Anaesthetics and labour analgesia
Local and general anaesthetics; epidural and spinal analgesia in labour
Local and general anaesthetics for FCPS Part 1: mechanism, doses, toxicity, epidural and spinal anatomy, and neuraxial complications in labour. Also covers general anaesthesia in pregnancy, placental transfer, muscle relaxants and malignant hyperthermia.
One of the most tested topics in past papers
How local anaesthetics work
- They block voltage-gated Na+ channels from inside the axon. They are weak bases: the un-ionised form crosses the membrane and the ionised form blocks the channel.
- Acidic (infected) tissue ionises the drug; bicarbonate speeds onset.
- pKa sets onset, lipid solubility potency, protein binding duration. Bupivacaine has the highest protein binding (about 95%) and the longest action.
- Differential block: thin and myelinated fibres need a lower concentration to block, so as the drug dilutes away from the injection site only thin fibres are blocked. Order: sympathetic (B), then pain and temperature (A-delta, C), then touch, then motor (A-alpha). The sympathetic level lies about two segments above the cold-sensation level and the motor level about two below. Cold is tested before surgery, because touch underestimates the block.
- Adrenaline slows absorption, prolonging action and allowing a higher dose. Cocaine itself vasoconstricts; ropivacaine has some intrinsic vasoconstrictor action at low concentration.
- Percentage to dose: x% = 10x mg/mL, so 2% lidocaine is 20 mg/mL. Adrenaline 1:100,000 = 10 micrograms/mL.
| Group | Examples | Metabolism | Notes |
|---|---|---|---|
| Esters | Procaine, cocaine, benzocaine, chloroprocaine | Plasma cholinesterase | PABA metabolite causes true allergy more often |
| Amides (two letter i) | Lidocaine, bupivacaine, prilocaine, ropivacaine | Liver | Prilocaine: methaemoglobinaemia, used for Bier's block |
| Agent | Maximum dose | Key point | |
| Lidocaine | 3 mg/kg plain, 7 mg/kg with adrenaline | Rapid onset, intermediate duration | |
| Bupivacaine | 2 mg/kg | Longest acting, most cardiotoxic; never for Bier's block | |
| Levobupivacaine, ropivacaine | Similar | Pure S-enantiomers: less cardiotoxic, less motor block, so preferred |
Systemic toxicity
- CNS first: perioral tingling, metallic taste, tinnitus, light-headedness, slurred speech, then seizures; then arrhythmia and arrest. Perioral tingling is the earliest sign of lidocaine toxicity, usually from accidental intravascular injection.
- Bupivacaine binds cardiac Na+ channels tightly: broad-complex arrhythmia, ventricular fibrillation and resistant cardiac arrest.
- Treat with airway, oxygen, a benzodiazepine for fits and 20% lipid emulsion.
- At term alpha-1 acid glycoprotein falls, raising the free fraction of bupivacaine.
- In an acidotic fetus local anaesthetic ionises and is trapped.
Neuraxial anatomy
- Midline layers: skin, subcutaneous tissue, supraspinous ligament, interspinous ligament, ligamentum flavum (the last ligament pierced before the epidural space, felt as loss of resistance). In the paramedian approach the needle bypasses the supraspinous and interspinous ligaments, but the ligamentum flavum is still the last.
- A spinal needle goes on through dura and arachnoid into the subarachnoid space (CSF).
- The epidural space runs from the foramen magnum to the sacral hiatus, is widest in the lumbar region (about 5–6 mm at L2) and holds fat and the valveless internal vertebral venous plexus.
- In pregnancy the engorged epidural venous plexus reduces CSF volume, so about a third less drug gives the same spinal height, and catheters enter veins more often. Lying supine worsens the engorgement.
Epidural and spinal analgesia in labour and caesarean section
- Labour needs block of T10–L1 (first stage) and S2–S4 (second stage). A pudendal block (S2–S4) is given near the ischial spine.
- Epidural fentanyl acts on dorsal horn mu receptors and is synergistic with local anaesthetic, so 0.1% bupivacaine suffices: good analgesia with little motor block, so women can move and push.
