Local Anaesthetics

Local anaesthetics are drugs that temporarily and reversibly block nerve conduction in a defined area, removing sensation (and at higher doses, movement) without putting the patient to sleep. In orthopaedics they are everywhere: infiltrating a wound, performing a digital block, doing a haematoma block for a wrist fracture, providing a peripheral nerve block for postoperative pain, and as part of spinal anaesthesia for lower-limb surgery.

For the exam, three threads run through this topic. The first is how they work - blocking sodium channels and the chemistry that decides onset, potency, and duration. The second is how to use them safely - the two drug classes, the use of adrenaline, and above all the maximum safe dose. The third is what goes wrong - recognising and treating local anaesthetic systemic toxicity before it becomes a fatal cardiac arrest. Get those three right and you can answer almost any question on this subject.

A nerve fires by letting sodium ions rush in through voltage-gated channels, which produces the action potential. Local anaesthetics enter the nerve and plug these sodium channels from the inside, so the action potential cannot rise and the message stops. The block is reversible: as the drug washes away, the channels reopen and the nerve recovers.

To reach the inside of the nerve, the drug must first cross the fatty nerve membrane. Each molecule exists in two forms - an unionised (lipid-soluble) form that crosses the membrane, and an ionised (charged) form that actually blocks the channel once inside. The balance between the two depends on the drug's pKa and the surrounding pH, which explains several exam favourites.

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Nerve fibres are not all blocked at once. Small, thin pain and autonomic fibres are blocked first, then touch and temperature, and the large motor fibres last. This differential block is why a patient may be pain-free yet still able to move a little, and it is a neat point to mention in a viva.

Every local anaesthetic is either an amide or an ester, decided by the chemical link in the middle of the molecule. The distinction matters for metabolism and for allergy.

The maximum safe dose is the highest-yield practical point in this topic. Doses are by body weight, and you must convert the concentration to milligrams first.

LAST occurs when the blood level of local anaesthetic rises high enough to poison the brain and heart. It usually follows accidental intravascular injection or simply giving too large a dose. It is the emergency every user of these drugs must be able to recognise and treat.

Classic teaching is that central nervous system signs come first, but cardiovascular collapse can be the first sign, especially with bupivacaine. Prevention is better than cure: use the lowest effective dose, aspirate before injecting, inject slowly in small increments, and use ultrasound guidance to see the needle and avoid vessels.

Local anaesthetics touch nearly every part of orthopaedic practice. In the emergency department you use them for haematoma blocks to reduce a Colles' fracture, for digital blocks, and for wound infiltration. In theatre they appear in peripheral nerve blocks, periarticular infiltration after joint replacement, and spinal anaesthesia. On the ward they underpin multimodal, opioid-sparing pain relief. The exam tests this breadth in several ways: a basic-science viva on mechanism and the amide-versus-ester distinction, a safety question on calculating the maximum dose, and a CIM or clinical scenario on recognising and treating LAST. Knowing the mechanism, the safe dose, and the emergency lets you answer confidently and, more importantly, practise safely.

• Major guidelines (for example the American Society of Regional Anesthesia and Pain Medicine, and the Association of Anaesthetists in the UK) agree on the core safety message: calculate the maximum dose, aspirate and inject incrementally, use ultrasound guidance where possible, and keep intravenous lipid emulsion 20 percent immediately available wherever local anaesthetics are used.
• Where guidance differs is mostly in the small print of LAST treatment - the exact lipid emulsion bolus and infusion regimen and the maximum cumulative dose vary slightly between national protocols, so candidates are expected to follow their local protocol rather than memorise a single set of numbers.
• Maximum-dose figures quoted in textbooks vary modestly between countries and formularies; the safe approach is to know the commonly cited adult values (lignocaine 3 mg/kg, with adrenaline 7 mg/kg, bupivacaine 2 mg/kg) and to reduce them in vulnerable patients.
• Global practice variation reflects drug availability and cost more than disagreement on principle - long-acting and liposomal preparations are used selectively, and registry and trial evidence has tempered early enthusiasm for liposomal bupivacaine where it offers little over standard agents within a multimodal pathway.