Local anesthetic systemic toxicity
Why examiners ask this
LAST is the regional anesthesia crisis with a specific antidote and a modified ACLS algorithm, so the examiner expects a precise, ordered response and then asks why each modification exists. It tests organization under pressure, application of knowledge about lipid emulsion dosing, and judgment about prevention: maximum doses, ultrasound, and the patients at highest risk. It also appears in disguise, late, after a fascial plane block or in a post-anesthesia care unit.
The 60-second answer
I stop injecting and call for help and the lipid kit. My priorities are the airway and seizure control: 100% oxygen and ventilation, because hypoxia and acidosis worsen toxicity, and a benzodiazepine for seizures; if only propofol is available I give it in small increments, such as 20 mg.1 At the first sign of cardiovascular toxicity, I give 20% lipid emulsion: over 70 kg, a bolus of about 100 mL over 2–3 minutes and about 250 mL infused over 15–20 minutes; under 70 kg, 1.5 mL/kg over 2–3 minutes and then 0.25 mL/kg/min.1 If the patient remains unstable I repeat the bolus and double the infusion, continue the infusion for at least 15 minutes after stability, and stay under a maximum of 12 mL/kg.1 If the patient arrests, I start CPR with epinephrine in small doses and alert the nearest bypass team. I observe for 2 hours after an isolated seizure and 4–6 hours after cardiovascular instability.1
Decision points and the "why"
- Lipid early, not last — it creates a lipid sink and shuttles drug away from the heart, and has direct inotropic effects. I give it at the first cardiovascular sign, not after ACLS fails; the order of bolus and infusion and the method of infusion are not critical.1
- Small epinephrine doses — large doses worsen arrhythmia and impair lipid efficacy; I start with less than 1 mcg/kg.1
- Avoid certain drugs — vasopressin, calcium-channel blockers, beta-blockers and other local anesthetics such as lidocaine for arrhythmias.1 Amiodarone is my antiarrhythmic.
- Propofol is not a substitute for lipid — the 10% lipid in propofol is too little, and the dose required would cause cardiovascular depression.
- Prolonged resuscitation — bupivacaine binds sodium channels tightly and dissociates slowly, so recovery can take more than an hour; this is why cardiopulmonary bypass is a realistic rescue.
- Prevention — ultrasound guidance, the lowest effective dose, aspiration and incremental injection every 3–5 mL, and an epinephrine marker. High-risk patients include the elderly, those with cardiac disease or low ejection fraction, liver disease, low muscle mass, and infants.
The complication they will inject
Twenty-five minutes after an uneventful bilateral erector spinae block with ropivacaine for a frail 78-year-old, the PACU nurse reports she is confused and has a wide-complex bradycardia. I tell the team this is late-onset LAST, because peak plasma levels after fascial plane blocks can occur 30 minutes or later. I call for the lipid kit, give oxygen, and give a 1.5 mL/kg lipid bolus with an infusion of 0.25 mL/kg/min.1 If she loses her pulse, I start CPR and small-dose epinephrine. I then calculate the dose she received against lean body weight, report the event to the LipidRescue registry, and review how bilateral volumes added up in a small patient.
Pitfalls that cost points
- Running standard ACLS with 1 mg epinephrine and vasopressin and forgetting lipid.
- Using lidocaine as the antiarrhythmic.
- Treating propofol as an acceptable lipid source.
- Stopping resuscitation early because the patient is not responding at 20 minutes.
- Forgetting that toxicity can be delayed after truncal and fascial plane blocks.
Rapid-why
Q: Why is bupivacaine more cardiotoxic than lidocaine? A: It binds sodium channels "fast in, slow out," so blockade accumulates at physiologic heart rates and recovery is slow.
Q: Why is the CNS-to-cardiovascular toxicity gap narrower with bupivacaine? A: The doses that cause seizures and arrhythmias are close together, so cardiovascular collapse can occur without warning seizures.
Q: Which blocks produce the highest plasma levels? A: In descending order: intercostal, caudal, epidural, brachial plexus, sciatic-femoral, subcutaneous; fascial plane blocks are high and slow to peak.
Q: Why do acidosis and hypercarbia matter? A: They increase free drug and ion-trap it in the cells, lowering the threshold for seizure and arrhythmia.
Numbers to know
| Item | Value |
|---|---|
| Lipid 20% bolus | 1.5 mL/kg over 2–3 min if <70 kg; ~100 mL over 2–3 min if >70 kg1 |
| Lipid infusion | 0.25 mL/kg/min if <70 kg; ~250 mL over 15–20 min if >70 kg; double if unstable1 |
| Lipid maximum | 12 mL/kg; continue ≥15 min after stable1 |
| Epinephrine in LAST arrest | Start <1 mcg/kg1 |
| Maximum bupivacaine | 2.5 mg/kg plain; 3 mg/kg with epinephrine |
| Maximum lidocaine | 4.5 mg/kg plain; 7 mg/kg with epinephrine |
| Observation after event | 2 h after seizure; 4–6 h after cardiovascular instability1 |
Links
- Epidural anesthesia and the test dose, Interscalene block and its complications, TAP, ESP, PECS, QL and fascia iliaca blocks (coming), Intravenous regional anesthesia (coming), Intraoperative cardiac arrest
- ASRA Practice Advisory on local anesthetic systemic toxicity (2020 checklist; ASRA reports an update under review for early 2027)2
Sources
- 1.Checklist for Treatment of Local Anesthetic Systemic Toxicity (LAST) · ASRA Pain Medicine, 2020 · asra.comPrintable checklist, 2020 v1.1 (Neal, Neal and Weinberg); source of all lipid, epinephrine, avoid-list and observation numbers.
- 2.Checklist for Treatment of Local Anesthetic Systemic Toxicity (LAST) - guideline page · ASRA Pain Medicine, 2020 · asra.comStates the 2020 checklist is under review with an update expected in early 2027.
Facts on this page were checked against these sources on Oct 14, 2026. Guidelines change; confirm doses against current institutional protocols.