📚 Antenatal Obstetric Complications - Key Points

1. VTE in Pregnancy - Diagnosis & Treatment

Diagnosis of DVT

• Clinical diagnosis of VTE is unreliable - always investigate promptly
• Symptoms: calf pain, redness, swelling - but legs are normally swollen in pregnancy, so unilateral symptoms = red flag
• Always ask about PE symptoms - a woman with PE may first present with DVT
• First investigation: Compression ultrasound (high sensitivity/specificity for proximal thrombosis)
• Calf vein thrombus alone rarely causes PE
• Venography = invasive (contrast + X-ray) but gives excellent visualization above and below the knee

Diagnosis of PE

• Most common presentation: mild breathlessness or inspiratory chest pain, mild tachycardia (>90 bpm), mild pyrexia (37.5°C)
• Investigations: ECG, chest X-ray, arterial blood gases (insufficient alone to diagnose/exclude)
• Also investigate lower limbs for DVT by ultrasound
• If tests normal but high clinical suspicion: V/Q scan or CTPA
• D-dimer: useful screening in non-pregnant women (high negative predictive value), but elevated physiologically in pregnancy - limited clinical use as a screening test

Treatment of VTE

• Warfarin: NOT recommended in pregnancy
  • Crosses placenta
  • Causes limb and facial defects (1st trimester)
  • Causes fetal intracerebral haemorrhage (2nd and 3rd trimesters)
  • Exception: women with mechanical heart valves
• LMWHs (Low Molecular Weight Heparins) = treatment of choice
  • Do not cross placenta
  • At least as safe and effective as UFH
  • Fewer haemorrhagic complications
  • Women self-inject and continue for the pregnancy duration
• Post-delivery: can switch to warfarin or stay on LMWH; both safe in breastfeeding
• Newer anticoagulants (fondaparinux, lepirudin): NOT licensed in pregnancy
• Graduated elastic stockings: use for initial DVT treatment; wear for 2 years to prevent post-thrombotic syndrome

Key Points - VTE Prevention

• Screen for thrombophilias in those with strong family/personal history of VTE
• Start treatment while awaiting diagnosis
• LMWHs = treatment of choice
• Compression stockings for 2 years post-DVT

2. Substance Abuse in Pregnancy

General

• ~1/3 of adults accessing drug services are women of reproductive age
• ~6,000 births/year in the UK to problem drug users
• Multidisciplinary care essential (financial, psychological, social problems often greater than physical)

Problems in Drug Addicts

• Social: housing, crime, children in care
• Coexistent addictions: alcohol, smoking
• Malnutrition: especially iron, vitamins B and C
• Risk of viral infections: HIV, hepatitis B
• Specific fetal and neonatal risks

Opioid Use (Heroin)

• Most commonly used; often combined with cocaine, amphetamines, benzodiazepines, cannabis
• Do NOT reduce opiate dose rapidly in pregnancy
• Sudden detoxification ("cold turkey") = dangerous, especially in 3rd trimester - causes fetal stress, distress, stillbirth
• Principle: administer lowest effective dose of methadone liquid in 3 divided doses/day
• Screen for hepatitis B and HIV routinely
• Multidisciplinary case conferences needed for delivery planning

3. Oligohydramnios & Polyhydramnios

Amniotic Fluid Basics

• Produced almost exclusively from fetal urine from 2nd trimester onwards
• Functions: protects from pressure/trauma, allows limb movement (postural development), enables fetal lung expansion

Oligohydramnios

• Defined as AFI < 5th centile for gestation
• AFI = sum of deepest vertical pool in all 4 abdominal quadrants (ultrasound)
• May be suspected if: clear fluid leaking from vagina, fetal poles feel hard and obvious, small-for-dates uterus

• Prognosis depends on cause; pulmonary hypoplasia and limb deformities common in severe early-onset (<24 weeks) oligohydramnios
• Renal agenesis / bilateral multicystic kidneys = lethal (life impossible without kidneys)

Polyhydramnios

• Defined as AFI > 95th centile
• Presentation: severe abdominal swelling/discomfort, abdomen distended out of proportion to gestation (increased SFH), tense/tender abdomen, fetal poles hard to palpate

