Anaesthesia for Obstetrics

Obstetric anaesthesia is a perennial NEET PG favourite because it weaves together altered maternal physiology, two patients (mother and foetus), and the two most lethal anaesthetic emergencies in pregnancy — failed intubation and aspiration (Mendelson syndrome). Master the physiological shifts first; almost every clinical decision flows from them.

Physiological changes of pregnancy relevant to anaesthesia

Pregnancy alters nearly every system, and these changes directly modify drug dosing, airway management, and haemodynamics under anaesthesia.

System	Change	Anaesthetic implication
Airway	Mucosal oedema, capillary engorgement, large breasts, weight gain, full dentition	Difficult mask ventilation & intubation; use smaller ETT (6.0–7.0 mm); avoid nasal instrumentation (epistaxis)
Respiratory	↑ Minute ventilation 50%, ↑ tidal volume, ↓ FRC 20%, ↑ O₂ consumption 20%	Rapid desaturation on apnoea; chronic compensated respiratory alkalosis (PaCO₂ ~30 mmHg)
Cardiovascular	↑ Cardiac output 40–50%, ↑ blood volume 40%, ↑ plasma > RBC mass	Physiological (dilutional) anaemia; aortocaval compression supine
Haematological	Hypercoagulable (↑ fibrinogen, factors VII–X)	↑ VTE risk; affects neuraxial timing if anticoagulated
GI	↓ Lower oesophageal sphincter tone, ↑ intragastric pressure, gastrin from placenta	High aspiration risk — treat all as full stomach from ~18–20 weeks
Renal/Hepatic	↑ GFR, ↓ plasma cholinesterase (~25%)	Altered drug clearance; suxamethonium action only mildly prolonged (rarely clinically significant)
CNS/Neuraxial	↑ Sensitivity to local anaesthetics, engorged epidural veins, ↓ epidural & CSF volume	Reduce neuraxial LA dose by ~30%; ↑ MAC requirement falls ~30%

High-yield: FRC falls while oxygen consumption rises — the pregnant patient desaturates dramatically faster during apnoea. This is why pre-oxygenation (denitrogenation) before any general anaesthetic in obstetrics is mandatory and non-negotiable.

High-yield: MAC (minimum alveolar concentration) of volatile agents is reduced by about 30% in pregnancy (progesterone, endorphins). Over-deepening causes uterine relaxation and hypotension.

Aortocaval compression (supine hypotension syndrome)

After ~20 weeks the gravid uterus compresses the IVC (and aorta) when supine, reducing venous return → ↓ cardiac output → hypotension, nausea, foetal distress.

Prevention: Left uterine displacement — 15° left lateral tilt or a wedge under the right hip. This applies during caesarean, neuraxial block, and resuscitation.

High-yield: During maternal CPR, manual left uterine displacement is preferred (rather than full lateral tilt) so effective chest compressions can continue. Plan perimortem caesarean within 4 minutes if no ROSC ("4-minute rule"), delivery by 5 minutes.

Analgesia for labour

Labour pain pathways are examinable:

• First stage (cervical dilatation, uterine contraction): visceral, T10–L1.
• Second stage (perineal distension via pudendal nerve): somatic, S2–S4.

**Stepwise options → ** Non-pharmacological → systemic opioids (pethidine, fentanyl, remifentanil PCA) → inhalational Entonox (50% N₂O + 50% O₂) → lumbar epidural / combined spinal-epidural (CSE) — the gold standard.

High-yield: Epidural analgesia is the most effective method of labour analgesia. It does not increase the caesarean section rate but may modestly prolong the second stage and increase instrumental delivery.

A low-concentration LA + opioid mix (e.g. 0.0625–0.1% bupivacaine/ropivacaine + fentanyl) gives a "walking epidural" — analgesia with preserved motor power.

Anaesthesia for caesarean section

Neuraxial vs general anaesthesia

Regional (neuraxial) is preferred for the vast majority of caesareans because it avoids airway manipulation, lowers aspiration risk, gives a more alert mother, allows skin-to-skin bonding, and reduces neonatal drug exposure and maternal mortality.

Feature	Spinal (subarachnoid)	Epidural	General anaesthesia
Onset	Fast (2–5 min)	Slow (15–20 min)	Fastest
Typical use	Elective & most emergency LSCS	Labour analgesia → top-up, or titration in cardiac disease	Failed/contraindicated neuraxial, crash LSCS, coagulopathy, maternal refusal
Drug volume	Small (hyperbaric bupivacaine 0.5% ~1.6–2.5 mL + opioid)	Large	—
Block quality	Dense, reliable	Slower, titratable	Complete
Hypotension	Marked, sudden	Gradual	Less neuraxial-type
Target level	T4 (nipple line) sensory block	T4	—

High-yield: The required sensory block height for caesarean is T4 (to cover peritoneal traction). Test with cold/pinprick; a block "to the nipple" is the classic teaching point.

