline infusion sonography) - intrauterine pathology

---

Treatment of AUB

• Endometrial ablation - destruction of functionalis; 80% satisfaction; not suitable if fertility desired
• Myomectomy - fibroids
• Hysterectomy - definitive; for completed family, failed medical treatment

---

PART III: AMENORRHOEA

---

Definitions

"A woman who previously menstruated can develop secondary amenorrhea, which is defined as absence of menstruation for three menstrual cycles or 3 months. A woman with regular cycles and a delay of menses of even a week may warrant assessment with a pregnancy test. It is advisable to evaluate a woman who has fewer than nine cycles per year or cycle length longer than 35 days." - Berek & Novak's Gynecology

"With a few exceptions, the causes of primary amenorrhea are similar to the causes of secondary amenorrhea. Therefore, it is important not to overemphasize a distinction between primary and secondary amenorrhea." - Berek & Novak's Gynecology

---

WHO Classification of Amenorrhoea

---

PRIMARY AMENORRHOEA

Framework

1. Is breast development present? (confirms oestrogen exposure)
2. Is the uterus present?
3. FSH level (hypergonadotropic vs hypogonadotropic)
4. Karyotype if indicated

---

A. PRIMARY AMENORRHOEA WITHOUT SECONDARY SEXUAL CHARACTERISTICS (No breast development)

1. Hypergonadotropic Hypogonadism (High FSH, Low oestrogen)

"Turner syndrome (45,X) and its variants represent the most common form of hypergonadotropic hypogonadism in women with primary amenorrhea... In one series, approximately 30% of patients with primary amenorrhea had an associated karyotypic abnormality." - Berek & Novak's Gynecology

• 17α-hydroxylase deficiency - life-threatening if untreated; hypertension, hypokalemia, no sex steroids; elevated progesterone; diagnosed by ACTH stimulation test
• Aromatase deficiency - cannot convert androgens to oestrogen

2. Hypogonadotropic Hypogonadism (Low FSH, Low oestrogen)

---

B. PRIMARY AMENORRHOEA WITH SECONDARY SEXUAL CHARACTERISTICS (Breast development present - oestrogen present)

1. UTERUS ABSENT → Outflow tract/anatomical cause

"Phenotypic females with complete congenital androgen insensitivity (previously called testicular feminization) have breast development, little or no axillary and pubic hair, and primary amenorrhea... The testes produce müllerian-inhibiting substance that induces the regression of the müllerian structures." - Berek & Novak's Gynecology

2. UTERUS PRESENT → Outflow tract obstruction

• Treatment: surgical incision of hymen; excision of septum

---

Diagnostic Approach to Primary Amenorrhoea

Primary Amenorrhoea
        |
Is breast development present?
    |                          |
   YES                        NO (No oestrogen)
    |                          |
Is uterus present?        Measure FSH
    |          |              |          |
   NO         YES          HIGH         LOW
    |          |              |          |
  AIS/MRKH  Outflow     Gonadal      Hypogonadotropic
  (check      obstruction  dysgenesis    hypogonadism
  karyotype) (imperforate  (Turner,     (Kallmann,
             hymen etc.)  Swyer)       CNS lesion)

---

SECONDARY AMENORRHOEA

Causes by System

1. HYPOTHALAMIC CAUSES (Most common overall)

"Stress, extreme weight loss, anorexia, excessive exercise, and low BMI are all associated with functional hypothalamic suppression, so good nutrition and optimal body weight should be encouraged to restore ovulation." - Berek & Novak's Gynecology

2. PITUITARY CAUSES

• Antipsychotics: phenothiazines, haloperidol, risperidone, clozapine
• Antidepressants: TCAs, MAOIs
• Antihypertensives: methyldopa, reserpine, calcium channel blockers
• Opiates, metoclopramide, H2 blockers
• Oestrogen-containing medications

3. OVARIAN CAUSES

• Idiopathic (30-90%)
• Genetic: FMR1 premutation (fragile X; 13-26% develop POI), Turner mosaics, BMP15 mutation, FOXL2 mutation
• Autoimmune: 20-40% of cases; anti-ovarian antibodies; associated with autoimmune thyroiditis, Addison's disease
• Iatrogenic: radiation, alkylating chemotherapy, bilateral oophorectomy
• Infections: mumps oophoritis (rare)
• Galactosaemia

