Local anesthetic systemic toxicity
Stem
A 52-year-old man, 85 kg, is having an ultrasound-guided supraclavicular block for an open reduction of a distal radius fracture. After 25 mL of 0.5% bupivacaine, he says his mouth tastes metallic and his ears are ringing, then becomes unresponsive and has a generalized seizure. Within a minute the ECG shows a widening QRS, heart rate 48, and blood pressure 72/40.
Question
What is happening, and what do you do?
Ideal answer
HeadlineLocal anesthetic systemic toxicity, neurologic and now cardiovascular: I stop injecting and call for help and the lipid kit.
- 100% oxygen and ventilation, because hypoxia and acidosis worsen toxicity.
- Benzodiazepine for the seizure; propofol only in small increments, such as 20 mg, if nothing else,1 because larger doses depress a poisoned heart.
- 20% lipid emulsion now, over 70 kg: a bolus of about 100 mL over 2–3 minutes, then about 250 mL over 15–20 minutes.1
- Still unstable: repeat the bolus, double the infusion, the infusion continued at least 15 minutes after hemodynamic stability, under 12 mL/kg.1
- Arrest: CPR, small-dose epinephrine, no vasopressin or lidocaine, nearest bypass team alerted, because large epinephrine doses worsen arrhythmia and bupivacaine recovery can take over an hour.
Watch for: recurrence, observing 4–6 hours after cardiovascular instability, 2 hours after an isolated seizure.1
Breaking down the answer
- Lipid early, not last — a lipid sink shuttles drug from the heart and is directly inotropic; I give it at the first cardiovascular sign, not after ACLS fails. Bolus-infusion order and infusion method are not critical.1
- Weight-based dosing — under 70 kg, 1.5 mL/kg over 2–3 minutes, then 0.25 mL/kg/min.1
- Why small epinephrine — large doses worsen arrhythmia and impair lipid efficacy: less than 1 mcg/kg.1 Also avoid calcium-channel blockers, beta-blockers and other local anesthetics for arrhythmias;1 amiodarone is my antiarrhythmic.
- Propofol is not a substitute for lipid — its 10% lipid is too little, and the dose required would cause cardiovascular depression.
- Prolonged resuscitation — bupivacaine dissociates slowly from sodium channels, so recovery can take more than an hour; cardiopulmonary bypass is a realistic rescue.
- Prevention — ultrasound, lowest effective dose, aspiration and incremental injection every 3–5 mL, an epinephrine marker. High risk: elderly, cardiac disease or low ejection fraction, liver disease, low muscle mass, infants.
Follow-up question
He stabilizes after one bolus, and the lipid infusion is stopped 15 minutes later. In recovery 25 minutes after that, the nurse reports he is confused again and has a wide-complex bradycardia. What do you do?
Follow-up answer
HeadlineRecurrent LAST: bupivacaine is still leaving the tissue depot once lipid has stopped, and I tell the team.
Lipid kit, oxygen, ventilation, another 100 mL bolus over 2–3 minutes as he is over 70 kg, and the infusion restarted at about 250 mL over 15–20 minutes,1 with a running total against the 12 mL/kg maximum, about 1 L for him.1 Pulseless: CPR, small-dose epinephrine, bypass team. I reassess rhythm, pressure and mental status after each bolus and restart his observation in a monitored bed. Then the dose against lean body weight, a LipidRescue registry report, and why aspiration and incremental injection did not catch it.
Pitfalls that cost points
- Reflexively giving the standard ACLS 1 mg epinephrine dose.
- 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-fire
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: Descending: intercostal, caudal, epidural, brachial plexus, sciatic-femoral, subcutaneous; fascial plane blocks are high and slow to peak, often 30 minutes or later.
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, Intravenous regional anesthesia, ACLS adapted to the operating room, Intraoperative cardiac arrest: care after return of circulation
- 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.