Anaesthetic emergencies

Local anaesthetic systemic toxicity (LAST)

Overview and approach

Systemic local-anaesthetic toxicity can cause neurological symptoms, seizures and cardiovascular collapse.

  • ANZCA advises that 20% lipid emulsion be immediately available wherever potentially toxic volumes of local anaesthetic are used1.
  • Usually caused by accidental intravascular injection or rapid absorption from vascular sites, such as intercostal blocks or mucous membranes5. Toxicity can occur some time after the initial injection2.
  • Maximum doses (guide only): lignocaine 3 mg/kg plain5; lignocaine 7 mg/kg with adrenaline6; bupivacaine 2 mg/kg5; prilocaine 6 mg/kg5. Product information says these are a guide only, and the safe dose may be substantially lower in patients with acute or chronic disease6.
  • 1 mL of 1% lignocaine = 10 mg5.
  • Why the brain signs come in that order: local anaesthetic first depresses inhibitory pathways in the cortex, leaving excitatory pathways unopposed, so twitching and seizures appear. Higher levels then cause generalised CNS depression7.
  • Cardiotoxicity: local anaesthetics block cardiac as well as nerve sodium channels. Bupivacaine is the most cardiotoxic of the common agents: arrhythmias can occur at about two-thirds of the dose that causes seizures, and arrest can occur without hypoxia or acidosis. Levobupivacaine and ropivacaine are only modestly safer7.
  • Which patients clear the drug slowly: amides are metabolised in the liver, so liver disease, heart failure and low liver blood flow (including during volatile anaesthesia) raise the risk. The half-life of lidocaine can rise from about 1.6 hours to over 6 hours in severe liver disease. Esters accumulate with atypical plasma cholinesterase7.

What pushes blood levels or toxicity up7.

FactorEffect
Injection sitePeak levels highest after intercostal blocks, then caudal and epidural, then brachial plexus; lowest after sciatic or femoral blocks and subcutaneous infiltration
Accidental intravascular injectionBypasses absorption entirely; maximum-dose rules give no protection
Slow metabolismLiver disease, heart failure, reduced liver blood flow (amides); atypical plasma cholinesterase (esters)
Hypoxia and acidosisMake toxicity worse at the same blood level
Added adrenalineSlows absorption and lowers the peak level (protective)
Assessment and clinical features

Recognise symptoms during/after injection, stop administration and call emergency help.

  • Early (CNS excitation): circumoral or tongue numbness, light-headedness, tinnitus, visual disturbance, slurred speech, restlessness, shivering, muscle twitching or tremor. Hypertension and tachycardia may occur early4,5.
  • Severe: sudden change in mental state, severe agitation or loss of consciousness, with or without tonic-clonic seizures2.
  • Cardiovascular: sinus bradycardia, conduction blocks, asystole and ventricular tachyarrhythmias. Cardiotoxicity can occur rapidly with little warning2,6.
  • The textbook sequence often fails: in a review of reported cardiac toxicity cases, CNS warning signs came first in only about 18%. Under general anaesthesia or a propofol infusion, cardiovascular collapse may be the first sign7.
  • Early symptoms of rising levels include circumoral and tongue numbness and a metallic taste, then nystagmus and muscle twitching before tonic-clonic seizures7.
Differentials and investigations

ABCDE, ECG and specialist/resuscitation assessment; presentations may be delayed or predominantly cardiovascular.

  • Consider drawing blood for analysis, but do not delay definitive treatment2.
  • Acidosis and hypoxia increase the risk and severity of toxicity, so ventilate well. Hyperventilation may help when there is metabolic acidosis2,6.
  • Seizures themselves worsen hypoxia and acidosis, which is another reason to control them quickly7.
Management and follow-up

Follow the current LAST rescue checklist, including appropriate airway/seizure care and lipid-emulsion therapy by the resuscitation team.