"POI has been defined as failure of ovarian estrogen production that occurs in a hypergonadotropic state at any age between menarche and 40 years... Autoimmune disorders have been associated with 20 to 40% of cases of POI that result in destruction of the ovary." - Tietz Textbook of Laboratory Medicine

• Serum FSH (>40 IU/L on two occasions ≥4 weeks apart)
• Karyotype if <35 years
• FMR1 premutation screening
• Anti-ovarian antibodies, adrenal antibodies
• DEXA scan (osteoporosis risk)

4. UTERINE / OUTFLOW TRACT CAUSES

"Intrauterine adhesions, referred to as Asherman syndrome, is more common with secondary amenorrhea or hypomenorrhea. Adhesions typically result from endometrial trauma during a surgical procedure, but may also result from..." - Berek & Novak's Gynecology

5. THYROID AND ADRENAL CAUSES

---

Investigation Protocol for Secondary Amenorrhoea

• FSH + LH → differentiate hypergonadotropic vs hypogonadotropic
• Prolactin → exclude hyperprolactinaemia
• TSH → thyroid disease
• E2 (oestradiol) → oestrogen status
• Testosterone + DHEAS → hyperandrogenism

• Give progestogen (medroxyprogesterone 10 mg × 10 days OR norethisterone 5 mg × 5 days)
• Bleed occurs → adequate oestrogen, anovulatory → WHO Group II (PCOS, hyperprolactinaemia)
• No bleed → either low oestrogen OR outflow tract obstruction

• Give combined oestrogen + progestogen cycle
• Bleed occurs → uterus present and functional; cause is low oestrogen (hypothalamic, pituitary, ovarian)
• No bleed → Asherman syndrome (outflow tract)

---

Treatment of Secondary Amenorrhoea

---

PART IV: MENOPAUSE

---

Definitions and Terminology

---

Pathophysiology of Menopause

1. Birth: ~1-2 million primordial follicles
2. Puberty: ~300,000-500,000 follicles
3. Menopause transition: Fewer than 1,000 follicles remain; insufficient to respond to FSH
4. Result: No follicular development → no oestradiol → no negative feedback → FSH and LH rise dramatically

"As estrogen continues to decline, an associated decrease in prolactin concentrations is noted. The decrease in estrogen concentrations gives rise to vasomotor instability and so-called 'hot flashes.'" - Tietz Textbook of Laboratory Medicine

"After menopause, the ovary continues to produce androgens, particularly testosterone and androstenedione, as a result of increased LH concentrations. The resulting decrease in the estrogen/androgen ratio is the cause of the hirsutism seen in some postmenopausal women." - Tietz Textbook of Laboratory Medicine

---

Clinical Features of Menopause

A. VASOMOTOR SYMPTOMS

• Most characteristic symptom; affects ~75-80% of women
• Sudden sensation of heat, flushing, sweating, palpitations; followed by chills
• Duration: 1-5 minutes
• Frequency: several per day to hourly; worse at night (night sweats)
• Mechanism: falling oestrogen → noradrenergic activation → altered central thermoregulatory set-point → inappropriate peripheral vasodilation

"The decline in ovarian function at menopause is associated with vasomotor symptoms in most women. The characteristic hot flashes may alternate with chilly sensations, inappropriate sweating, and (less commonly) paresthesias..." - Goodman & Gilman's Pharmacological Basis of Therapeutics

B. GENITOURINARY SYNDROME OF MENOPAUSE (GSM)

• Vulvovaginal atrophy: Dryness, loss of rugae, pale thin epithelium, loss of elasticity
• Dyspareunia (painful intercourse) - due to vaginal dryness
• Urinary: Urgency, frequency, dysuria, recurrent UTIs (atrophy of urethral epithelium)
• Vaginal pH rises (>5) due to loss of lactobacilli (normal <4.5)
• Unlike vasomotor symptoms, GSM does not improve without treatment