- Spinal heavy bupivacaine (in glucose) is denser than CSF and spreads with gravity. Caesarean section needs a block to T4.
- Hypotension is the commonest complication: sympathetic block causes vasodilatation, worsened by aortocaval compression; treat with tilt, fluids and phenylephrine. Uterine blood flow is not autoregulated.
- Also: urinary retention, shivering, opioid pruritus, Horner syndrome, and epidural haematoma if platelets are low (about 45 x 10^9/L rules it out).
- Intrathecal or epidural morphine is hydrophilic, spreads up the CSF and causes delayed respiratory depression (up to 12–24 hours); lipid-soluble fentanyl stays near the site.
- Test dose: 3 mL of 2% lidocaine through an epidural catheter producing rapid dense motor block and warm numb legs within minutes means the tip is subarachnoid; tachycardia or tinnitus means a vein. A full top-up through an unrecognised intrathecal catheter causes a total spinal (apnoea from C3–C5 block).
Post-dural puncture headache
- CSF leaks through the dural hole, the brain sags and pain-sensitive structures stretch; headache is worse on sitting, better lying flat.
- A pencil-point (Whitacre, Sprotte) needle parts the dural fibres rather than cutting them, leaving a smaller hole that closes; a large epidural needle puncture carries the highest risk.
- Abducent nerve (VI) palsy, with horizontal diplopia, is the commonest cranial nerve lesion because its long intracranial course over the petrous apex is stretched as the brain sags.
- Treat with an epidural blood patch. A headache with hypertension needs pre-eclampsia excluded.
General anaesthesia in pregnancy
- Airway mucosa is oedematous; smaller tube, avoid the nose.
- Aspiration (Mendelson syndrome): worst when pH below 2.5 and volume above 25 mL. 0.3 M sodium citrate (30 mL) is chosen because it is clear, non-particulate and acts at once; particulate antacids (magnesium trisilicate) cause pneumonitis if aspirated. It lasts only 20–30 minutes, so it is given just before induction, with an H2 blocker or PPI and rapid sequence induction.
- MAC falls 25–40% because progesterone lowers anaesthetic requirement; awareness at caesarean section is still relatively common. Volatiles cause dose-related uterine relaxation.
- Placental transfer: induction agents, opioids and volatiles cross. Quaternary (charged) neuromuscular blockers such as rocuronium and suxamethonium barely cross, so the baby is not paralysed.
- Fetal protection from propofol: umbilical venous blood passes first through the fetal liver, and via the ductus venosus mixes with IVC blood carrying no drug, so the drug is diluted before reaching the brain. Long induction-to-delivery intervals overcome this.
- Magnesium sulphate potentiates non-depolarising blockers (less acetylcholine release, less end-plate sensitivity): prolonged fade on train-of-four. Sugammadex also binds progestogens.
- Remifentanil PCA for labour (when epidural is contraindicated): ultra-short acting because non-specific tissue and plasma esterases hydrolyse it; apnoea risk needs saturation monitoring.
General anaesthetic agents and relaxants
| Agent | Key facts |
|---|---|
| Thiopental | Offset by redistribution; hypotension from venodilatation and myocardial depression with reflex tachycardia; avoid in porphyria |
| Propofol | Fast recovery, anti-emetic; hypotension |
| Ketamine | Dissociative, analgesic, raises BP, HR, intracranial and intraocular pressure, bronchodilator |
| Nitrous oxide | Analgesic, weak anaesthetic; expands air spaces; inactivates vitamin B12 |
| Suxamethonium | Depolarising, fastest onset; hyperkalaemia after burns or crush; prolonged apnoea with plasma cholinesterase deficiency |
| Rocuronium | Non-depolarising; high dose gives rapid intubating conditions when suxamethonium is contraindicated; reversed by sugammadex |
- Malignant hyperthermia (volatiles, suxamethonium): autosomal dominant ryanodine receptor defect. A patient whose relative died under anaesthesia should not receive suxamethonium or volatile agents; use total intravenous anaesthesia. Treat with dantrolene.