High-yield: Single-shot spinal is the technique of choice for elective and most category emergency caesareans — rapid, dense, reliable, minimal foetal drug transfer.

Spinal additives: intrathecal fentanyl (10–25 µg) improves intra-op quality; intrathecal/preservative-free morphine (~100 µg) gives prolonged post-op analgesia (watch delayed respiratory depression).

Mnemonic — absolute contraindications to neuraxial block

"PISCES": Patient refusal, Infection at site, Severe hypovolaemia/shock, Coagulopathy/anticoagulation, Elevated ICP, Stenotic valvular lesions (relative — severe aortic stenosis) / raised intracranial pressure.

Spinal-induced hypotension and its prevention

This is one of the single most tested obstetric anaesthesia topics. Sympathetic blockade + aortocaval compression → maternal hypotension → reduced uteroplacental perfusion → foetal acidosis.

**Prevention/treatment bundle → ** Left uterine displacement + IV co-load (crystalloid/colloid given with the block, more effective than pre-load) + prophylactic vasopressor infusion.

High-yield: Phenylephrine is now the vasopressor of choice for spinal hypotension at caesarean. As a pure α₁-agonist it best maintains maternal BP and foetal acid–base status (higher umbilical artery pH).

High-yield: Ephedrine (mixed α/β) crosses the placenta, increases foetal metabolic rate, and is associated with lower umbilical artery pH (foetal acidosis) — so it is now second-line, reserved for bradycardia + hypotension. Phenylephrine causes reflex maternal bradycardia.

Vasopressor	Mechanism	Effect on foetal pH	NEET role
Phenylephrine	Pure α₁	Best preserved	First line
Ephedrine	α + β	Lowers (acidosis)	Use if maternal bradycardia coexists
Noradrenaline	α >> β	Comparable to phenylephrine, less bradycardia	Emerging alternative

General anaesthesia in obstetrics — and its dangers

When GA is unavoidable (crash caesarean, coagulopathy, failed block, massive haemorrhage), the two killers dominate the exam.

**Rapid sequence induction (RSI) sequence → ** Aspiration prophylaxis → positioning with left tilt → pre-oxygenation 3 min / 8 vital-capacity breaths → pre-induction of propofol/thiopentone + suxamethonium → cricoid pressure (Sellick) → intubate with cuffed ETT → confirm with capnography → maintain with volatile + O₂/N₂O → extubate awake, on the side.

High-yield: Induction-to-delivery and uterine incision-to-delivery (U-D) intervals matter: a prolonged U–D interval (>180 s) correlates with foetal acidosis and lower Apgar regardless of technique.

Aspiration prophylaxis ("full stomach")

• Non-particulate antacid: 0.3 M sodium citrate (immediate ↑ gastric pH).
• H₂ blocker: ranitidine (now famotidine) — slower, reduces volume & acidity.
• Prokinetic: metoclopramide — ↑ gastric emptying, ↑ LOS tone.

High-yield: Mendelson syndrome = chemical aspiration pneumonitis from acidic gastric contents; danger threshold classically gastric volume >25 mL and pH <2.5. Particulate antacids are avoided — give clear non-particulate sodium citrate.

Failed intubation drill

Obstetric airways are the classic difficult airway. A failed obstetric intubation is an emergency with a defined plan.

**Failed intubation algorithm → ** Call for help → maintain cricoid + oxygenate by facemask/SAD (2nd-gen LMA, e.g. ProSeal/i-gel) → if oxygenation adequate and surgery urgent for maternal/foetal life, may proceed via LMA; otherwise wake the mother → "can't intubate, can't oxygenate" (CICO) → front-of-neck access (cricothyroidotomy).

High-yield: The cornerstone decision after failed obstetric intubation is "wake or proceed", driven by maternal oxygenation and urgency. Maternal safety (oxygenation) always takes priority over the foetus.

Drugs, placental transfer, and the neonate

Placental transfer follows passive diffusion — favoured by low molecular weight, high lipid solubility, low protein binding, and non-ionisation.

Drug	Crosses placenta?	Note
Induction agents (thiopentone, propofol)	Yes (lipophilic)	Single induction dose well tolerated by neonate
Suxamethonium	Negligible	Highly ionised, large dose needed for foetal effect → safe
Non-depolarising relaxants	Negligible	Quaternary, ionised → do not affect neonate
Opioids (pethidine, fentanyl, morphine)	Yes	Neonatal respiratory depression
Heparin	No	Large, polar → anticoagulant of choice in pregnancy
Warfarin	Yes	Teratogenic — avoid
Local anaesthetics	Yes (esp. lignocaine)	Bupivacaine highly protein-bound → least transfer, but most cardiotoxic to mother

High-yield: Pethidine (meperidine) given in labour causes neonatal respiratory depression; its active metabolite norpethidine has a long half-life (~60 h in neonate). Reverse neonatal opioid depression with naloxone (never give naloxone to the neonate of an opioid-dependent mother — precipitates withdrawal/seizures).

