Local Anaesthetic Systemic Toxicity (LAST)

Quick Answer

Local anaesthetic systemic toxicity (LAST) is a life-threatening emergency occurring when local anaesthetics enter systemic circulation, causing CNS and cardiovascular toxicity. Incidence: 0.1-0.3% of peripheral nerve blocks, 0.01-0.02% of epidurals. Pathophysiology: Sodium channel blockade in CNS (seizures, coma) and myocardium (conduction block, negative inotropy); bupivacaine most cardiotoxic due to strong binding and long dissociation from sodium channels. Clinical phases: Prodromal (tinnitus, perioral numbness, metallic taste, visual disturbances, agitation—CNS excitation), seizure activity (generalized tonic-clonic, then CNS depression/coma), cardiovascular collapse (hypotension, arrhythmias—bupivacaine/ropivacaine cause refractory VT/VF), cardiac arrest (PEA or asystole). Risk factors: Injection into vascular tissue (injection pain), high doses, intravascular injection (negative aspiration not 100% sensitive), rapid absorption (intercostal, caudal), low protein binding (pregnancy, elderly), metabolic impairment (liver/renal failure), cardiac disease (reduced tolerance). Prevention: Aspirate before injection, test dose 3-5 mL with adrenaline (tachycardia indicates IV placement), incremental dosing, ultrasound guidance (reduces volume needed, allows visualization of vessels), total dose limits, careful patient selection. Immediate management: Stop injection, call for help, airway management with 100% oxygen, seizure control (benzodiazepines preferred—midazolam 2-5 mg IV, avoid propofol/high-dose barbiturates which worsen cardiovascular depression), cardiovascular support (fluids, vasopressors—phenylephrine, adrenaline; standard ACLS), LIPID EMULSION (20% Intralipid)—cornerstone of treatment: bolus 1.5 mL/kg (100 mL/70 kg) over 1 minute, then infusion 0.25 mL/kg/min (approximately 18 mL/min for 70 kg), repeat bolus if cardiovascular collapse, continue infusion until hemodynamic stability; lipid emulsion acts as "lipid sink" sequestering lipophilic local anaesthetics, also provides fatty acid substrate for myocardial energy. Refractory arrest: Continue CPR, repeated lipid emulsion boluses, prolonged resuscitation may be successful (bupivacaine-induced arrest may require >60-90 minutes CPR before return of circulation). Arrhythmia management: Avoid amiodarone/procainamide (class I antiarrhythmics add to sodium channel blockade); bretylium historically used but unavailable; standard ACLS with emphasis on lipid emulsion. Post-resuscitation: ICU admission, monitoring for recurrent toxicity (rebound as local anaesthetic redistributes), neurological assessment. Documentation and reporting: Incident reporting, patient follow-up, allergy clinic referral. ANZCA guidelines: Immediate availability of lipid emulsion in all sites performing regional anaesthesia; regular training in LAST recognition and management. Indigenous populations: No specific differences in LAST risk; standard protocols apply. [1-10]