• Maternal: Diabetes, placental (chorioangioma, arteriovenous fistula)
• Fetal: Multiple gestation (TTTS), idiopathic, oesophageal/duodenal atresia, TOF fistula, neuromuscular condition, anencephaly

• Establish cause, relieve discomfort (amniodrainage), assess preterm labour risk
• Polyhydramnios from maternal diabetes: correct glycaemic control first - fluid should correct itself
• Twin-to-twin transfusion syndrome (TTTS): recipient sac gets polyhydramnios, donor sac gets oligohydramnios - rapidly fatal; treat with amniodrainage or laser ablation of placental vascular connections

4. Fetal Malpresentation at Term

Breech Presentation

• Malpresentation = not cephalic
• Breech occurs in 3-4% of term pregnancies
• Three types:
  1. Extended (Frank) breech - commonest (hips flexed, knees extended)
  2. Flexed (Complete) breech - hips and knees flexed
  3. Footling breech - foot presents first (cord and foot prolapse risks)

Predisposing Factors for Breech

• Maternal: fibroids, uterine abnormalities (bicornuate), previous uterine surgery
• Fetal/placental: multiple gestation, prematurity, placenta praevia, fetal abnormality (anencephaly, hydrocephalus), neuromuscular condition, oligo/polyhydramnios

Antenatal Management of Breech

• Confirm at 36 weeks with ultrasound (check AFI, placental site, biometry, fetal leg position, any anomalies)
• Three management options:
  1. ECV (External Cephalic Version)
  2. Vaginal breech delivery
  3. Elective caesarean section - evidence suggests this is the best method for term breech singleton

5. External Cephalic Version (ECV)

• Reduces caesarean sections due to breech
• Success rate ~50% (higher in multiparous women)
• Performed at ≥37 completed weeks by experienced obstetrician at/near delivery facilities
• Use tocolytic (e.g. nifedipine) - improves success rate
• Woman positioned: flat with left lateral tilt, bladder emptied
• Fetal heart rate trace before and after procedure
• Give anti-D if rhesus negative
• Duration: ≤10 minutes; abandoned if difficult

Contraindications to ECV

• Fetal abnormality (e.g. hydrocephalus)
• Placenta praevia
• Oligohydramnios or polyhydramnios
• History of antepartum haemorrhage
• Previous caesarean or myomectomy scar
• Multiple gestation
• Pre-eclampsia or hypertension
• Already planned caesarean section

Risks of ECV

• Placental abruption
• Premature rupture of membranes
• Cord accident
• Transplacental haemorrhage (give anti-D to rhesus-negative women)
• Fetal bradycardia

6. Vaginal Breech Delivery

Pre-requisites (Feto-maternal)

• Presentation: extended (frank) OR flexed breech
• No evidence of feto-pelvic disproportion; estimated fetal weight <3,500 g
• No fetal head hyperextension; no abnormalities precluding safe vaginal delivery

Management of Labour

• Careful monitoring of fetal wellbeing and progress
• Epidural analgesia: optional but advantageous (prevents premature pushing)
• Fetal blood sampling from buttocks for acid-base assessment
• Experienced operator must be available

Delivery Technique ("Masterly Inactivity" = hands-off)

• Buttocks: episiotomy only when anus seen over fourchette
• Legs: flexed = deliver spontaneously; extended = use Pinard's manoeuvre
• Shoulders: allow natural rotation; Loveset's manoeuvre copies natural rocking movements to deliver arms
• Head: Mauriceau-Smellie-Veit manoeuvre - finger in mouth + one on each maxilla, downward then upward traction; if fails, use forceps (assistant holds baby up while forceps applied)

Key Complication

• Baby getting "stuck" - do not pull; do not rush; interference paradoxically increases obstruction risk

7. Other Fetal Malpresentations

Transverse Lie

• Fetal long axis perpendicular to maternal long axis = shoulder presentation
• Oblique lie: fetal axis at ~45° to maternal axis
• Both at risk of cord prolapse on membrane rupture
• Diagnosis: asymmetrical abdomen on inspection, SFH less than expected, head/buttocks in iliac fossa, empty pelvis on palpation
• Cannot deliver vaginally (except very preterm/small babies)
• Unstable lie at term = admit to antenatal ward; deliver by caesarean if not cephalic in early labour or if membranes rupture spontaneously
• In multiparous women: unstable lie often corrects itself in early labour if membranes intact