C. PSYCHOLOGICAL/NEUROLOGICAL SYMPTOMS

• Mood changes, irritability, emotional lability
• Sleep disturbances (related to night sweats)
• Cognitive changes ("brain fog") - concentration, memory
• Depression (increased risk perimenopausally)
• Headaches (fluctuating oestrogen)
• Reduced libido

D. LONG-TERM CONSEQUENCES

---

Diagnosis of Menopause

"In general, menopause may be diagnosed in women over the age of 45 on the basis of menstrual history and age without relying on laboratory test results, although serum FSH values may be helpful." - Tietz Textbook of Laboratory Medicine

• Clinical: 12 consecutive months of amenorrhoea without other cause in appropriate age group
• Biochemical: FSH >40 IU/L (on two occasions, 4-6 weeks apart) + E2 <30 pg/mL
• Important: In women on combined OCP or HRT, FSH may be suppressed - cannot use for diagnosis while on these medications
• Perimenopausal hCG can be falsely mildly elevated - FSH >45 IU/L makes pregnancy unlikely

---

Hormone Replacement Therapy (HRT / MHT)

Indications

1. Vasomotor symptoms (primary indication) - most effective treatment
2. Genitourinary syndrome of menopause (local oestrogen highly effective)
3. Prevention of osteoporosis (reduces fracture risk)
4. Premature menopause / POI - strongly indicated until natural age of menopause (~51 years)
5. Cardiovascular benefit (if started early - "timing hypothesis")

"In general, the benefits of HRT before age 60 or within 10 years of menopause are considered to outweigh the risks associated with treatment." - Tietz Textbook of Laboratory Medicine

Types of HRT

Routes of Administration

Benefits and Risks

• Vasomotor symptom relief (~90%)
• Prevention and treatment of osteoporosis (reduces vertebral fracture by ~40%, hip fracture by ~25%)
• Relief of GSM
• Cardiovascular protection if started within 10 years of menopause ("timing/window hypothesis" - based on WHI re-analysis)
• Modest reduction in colorectal cancer risk (combined HRT)
• Possible reduction in cognitive decline if started early

• Personal history of breast cancer
• Personal history of endometrial cancer (relative)
• Active or recent thromboembolic disease
• Active liver disease
• Unexplained vaginal bleeding (investigate first)
• Oestrogen-dependent tumours

"HRT consisting of estrogen alone (ET) is associated with an increased risk of endometrial cancer and is contraindicated in women with an intact uterus... Because of the increased risk of uterine cancer associated with ET, HRT consisting of estrogen and a progestogen (EPT) is indicated in women with an intact uterus, but it is recommended that these women limit their duration of therapy because the risk of breast cancer increases after 3 to 5 years of EPT treatment." - Tietz Textbook of Laboratory Medicine

Non-Hormonal Alternatives for Vasomotor Symptoms

---

SUMMARY TABLES

Normal Menstrual Cycle Parameters

Amenorrhoea - Diagnostic Approach

Menopause Summary

---

• Berek & Novak's Gynecology - Menstrual cycle, primary and secondary amenorrhoea (Chapters 7, 34)
• Robbins, Cotran & Kumar Pathologic Basis of Disease - Endometrial histology, menstrual cycle pathology
• Tietz Textbook of Laboratory Medicine, 7th Edition - Hormonal profiles, menopause, AUB
• Rosen's Emergency Medicine - PALM-COEIN AUB classification
• Goodman & Gilman's Pharmacological Basis of Therapeutics - Vasomotor symptoms, HRT pharmacology
• Costanzo Physiology - HPO axis, menstrual cycle events
• Williams Obstetrics and DC Dutta's Textbook of Obstetrics and Gynecology knowledge base - Clinical framework throughoutThe chapter is complete. Here's a quick orientation:

---

• Primary amenorrhoea: Turner syndrome, Swyer syndrome, Kallmann (anosmia), MRKH, Complete AIS (AIS vs MRKH differentiating table), imperforate hymen - all with diagnostic algorithms
• Secondary amenorrhoea: WHO 4-group classification, systematic causes (hypothalamic FHA, Sheehan syndrome, prolactinoma, Asherman syndrome, POI with FMR1/autoimmune causes), progestogen withdrawal test interpretation, full investigation protocol