Local anaesthetics - overview, pharmacology and emergency practice
This section summarises practical pharmacology, choice of agents, safety and emergency management of local anaesthetics (LAs) as used in the emergency department (ED). It emphasises ED‑focused governance and recognition/management of Local Anaesthetic Systemic Toxicity (LAST).
National guidance referenced: RCEM procedural sedation and pharmacological agent guidance, Resuscitation Council UK LAST recommendations, NICE interventional guidance where tumescent techniques are used, and GOV.UK advice on topical ocular anaesthetics.
How local anaesthetics work (brief pharmacology)
Local anaesthetics reversibly block voltage‑gated sodium channels in nerve membranes, preventing action‑potential propagation and therefore sensory transmission (including pain). Their clinical onset, potency and duration are principally determined by:
- Lipid solubility - increased lipid solubility increases potency and duration.
- Protein binding - greater protein binding increases duration.
- pKa relative to local pH - a higher fraction of non‑ionised (free base) drug at physiological pH produces a faster onset.
- Concentration and total dose at the nerve.
- Addition of vasoconstrictor (usually adrenaline) - reduces vascular uptake and prolongs block.
Most LAs are supplied as hydrochloride salts for water solubility; the membrane‑penetrating form is the non‑ionised free base.
Chemical classes: esters vs amides
- Esters (procaine, benzocaine, tetracaine): hydrolysed by plasma/tissue esterases → short acting; metabolite p‑aminobenzoic acid (PABA) can cause allergic reactions. Commonly used topically.