8. Post-term Pregnancy

• Defined as ≥42 weeks' gestation
• Affects ~10% of all pregnancies; aetiology unknown
• Accurate dating essential (first-trimester crown-rump length ultrasound)
• Associated with: increased risk of stillbirth and perinatal death, increased risk of prolonged labour and caesarean section
• Two strategies to reduce adverse outcome: fetal surveillance and induction of labour

Exam tip: The bold/underlined items in the book are the highest-yield facts - focus on LMWH for VTE, AFI cut-offs for amniotic fluid disorders, ECV contraindications/risks, and the three manoeuvres for vaginal breech delivery (Pinard's, Loveset's, Mauriceau-Smellie-Veit).

📚 Antenatal Obstetric Complications - Key Points (Pages 96-102)

1. Post-term Pregnancy (continued) & Antepartum Haemorrhage

When to Induce Immediately Post-dates

• Reduced amniotic fluid on scan
• Reduced fetal growth
• Reduced fetal movements
• Abnormal/non-perfect CTG
• Mother is hypertensive or has a significant medical condition

Key Counselling Point

• No test can guarantee baby's safety beyond 42 weeks
• Perinatal mortality is at least doubled beyond 42 weeks
• Post-term labour more likely to need caesarean section (uterus reluctant to contract properly)

2. Vaginal Bleeding in Pregnancy (Antepartum Haemorrhage - APH)

Definitions

• Bleeding < 24 weeks = threatened miscarriage
• Bleeding from 24 weeks to delivery = Antepartum Haemorrhage (APH)
• Incidence of APH = 3%; causes: 1% placenta praevia, 1% placental abruption, 1% other causes

Causes of APH

• Placental abruption
• Placenta praevia
• Vasa praevia

• Cervicitis
• Cervical ectropion
• Cervical carcinoma
• Vaginal trauma
• Vaginal infection

History to Take

• How much bleeding?
• Triggering factors (e.g. postcoital bleed)?
• Associated with pain or contractions?
• Is the baby moving?
• Last cervical smear (date/normal or abnormal)?

Examination

• Pulse, blood pressure
• Is the uterus soft or tender and firm?
• Fetal heart auscultation/CTG
• Speculum vaginal examination - particularly to visualize cervix and confirm placenta is not praevia (use portable ultrasound)
• Never perform digital vaginal examination until placenta praevia is excluded

Investigations

• Full blood count, clotting; if suspected praevia/abruption: cross-match 6 units of blood
• Ultrasound: fetal size, presentation, amniotic fluid, placental position and morphology

Management

• Minimal bleeding with clearly local cause: symptomatic management (e.g. antifungal for candidiasis), as long as cervical carcinoma excluded
• Significant APH: see Chapter 14 (Obstetric emergencies)
• APH must always be taken seriously - a pale, tachycardic woman with a painful, firm abdomen and reduced fetal movements = emergency (possible placental abruption)

3. Rhesus Isoimmunization

The Basics

• Blood groups: ABO system (O, A, B, AB) + Rhesus system (C, D, E antigens)
• D antigen = most clinically important rhesus antigen
• Mismatch between fetus and mother → fetal red cells cross to maternal circulation → maternal sensitization → Haemolytic Disease of the Fetus and Newborn (HDFN)
• Rhesus system most commonly associated with severe haemolytic disease

How Rhesus Disease Develops (3 Stages)

1. Rhesus-negative mother conceives rhesus-positive baby
2. Fetal cells enter maternal circulation in sufficient volume → maternal antibody response
3. Maternal antibodies cross placenta → immune destruction of fetal red cells

First vs. Subsequent Pregnancies

• First pregnancy: primary response is weak - mainly IgM antibodies that do NOT cross the placenta → no disease
• Subsequent pregnancy with rhesus-positive baby: re-sensitization → B-cells produce IgG antibodies that DO cross the placenta → fetal haemolysis → severe anaemia → fetal death if untreated
• Disease gets worse with successive pregnancies

Prevalence

• D-rhesus negativity = 15% of UK Caucasian population (lower in other ethnic groups)
• ~55% of UK Caucasian males are heterozygous for D antigen → ~two-thirds of rhesus-negative mothers expected to carry a rhesus-positive fetus

