Local anaesthetic systemic toxicity

01Core principlesThe concepts and mechanisms needed to understand the subject.

Local-anaesthetic systemic toxicity occurs when a sufficient concentration reaches the brain or heart, most often through inadvertent intravascular injection, excessive total dose, rapid absorption or impaired clearance. Early subjective symptoms such as metallic taste, tinnitus or circumoral tingling may be absent, hidden by sedation or bypassed by a rapid intravascular injection. Severe toxicity can therefore present directly with seizure or cardiovascular collapse.

Risk depends on the drug, site vascularity, dose, injection speed, patient mass and physiology. Total exposure includes surgeon infiltration, multiple blocks, boluses and continuous infusions. Frailty, pregnancy, childhood, critical illness and cardiac, hepatic or renal dysfunction change the margin of safety. Product-specific dose limits and specialist adjustment matter more than memorising one universal maximum.

Resuscitation differs from routine cardiac-arrest treatment. Oxygenation and ventilation limit acidosis and hypercarbia. The June 2023 Association Quick Reference Handbook gives a 20% lipid emulsion bolus followed by infusion, with repeat boluses and infusion escalation for persistent cardiovascular instability. During arrest it advises reduced adrenaline dosing and avoiding vasopressin. Recovery may take more than an hour.

After stabilisation, the patient requires transfer to a suitable monitored area, repeated clinical review and surveillance for complications including pancreatitis after lipid treatment. The event, cumulative dose, timeline and response should be recorded and reported. Future records must clearly describe the reaction without automatically labelling every local anaesthetic as an IgE allergy.

Key points

Stop injection and all pumps immediately when LAST is suspected; call for senior help, the cardiac-arrest trolley and the lipid rescue pack.
Give 100% oxygen, maintain or secure the airway and ventilate effectively while avoiding hypercarbia, which can worsen toxicity.
Use 20% lipid emulsion: initial 1.5 mL/kg intravenous bolus over 2–3 minutes, then 15 mL/kg/hour infusion, following the QRH repeat and maximum-dose instructions.
Treat seizure with small incremental benzodiazepine doses; propofol or thiopental can worsen myocardial depression in an unstable patient.
If cardiac arrest occurs, start CPR, use the modified LAST drug approach and prepare for prolonged resuscitation or cardiopulmonary bypass where available.
Prevent LAST by calculating cumulative dose from every source, selecting the lowest effective concentration and dose, injecting incrementally and maintaining monitoring and rescue readiness.

02Mechanisms and patternsImportant relationships and how to distinguish them.

Neurological prodrome

Circumoral numbness, metallic taste, tinnitus, dizziness, agitation or confusion after injection may precede seizure but can be absent.

Severe neurological toxicityRed flag

Sudden altered consciousness or tonic-clonic convulsion during or after local anaesthetic should trigger the LAST drill.

Cardiac toxicityRed flag

Bradycardia, conduction delay, wide complexes, ventricular arrhythmia, hypotension and asystole indicate life-threatening myocardial and electrical toxicity.

Delayed presentation

New symptoms after apparently uncomplicated injection or during an infusion remain compatible with systemic toxicity.

Masked presentation

General anaesthesia or deep sedation removes subjective warning symptoms, leaving monitor changes and cardiovascular deterioration as the first clues.

Important alternatives

High neuraxial block, anaphylaxis, embolism, haemorrhage, hypoxia and drug error can mimic parts of LAST and must be assessed during resuscitation.

Red flags requiring action

Sudden agitation, altered mental state, loss of consciousness or tonic-clonic seizure after local anaesthetic requires immediate treatment for possible toxicity.
Bradycardia, conduction block, ventricular arrhythmia, hypotension or asystole may be the first recognised manifestation under sedation or general anaesthesia.
Toxicity can appear after the injection, through cumulative infiltration or during a continuous infusion; finishing the block does not end surveillance.
Propofol is not a substitute for 20% lipid emulsion in the LAST rescue regimen.
During LAST cardiac arrest, the Association QRH specifies smaller adrenaline doses of no more than 1 microgram/kg and avoidance of vasopressin.
Children, pregnancy, frailty, critical illness and cardiac, renal or hepatic dysfunction increase risk and require specialist dosing rather than routine adult extrapolation.

03Interpreting evidenceInformation, measurements and their limitations.

Reasoning sequence

Consider the information, its meaning and its limitations before deciding what follows.

01
Immediate ABC and monitor review
Why
Detect airway failure, seizure, arrhythmia and circulatory collapse while treatment begins.
Interpretation and limitations
Diagnosis is clinical and treatment should not wait for a confirmatory concentration; relate deterioration to the injection timeline and all administered drugs.
02
Twelve-lead ECG
Why
Characterise conduction delay or arrhythmia after initial stabilisation.
Interpretation and limitations
Wide complexes, block or ventricular arrhythmia support cardiac toxicity and guide ongoing monitored care, but a later normal trace does not exclude a transient event.
03
Blood gas with electrolytes
Why
Identify acidosis, hypercarbia, hypoxaemia and metabolic contributors that worsen toxicity.
Interpretation and limitations
Correct ventilation and perfusion promptly; severe abnormalities may reflect arrest as well as drug effect and should be trended.
04
Cumulative local-anaesthetic reconstruction
Why
Calculate total drug exposure across blocks, infiltration, additives and pumps.
Interpretation and limitations
Compare with the exact product and patient-specific plan; an apparent single safe dose may become excessive when multiple sources are combined.
05
Amylase or lipase after lipid rescue
Why
Screen for pancreatitis during monitored follow-up after substantial lipid administration.
Interpretation and limitations
Interpret with symptoms and serial clinical review; the QRH advises daily measurement after the event.

