Before infiltrating a groin hernia repair under local anaesthesia in an 80 kg man, the registrar calculates maximum doses and rehearses toxicity management. Which account of local anaesthetic pharmacology is correct?
- ALocal anaesthetics have no maximum dose provided injection is slow
- BA 1% solution contains 1 mg/mL
- CSodium-channel blockade; lidocaine 3 mg/kg plain, 7 mg/kg with adrenaline (1% = 10 mg/mL); toxicity moves from tingling to seizures, treated with 20% lipid emulsion
- DBupivacaine is the least cardiotoxic agent and therefore the safest choice for intravenous regional anaesthesia
- ELipid emulsion has no role in local anaesthetic toxicity
Show answer and explanation
Correct answer: C
Local anaesthetic pharmacology is arithmetic plus an emergency drill, and both are examinable. Mechanism: weak bases crossing the membrane un-ionised, then blocking voltage-gated sodium channels from within — smaller and myelinated fibres first (pain and temperature before touch and motor), and inflamed acidic tissue resisting (the ionised fraction rises — why abscess infiltration works poorly). Arithmetic: concentration to mass — a 1% solution is 10 mg/mL (0.25% = 2.5 mg/mL) — then dose to weight: lidocaine ~3 mg/kg plain (240 mg for 80 kg: 24 mL of 1%) and ~7 mg/kg with adrenaline 1:200,000, the vasoconstrictor slowing systemic absorption, prolonging block and reducing bleeding (traditional caution in digits, nose and penis persists in exams); bupivacaine ~2 mg/kg (longer-acting, motor-sparing at low concentrations — the wound-infiltration workhorse) with the crucial caveat of its cardiotoxicity: avid, slowly reversible cardiac sodium-channel binding means ventricular arrhythmia and arrest can PRECEDE neurological warning, why it is absolutely contraindicated in intravenous regional anaesthesia (Bier's block — prilocaine's territory) and why levobupivacaine exists. Toxicity (LAST) usually follows inadvertent intravascular injection or cumulative overdose: perioral paraesthesia, metallic taste, tinnitus, agitation → seizures → conduction block, arrhythmia, collapse. The drill: stop injecting, call for help, airway and 100% oxygen, benzodiazepines for seizures, ALS modified (avoid lidocaine as an anti-arrhythmic; prolonged resuscitation justified) — and the specific antidote: 20% lipid emulsion (Intralipid) bolus 1.5 mL/kg then infusion per AAGBI guideline, the 'lipid sink' every theatre and ED must stock and every surgeon infiltrating must know. Prevention completes it: aspirate before injecting, incremental dosing, know the running total across field blocks and infiltration.
Why the others are wrong: A, B, D and E — maxima are real and weight-based; 1% = 10 mg/mL; bupivacaine is the MOST cardiotoxic and banned from Bier's block; lipid emulsion is the rescue.
Key point: Sodium-channel blockers with hard ceilings — lidocaine 3 (plain)/7 (with adrenaline) mg/kg, bupivacaine 2 mg/kg, 1% = 10 mg/mL — LAST runs mouth-tingling → seizures → bupivacaine's early cardiac arrest, and the answer is stop, support, and 20% lipid emulsion by protocol.
Guidelines: AAGBI safety guideline on local anaesthetic systemic toxicity: calculate maximum doses before infiltration (lidocaine 3 mg/kg, 7 mg/kg with adrenaline; bupivacaine 2 mg/kg), and treat toxicity with immediate cessation, airway support and intravenous lipid emulsion per the published protocol.