Potential Sensitizing Events

• Miscarriage
• Termination of pregnancy
• Antepartum haemorrhage
• Invasive prenatal testing (CVS, amniocentesis, cordocentesis)
• Delivery

4. Preventing Rhesus Isoimmunization

Anti-D Immunoglobulin

• Given intramuscularly to rhesus-negative mothers
• "Mops up" circulating rhesus-positive fetal cells before the immune response is triggered
• Must be given as soon as possible after a sensitizing event, within 72 hours

Dose Protocol by Gestation

Kleihauer Test

• Tests maternal blood to determine the proportion of fetal cells in maternal circulation
• Relies on fetal red cells' resistance to denaturation by alcohol/acid
• Calculates size of feto-maternal transfusion and amount of extra anti-D Ig required

Routine Antenatal Prophylaxis (RAADP)

• All unsensitized rhesus-negative women should be offered anti-D prophylaxis:
  • Single dose at 28 weeks, OR
  • Two doses at 28 and 34 weeks

5. Signs of Fetal Anaemia (from Rhesus Disease)

• Polyhydramnios
• Enlarged fetal heart
• Ascites and pericardial effusions
• Hyperdynamic fetal circulation - detected by Doppler (increased velocities in middle cerebral artery or aorta)
• Reduced fetal movements
• Abnormal CTG with reduced variability → eventually a sinusoidal trace

Note: Features not obvious unless fetal haemoglobin is <6 g/dl

6. Management of Rhesus Disease in a Sensitized Woman

Monitoring

• Monitor antibody levels every 2-4 weeks from booking
• Use IU/ml method (more clinically relevant than titre)

• Once antibodies rise: assess for fetal anaemia using MCA (Middle Cerebral Artery) Doppler - peak velocity correlates reliably with fetal anaemia; sensitivity ~100%
• Invasive monitoring (amniotic fluid bilirubin) is now replaced by non-invasive MCA Doppler

Treatment Options for Fetal Anaemia

• Delivery (if fetus sufficiently mature)
• Intrauterine fetal blood transfusion (if too premature to deliver)
  • Life-saving for severely anaemic premature fetus
  • Restores haemoglobin levels; prevents hydrops/death
  • Side-effect: suppresses fetal erythropoiesis

Routes of Fetal Transfusion

1. Umbilical vein at cord insertion (preferred - ideally through amniotic sac, NOT through placenta)
2. Intrahepatic vein
3. Peritoneal cavity (less effective but useful in early gestations)
4. Fetal heart

Transfused Blood Specifications

• RhD negative
• Crossmatched with maternal sample
• Densely packed (Hb ~30 g/l) - small volumes
• White cell depleted and irradiated
• Screened for infection including CMV

At Delivery

• Neonatologist must be present if baby is anaemic or has had multiple transfusions
• Cord blood taken at delivery for: blood count, blood group, indirect Coombs test
• Blood ready for possible exchange transfusion

7. ABO Incompatibility

• Occurs when mother is blood group O and baby is A or B
• Anti-A and anti-B antibodies naturally present in maternal circulation (secondary to sensitization against food/bacteria)
• ABO incompatibility can occur in the first pregnancy (unlike rhesus disease)
• However: most anti-A and anti-B antibodies are IgM → do NOT cross the placenta
• A and B antigens are not fully developed in the fetus
• Result: generally only mild haemolytic disease - may cause unexpected jaundice in an otherwise healthy term infant

8. New Developments

• Cell-free fetal DNA (cffDNA) from maternal blood samples (between 16-20 weeks) can determine fetal rhesus genotype non-invasively with ~100% accuracy
• This allows selective use of anti-D (avoiding prophylaxis in the ~40% of rhesus-negative women carrying a rhesus-negative fetus)
• Routine fetal rhesus typing from maternal blood has been introduced in Denmark and Netherlands; not yet recommended in the UK

Key Learning Points Summary

• Rhesus disease gets worse with successive pregnancies
• If the father is rhesus negative → fetus cannot be rhesus positive → no risk
• If father is rhesus positive and heterozygous → 50% chance baby is positive; if homozygous → 100% chance
• Anti-D is only prophylaxis - useless once sensitization has occurred
• Invasive prenatal testing (CVS, amniocentesis) may boost antibody levels in already sensitized women → avoid where possible