Classify local anaesthetics. Describe their mechanism of action, techniques of use and systemic toxicity.

Definition and Mechanism

The drug is a weak base, supplied as an acidic hydrochloride salt → In tissue at pH 7.4, part converts to the unionised, lipid-soluble form → Only the unionised form crosses the axonal membrane → Inside the axon it re-ionises to the cationic form → The cation binds the voltage-gated sodium channel from the inside → Sodium influx is blocked → no depolarisation → conduction fails → Binding is greatest to open and inactivated channels — hence use-dependent (frequency-dependent) block: rapidly firing fibres are blocked preferentially

Classification

Order of Blockade and Techniques

• Fibres are blocked in order of increasing size and myelination — autonomic (B) → pain and temperature (C and A-delta) → touch → pressure → motor (A-alpha); recovery is in the reverse order
• This is why a patient still feels touch and pressure after pain has gone, and must be reassured that they will feel movement but not pain
• Techniques — surface (topical); infiltration; field block; nerve block (including brachial plexus); intravenous regional (Bier block); spinal (subarachnoid); and epidural
• Spinal against epidural — spinal uses a small dose into cerebrospinal fluid below L1 with rapid dense block and a risk of post-dural-puncture headache; epidural uses a larger dose into the epidural space, has slower onset, allows a catheter for continuous infusion, and is widely used for labour analgesia

Adrenaline with Local Anaesthetics

• Usually 1:200,000. It causes vasoconstriction, which (1) prolongs the block, (2) reduces systemic absorption and so toxicity, (3) allows a larger maximum dose, and (4) provides a bloodless field
• Never use adrenaline in end-artery territories — fingers, toes, nose, ears and penis — where vasoconstriction risks ischaemic necrosis
• Avoid in patients with ischaemic heart disease, uncontrolled hypertension, thyrotoxicosis, and those on tricyclic antidepressants or MAO inhibitors

Systemic Toxicity

Excessive dose, or inadvertent intravascular injection → Early CNS excitation — because inhibitory neurons are blocked first: perioral tingling and numbness of the tongue, metallic taste, tinnitus, light-headedness, visual disturbance, restlessness, muscle twitching → convulsions → CNS depression — unconsciousness, respiratory arrest → cardiovascular collapse — myocardial depression, arrhythmia, asystole; occurs at a higher dose than the CNS effects for most agents, but with bupivacaine the cardiac and CNS thresholds are close, and resuscitation is notoriously difficult

• Management — stop the injection; airway, oxygen and ventilation; benzodiazepine for seizures; standard resuscitation; and intravenous lipid emulsion ("lipid rescue"), which acts as a "lipid sink" drawing the drug out of cardiac tissue — it has produced dramatic recoveries from bupivacaine cardiotoxicity
• Prevention is everything — calculate the maximum dose by weight, aspirate before every injection, inject slowly in divided doses, and maintain verbal contact with the patient so that early CNS symptoms are noticed

Comparison of Spinal and Epidural Anaesthesia

Applied Aspects

• Know the maximum safe doses — lignocaine 3 mg/kg plain and 7 mg/kg with adrenaline; bupivacaine 2 mg/kg. Overdose in children is a recognised cause of death and follows from failing to calculate by weight
• Always check whether the ampoule contains adrenaline before a ring block
• Resuscitation equipment and lipid emulsion must be immediately available wherever regional anaesthesia is performed
• True allergy is rare and almost always to an ester or to the preservative methylparaben; a patient labelled "allergic to lignocaine" usually had a vasovagal reaction or an adrenaline effect, and can often be safely tested
• Local anaesthesia is safe, cheap and underused in India — a great deal of minor surgery can be done under local or regional block without the cost and risk of general anaesthesia
• Methaemoglobinaemia from prilocaine or benzocaine presents with cyanosis unresponsive to oxygen and a normal arterial oxygen tension; treated with methylene blue
• Warm the solution and buffer with bicarbonate to reduce the sting of infiltration, and inject slowly through a fine needle
• Spinal anaesthesia causes sympathetic blockade with hypotension and bradycardia, which is anticipated with fluid preloading and vasopressors rather than treated after the event
• Post-dural-puncture headache is postural, worse on sitting up, and treated with fluids, caffeine, analgesia and, if persistent, an epidural blood patch; a fine pencil-point needle reduces the incidence
• Cauda equina syndrome is a rare but devastating complication of excessive or maldistributed spinal anaesthetic, and is the reason continuous spinal microcatheters were withdrawn
• Regional anaesthesia is contraindicated over infected skin, in coagulopathy or on anticoagulants, in raised intracranial pressure, and where the patient refuses
• Epidural haematoma is the feared complication in an anticoagulated patient, and specific time intervals must be observed between the last dose and needle insertion or catheter removal
• Lignocaine is also an antiarrhythmic, and the same sodium channel blockade underlies both actions — a useful reminder that a drug’s mechanism, not its label, predicts what it does
• Topical anaesthesia of the airway abolishes protective reflexes, so the patient must not eat or drink until they return, or aspiration follows
• Ultrasound guidance has transformed nerve blocks, improving success rates and reducing both the dose needed and the risk of intravascular injection
• Never leave a patient alone after a regional block; toxicity may appear several minutes after injection as absorption continues