- Entonox (50% N2O, 50% O2): start at the onset of a contraction. Pethidine: norpethidine causes fits, MAOI interaction, neonatal respiratory depression; it was traditionally preferred to morphine as it causes less smooth muscle (biliary) spasm.
Remember Loss of resistance at the ligamentum flavum marks the epidural space; a spinal needle goes on through dura and arachnoid.
Exam trap Hypotension, not headache, is the commonest complication of neuraxial block.
Exam trap Bupivacaine is the most cardiotoxic local anaesthetic; prilocaine, not bupivacaine, is used for Bier's block.
How FCPS asks about this
- Fibres blocked first by local anaesthetic: thin B and C fibres (sympathetic, pain) before motor.
- Ligament pierced last in an epidural (midline or paramedian): ligamentum flavum.
- Epidural opioid causing delayed respiratory depression: morphine (hydrophilic).
- Earliest sign of lidocaine toxicity: perioral tingling, light-headedness, tinnitus.
- Bupivacaine toxicity: resistant ventricular arrhythmias and cardiac arrest; treat with lipid emulsion.
- Prolonged apnoea after suxamethonium: plasma cholinesterase deficiency.
- Why the baby is not paralysed at GA caesarean: quaternary relaxants barely cross the placenta.
Test yourself on this topic
5 of the 60 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
After a spinal anaesthetic in labour, the mother's systolic BP falls to 80 mmHg for four minutes. The CTG shows a fetal bradycardia that recovers once her BP is restored. Why is the fetus so sensitive to the maternal BP?
Answer: Uterine blood flow is not autoregulated
The spiral arteries are remodelled by trophoblast into wide, low-resistance channels with little smooth muscle, so uteroplacental flow cannot autoregulate. Flow is directly proportional to maternal perfusion pressure. A fall in maternal BP therefore reduces intervillous perfusion and fetal oxygen supply at once, causing fetal bradycardia. Restoring maternal BP restores flow.
Uteroplacental perfusion
- Remodelled spiral arteries
- No autoregulation
- Flow follows maternal BP
- Hypotension: fetal bradycardia
Remember Mother's pressure is the baby's pressure.
Exam trap Uterine vessels are already maximally dilated, so vasodilators cannot improve flow during hypotension.
Why the other options are wrong
- The fetal heart lacks a vagal supply The fetal heart has vagal innervation; vagal responses cause decelerations.
- The spinal drug crosses to the fetus Spinal doses give negligible fetal drug levels.
- Maternal oxygen saturation falls A spinal does not lower maternal saturation.
- Fetal haemoglobin gives up oxygen poorly HbF holds oxygen tightly but this does not explain the pressure dependence.
A labouring woman with a lidocaine epidural has a fetus whose scalp blood pH is 7.10. After delivery the fetal-to-maternal ratio of lidocaine is higher than in babies born with a normal pH. What explains this?
Answer: Ion trapping in acidotic fetal blood
Lidocaine is a weak base (pKa about 7.9). The un-ionised form crosses the placenta. In acidotic fetal blood more of it becomes ionised, and ionised drug cannot cross back, so it accumulates in the fetus. This ion trapping raises fetal levels of local anaesthetics and opioids when the fetus is acidotic. Fetal protein binding is actually lower than maternal, and there is no active placental transport.
Ion trapping
- Local anaesthetics are weak bases
- Un-ionised form crosses placenta
- In acidic fetal blood it ionises
- Ionised drug is trapped in fetus
Remember Acidotic fetus traps basic drugs.
Exam trap The same mechanism traps weak bases in breast milk, which is slightly more acidic than plasma.
Why the other options are wrong
- Lower fetal hepatic blood flow Hepatic flow does not explain the pH-related difference.
- Higher protein binding in fetal plasma Fetal plasma binds local anaesthetics less than maternal plasma.
- Active transport of lidocaine by placenta Lidocaine crosses by passive diffusion.
- Slower fetal renal excretion Renal excretion is too slow to matter acutely.
After several top-ups of her labour epidural, a woman develops a small right pupil and mild drooping of the right upper eyelid, with no limb weakness. The signs fade when the infusion is reduced. Which structures has the local anaesthetic reached?