04Applied reasoningWorked examples connecting principles to decisions.

01Worked case: emergencySeizure during a peripheral nerve blockAn adult becomes agitated and convulses seconds after local-anaesthetic injection.

1Stop injection and any infusion, call for help, summon the arrest trolley and lipid pack, give 100% oxygen and establish effective airway ventilation and intravenous access.
2Control seizure with small incremental benzodiazepine doses and assess rhythm and perfusion; begin 20% lipid emulsion promptly if severe toxicity is suspected.
3Give an initial 1.5 mL/kg lipid bolus over 2–3 minutes and start 15 mL/kg/hour, then follow the QRH repeat-bolus, doubled-infusion and 12 mL/kg cumulative ceiling instructions.
4If arrest occurs, start continuous CPR, use adrenaline doses no greater than 1 microgram/kg, avoid vasopressin and consider prolonged resuscitation with bypass support.

02PreventionMultiple local-anaesthetic sources plannedThe anaesthetist and surgeon both plan regional injection or infiltration during the same operation.

1Agree the exact drugs, concentrations, maximum cumulative amount and division between operators before either injection starts.
2Adjust for body size, frailty, pregnancy and organ disease, use the lowest effective dose and document all administrations in a shared record.
3Inject incrementally with appropriate aspiration and monitoring, maintain verbal contact when feasible, and keep the lipid rescue pack accessible.

03AftercareRecovery after lipid rescueCirculation and neurological status have recovered after treatment of suspected LAST.

1Transfer to an appropriately monitored clinical area and continue rhythm, neurological, respiratory and haemodynamic observation for recurrence.
2Review clinically for pancreatitis and check amylase or lipase daily as advised by the QRH after lipid administration.
3Record and report the incident, explain it to the patient, and create an accurate future anaesthetic alert describing the suspected mechanism and drugs.

05Relevant medicines and safetySpecific regimens and precautions where medicines are relevant.

Provides lipid rescue during severe neurological or cardiovascular local-anaesthetic toxicity.

Twenty percent lipid emulsion

Give 1.5 mL/kg intravenously over 2–3 minutes, then infuse 15 mL/kg/hour under the current QRH regimen.

Repeat boluses at five and ten minutes and double the infusion for persistent instability as directed; do not exceed 12 mL/kg cumulative dose and do not substitute propofol.

Controls seizure without the same degree of myocardial depression associated with large induction-agent doses.

Benzodiazepine for seizure

Use a small incremental intravenous dose titrated to terminate convulsion while ventilation is supported.

Any sedative can impair airway and breathing; propofol or thiopental needs particular caution when cardiac function is already depressed.

Supports coronary and systemic perfusion in cardiac arrest modified for local-anaesthetic toxicity.

Adrenaline during LAST arrest

Use small intravenous doses no greater than 1 microgram/kg while high-quality CPR and lipid rescue continue.

This differs from routine 1 mg ALS dosing in the QRH LAST drill; avoid vasopressin and seek expert help for prolonged refractory collapse.

06Checking understandingVerify the reasoning, revisit uncertainties and apply feedback.

Maintain ECG, blood pressure, oxygen saturation and capnography when ventilation is assisted throughout resuscitation and transfer.
Track cumulative lipid dose, repeat bolus times, infusion rate, adrenaline exposure and the response of rhythm and circulation.
Continue neurological and cardiac observation after apparent recovery because toxicity can recur or have been delayed from the original injection.
After lipid therapy, perform regular clinical review for pancreatitis with daily amylase or lipase under the QRH aftercare plan.
Before future regional anaesthesia, review the full event rather than relying on a nonspecific allergy label.

07Special situationsVariants, exceptions and circumstances that change the usual approach.

Subjective signs may vanish

Sedation and general anaesthesia can hide tinnitus or metallic taste, so sudden monitor and circulation changes may be the first evidence.

Every syringe contributes

Safe planning adds surgeon infiltration, anaesthetist blocks, wound catheters and infusions rather than checking each source in isolation.

Ventilation is treatment

Hypoxia, acidosis and hypercarbia potentiate toxicity, making prompt oxygen delivery and effective ventilation central to resuscitation.

The arrest algorithm changes

Reduced adrenaline and avoidance of vasopressin are deliberate QRH modifications, so the lipid rescue card should be read during the event.

Allergy is a different mechanism

A toxic plasma concentration does not by itself establish IgE-mediated allergy, and imprecise labelling may unnecessarily restrict future care.

08Common pitfallsFrequent interpretation and management errors.

01
Continuing a wound infusion or second syringe after stopping only the most obvious local-anaesthetic injection.
02
Waiting for a drug concentration before starting airway support and lipid rescue in a compatible severe presentation.
03
Using propofol as the lipid source instead of giving 20% lipid emulsion.
04
Giving routine full-dose adrenaline repeatedly during a LAST arrest despite the specific reduced-dose algorithm.
05
Ignoring delayed symptoms because the injection itself appeared uneventful.
06
Calculating each operator’s dose separately and overlooking excessive cumulative exposure.

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