  • Stop injecting, call for help, airway and 100% oxygen, IV access, control seizures with a benzodiazepine2,3. Lipid emulsion 20%: bolus then infusion per the checklist, repeat if unstable and continue after stability, with a maximum total dose3. Avoid lidocaine, beta-blockers, calcium-channel blockers and vasopressin; use low-dose adrenaline for hypotension3. Observe for 2 hours after a seizure and 4-6 hours after cardiovascular instability3.
  • Seizures: benzodiazepine preferred. If only propofol is available, give small doses (e.g. 20 mg increments)3.
  • 20% lipid emulsion, ASRA checklist (2020): give early; the order of bolus and infusion is not critical3.
    • Under 70 kg: bolus about 1.5 mL/kg over 2-3 minutes, then infuse about 0.25 mL/kg/min (consider a pump if under 40 kg)3.
    • Over 70 kg: bolus about 100 mL over 2-3 minutes, then infuse about 250 mL over 15-20 minutes3.
    • If still unstable: repeat the bolus and double the infusion. Continue for at least 15 minutes after haemodynamic stability. Maximum dose about 12 mL/kg3.
  • AAGBI 2010 regimen (ANZCA-endorsed; used in some Australian kits): 1.5 mL/kg over 1 minute plus infusion at 15 mL/kg/h. After 5 minutes, give up to two repeat boluses 5 minutes apart and double the infusion to 30 mL/kg/h if needed. Maximum cumulative dose 12 mL/kg, which is about 840 mL for 70 kg2,4.
  • Arrhythmia or hypotension: use smaller-than-usual adrenaline doses (start at ≤1 microgram/kg). Avoid local anaesthetics (including lignocaine as an antiarrhythmic), beta-blockers, calcium-channel blockers and vasopressin2,3. Propofol is not a substitute for lipid2.
  • How lipid emulsion probably works: it soaks up lipid-soluble local anaesthetic from plasma (the "lipid sink"), lowering the amount at the heart and brain. This does not fully explain the effect; it may also restore energy production in the heart, since bupivacaine blocks fatty acid transport into mitochondria7.
  • Propofol cannot stand in for lipid emulsion, because the volume needed would deliver a lethal dose of propofol7.
  • Cardiac arrest: start CPR and continue it throughout lipid therapy. Arrhythmias may be very refractory, and recovery may take more than 1 hour. Consider cardiopulmonary bypass if available2,3.
  • Follow-up: observe 2 hours after a seizure and 4-6 hours after cardiovascular instability, in a monitored area2,3. After lipid, exclude pancreatitis with clinical review and daily amylase or lipase for 2 days2. Report the incident and lipid use (international registry, lipidregistry.org)2.
Red flags and clinical pearls

Dose limits, incremental injection and monitoring reduce risk but do not eliminate it; standard resuscitation drug choices may need modification.

  • LAST resuscitation differs from standard ALS: lower adrenaline doses, no lignocaine, no vasopressin3.
  • Calculate the maximum dose before injecting, and inject slowly with frequent aspiration5,6.
  • Know where the nearest lipid emulsion is kept before starting any block2,4.
  • A benzodiazepine premedication raises the seizure threshold but does nothing for cardiotoxicity, and it can hide the CNS warning signs of a dangerous level7.
  • Test doses and giving the total dose in small fractions became standard because of cardiac arrests with concentrated bupivacaine in epidural anaesthesia7.
References
  1. ANZCA Essential Medications List (July 2026)
  2. AAGBI: Management of severe local anaesthetic toxicity
  3. ASRA: Local anesthetic systemic toxicity checklist
  4. SESLHD: Intralipid - management of severe local anaesthetic toxicity (adult)
  5. NHS Scotland Emergency Medicine: Local anaesthesia (reviewed 2011)
  6. Australian Product Information: 2% Xylocaine DENTAL with adrenaline 1:80,000 (Dentsply Sirona)
  7. Katzung BG, Trevor AJ, editors. Basic and Clinical Pharmacology. 13th ed. New York: McGraw-Hill Education; 2015. Chapter 26, Local anesthetics.

Last updated from Sen’s notes on 22 October 2026.