High-yield: Bupivacaine is the most cardiotoxic local anaesthetic; accidental IV injection causes refractory ventricular arrhythmias. Treat Local Anaesthetic Systemic Toxicity (LAST) with 20% Intralipid (lipid emulsion) "lipid rescue" plus standard resuscitation. Avoid the 0.75% concentration in obstetrics (historic FDA warning).

Specific high-yield obstetric emergencies

Pre-eclampsia / eclampsia

• Drug of choice for seizure prophylaxis & treatment: magnesium sulphate (loading then infusion).
• **MgSO₄ toxicity sequence → ** loss of deep tendon reflexes (first sign, ~4 mmol/L) → respiratory depression → cardiac arrest. Antidote: IV calcium gluconate. Monitor patellar reflex, RR, urine output.
• Mg potentiates non-depolarising neuromuscular blockers → reduce relaxant dose.
• Antihypertensives: labetalol, hydralazine, nifedipine. Neuraxial preferred if platelets adequate (usually >75–80 ×10⁹/L and no rapidly falling count/coagulopathy).

High-yield: In severe pre-eclampsia, regional anaesthesia is preferred over GA — GA risks a dangerous pressor (hypertensive) response to laryngoscopy → intracerebral haemorrhage, plus airway oedema makes intubation harder. Obtund the pressor response (opioid/labetalol/lignocaine) if GA is unavoidable.

Amniotic fluid embolism (AFE)

Sudden cardiovascular collapse, hypoxia, and DIC during labour/immediately postpartum. Diagnosis is clinical/of exclusion; management is supportive (oxygenation, circulatory support, treat DIC). High mortality.

Postpartum haemorrhage (PPH)

• Uterine atony is the commonest cause. Drug ladder: oxytocin (first line) → ergometrine (avoid in hypertension/pre-eclampsia) → carboprost (15-methyl PGF₂α) (avoid in asthma) → misoprostol → tranexamic acid.

Recently asked / exam angle

• Vasopressor of choice for spinal hypotension at caesarean → phenylephrine (ephedrine causes foetal acidosis / lower umbilical pH). Repeatedly tested.
• Required sensory block level for caesarean → T4.
• MAC change in pregnancy → decreased ~30%.
• FRC in pregnancy → decreased ~20% (with rapid desaturation) — a favourite physiology one-liner.
• Aspiration prophylaxis agent that raises pH immediately → sodium citrate (non-particulate).
• Mendelson syndrome thresholds → volume >25 mL, pH <2.5.
• Antidote to MgSO₄ toxicity → calcium gluconate; first sign → loss of deep tendon reflexes.
• LAST treatment → 20% lipid emulsion (Intralipid).
• Most cardiotoxic LA → bupivacaine; least placental transfer → bupivacaine (high protein binding) — a frequent "trick" pairing.
• Pethidine metabolite causing prolonged neonatal effect → norpethidine.
• Perimortem caesarean timing → within ~4 minutes of arrest.
• Preferred technique for elective LSCS → single-shot spinal; preferred in severe pre-eclampsia → neuraxial over GA.
• Post-dural puncture headache (PDPH): postural (worse upright), frontal/occipital, after dural breach (more with larger/cutting needles). Treatment of choice if conservative measures fail → epidural blood patch. Use pencil-point (Whitacre/Sprotte) atraumatic needles to reduce incidence.

Rapid revision

1. Treat every pregnant patient from ~18–20 weeks as a full stomach — RSI with cricoid pressure for GA.
2. FRC ↓, O₂ consumption ↑ → fast desaturation → always pre-oxygenate.
3. MAC of volatiles ↓ ~30%; reduce neuraxial LA dose ~30% (engorged epidural veins, ↓ CSF volume).
4. Left uterine displacement / 15° left tilt prevents aortocaval compression from 20 weeks.
5. T4 block required for caesarean; single-shot spinal is the technique of choice.
6. Phenylephrine = vasopressor of choice for spinal hypotension; ephedrine → foetal acidosis.
7. Co-loading with fluids beats pre-loading for preventing spinal hypotension.
8. Aspiration prophylaxis: sodium citrate + ranitidine/famotidine + metoclopramide; Mendelson threshold >25 mL, pH <2.5.
9. Bupivacaine = most cardiotoxic LA, least placental transfer; lipid emulsion rescues LAST.
10. Suxamethonium and non-depolarising relaxants do NOT cross the placenta; opioids do → neonatal respiratory depression (reverse with naloxone).
11. Severe pre-eclampsia → prefer regional; GA risks pressor response → ICH; MgSO₄ for seizures, calcium gluconate antidote.
12. Failed obstetric intubation → oxygenate via 2nd-gen LMA, decide "wake or proceed"; maternal oxygenation > foetus.