Answer: Preganglionic sympathetic fibres at T1–T2
This is Horner syndrome from high spread of the epidural. Sympathetic supply to the eye begins as preganglionic fibres leaving the cord at T1 (and T2) in the ventral roots, which ascend to the superior cervical ganglion. Cephalad spread of local anaesthetic in the epidural space blocks these fibres, causing miosis and partial ptosis. It is usually harmless and resolves as the block recedes.
Horner syndrome after epidural
- High spread to T1–T2 roots
- Blocks preganglionic sympathetics
- Miosis and partial ptosis
- Usually benign; reduce the infusion
Remember Small pupil means the block has climbed high.
Exam trap Horner syndrome warns of high spread, so check for arm weakness and breathing difficulty.
Why the other options are wrong
- Cervical sympathetic chain in the neck An epidural does not reach the neck tissues; it blocks the roots at their origin.
- Oculomotor nerve in the cavernous sinus Oculomotor palsy gives a dilated pupil and complete ptosis.
- Ciliary ganglion in the orbit Ciliary ganglion block gives a dilated pupil.
- Edinger–Westphal nucleus in the midbrain This is parasympathetic; its loss would dilate the pupil.
Two hours after a caesarean section under spinal anaesthesia with intrathecal morphine, a woman has intense itching of her face and upper trunk. There is no rash, wheal or wheeze. What is the mechanism of the itching?
Answer: Central mu-opioid receptor activation
Pruritus is the commonest side effect of neuraxial opioids. Spread of opioid in the CSF activates mu receptors in the dorsal horn and the trigeminal nucleus, which explains the facial distribution. It is not a histamine or allergic effect and responds poorly to antihistamines, but is relieved by low-dose naloxone or a mixed agonist-antagonist such as nalbuphine, which reverse the itch while sparing much of the analgesia.
Neuraxial opioid itch
- Commonest side effect of intrathecal opioid
- Central mu receptors, trigeminal nucleus
- Face, neck, upper trunk
- Treat: low-dose naloxone or nalbuphine
Remember Spinal opioid itch is central, not histamine.
Exam trap Antihistamines may only help by sedation; they do not treat the cause.
Why the other options are wrong
- Histamine release from skin mast cells Histamine release causes flushing or wheals after IV morphine, not this facial itch.
- IgE-mediated allergy to morphine There are no features of allergy.
- Retention of bile salts in the skin Bile salts cause the itch of cholestasis, not this acute pattern.
- Allergy to the local anaesthetic Amide local anaesthetic allergy is very rare and would cause rash or wheeze.
A labour epidural is topped up with 15 mL of 0.5% bupivacaine for an emergency caesarean section. Within minutes the woman has weak hands, a weak voice and then stops breathing. Block of which nerve roots stops her breathing?
Answer: C3 to C5
This is a high or total spinal, usually because the catheter has migrated into the subarachnoid space. Local anaesthetic spreading up the CSF blocks the cervical roots: weak hands indicate C6 to T1, and apnoea follows when the phrenic nerve roots (C3, C4, C5) supplying the diaphragm are blocked. Intercostal (T1 to T11) block alone reduces breathing but does not cause apnoea while the diaphragm works.
Total spinal
- Spread of drug up the CSF
- Weak hands: C6–T1 blocked
- Apnoea: phrenic C3–C5 blocked
- Treat: airway, ventilation, vasopressors
Remember C3, 4, 5 keep the diaphragm alive.
Exam trap Consciousness may be lost from brainstem spread or low perfusion; the mother is not under general anaesthesia and needs sedation once ventilated.
Why the other options are wrong
- T1 to T6 Intercostal paralysis weakens breathing, but the diaphragm keeps her breathing.
- T7 to T12 Lower intercostal and abdominal muscles are not essential for quiet breathing.
- C6 to C8 These roots explain weak hands, not apnoea.
- L1 to L3 Lumbar roots supply the legs.
Where this sits in the CPSP syllabus
- Obstetrics & Gynaecology, Paper 2: Drugs in obstetrics and gynaecology, Local and general anaesthetics; epidural and spinal analgesia in labour
Read next
Drug dose pages
Doses, cautions and practical tips for drugs in this chapter.