Two Local Anesthetics, One Seizure
A 44-year-old woman (72 kg, ASA II, no comorbidities) presents for open reduction and internal fixation of a distal radius fracture. You perform an ultrasound-guided supraclavicular brachial plexus block with 30 mL of 0.5% bupivacaine and 15 mL of 2% lidocaine containing 1:200,000 epinephrine, injected incrementally over six minutes with negative aspiration before and during each aliquot. Twenty minutes after the last injection she reports a metallic taste and tinnitus, becomes agitated, and then has a 40-second generalized tonic-clonic seizure. Between convulsions, blood pressure is 168/104 mmHg, heart rate 112 in sinus rhythm, and SpO2 is 94% on 6 L/min by face mask. The surgeon has already made the incision and the tourniquet is inflated.
1. Calculate the dose of each drug in milligrams and mg/kg. Which agent most likely drove the toxicity, and how do you reconcile the doses with the event?
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Doses:
- Bupivacaine 0.5% = 5 mg/mL. 30 mL = 150 mg, or 150/72 = 2.1 mg/kg.
- Lidocaine 2% = 20 mg/mL. 15 mL = 300 mg, or 300/72 = 4.2 mg/kg.
- Total 450 mg, or 6.25 mg/kg of local anesthetic.
Interpretation: the lidocaine dose sits well below the 7 mg/kg figure usually quoted when epinephrine is added, and the bupivacaine dose is only just above the 2 mg/kg figure. Neither is a classic massive overdose; this is exactly the point. Published maximum doses are statistical constructs derived from population data, not individual thresholds, and the real determinant is the plasma concentration achieved, which depends on vascularity of the injection site, speed of injection, protein binding, and cardiac output.
Why bupivacaine dominates: it is far more lipid-soluble and protein-bound, blocks cardiac sodium channels with slow dissociation kinetics, and produces seizures and cardiovascular collapse at lower plasma concentrations than lidocaine. The supraclavicular region is highly vascular and adjacent to the subclavian vessels, so a fraction of any injection can enter the circulation despite negative aspiration. Treat this as bupivacaine-predominant toxicity.
2. Give the immediate management sequence, including the lipid emulsion regimen for this patient with the arithmetic shown.
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Sequence: stop injecting, call for help, secure the airway and give 100% oxygen, terminate the seizure with a benzodiazepine (small incremental doses, watching blood pressure), attach a defibrillator, and start lipid emulsion early rather than waiting for cardiovascular collapse.
Lipid arithmetic (72 kg, 20% emulsion):
- Bolus 1.5 mL/kg = 108 mL over about one minute.
- Infusion 0.25 mL/kg/min = 18 mL/min, roughly 1080 mL/h, continued for at least 15 minutes after circulatory stability.
- Repeat the bolus once or twice (1.5 mL/kg each) if instability persists.
- Ceiling approximately 12 mL/kg = 864 mL for this patient.
Additional principles: keep epinephrine boluses small (1 microgram/kg or less) because large doses worsen lipid-facilitated arrhythmias; avoid vasopressin, calcium channel blockers, beta blockers, and lidocaine for the seizure; amiodarone is acceptable for ventricular arrhythmia; propofol is a poor choice in a hypotensive patient. Note that the epinephrine in the lidocaine solution provides no protection against bupivacaine cardiotoxicity. After stabilization, monitor with continuous ECG and pulse oximetry for several hours, because recrudescence after apparent recovery is well described.
3. Thirty minutes later the seizure has stopped but the ECG shows a QRS of 140 ms and runs of ventricular tachycardia with a MAP of 50 mmHg. What is your priority order and why?
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Priority: continue and if necessary re-bolus lipid emulsion, correct hypoxia and acidosis (the two biggest amplifiers of bupivacaine cardiotoxicity), and treat unstable ventricular tachycardia with synchronized or unsynchronized shock as appropriate rather than with further negative inotropes.
Reasoning: bupivacaine blocks the cardiac sodium channel and dissociates slowly; a wide QRS is the electrocardiographic signature. Lipid works by creating an intravascular lipid phase that sequesters the drug and by supplying free fatty acids to a myocardium that has been deprived of them. Because the drug is still present in tissue, the lipid infusion must continue - a single bolus is not a course.
Practical points:
- Sodium bicarbonate is reasonable for a wide-complex rhythm in the setting of sodium-channel blockade, but it is an adjunct, not a substitute for lipid.
- Start an epinephrine infusion at low dose rather than repeated large boluses.
- Call for cardiopulmonary bypass early if there is no response; it is the definitive rescue for refractory local anesthetic cardiotoxicity.
- Once stable, document the event, keep the patient monitored, and arrange allergy/anesthetic follow-up so that the record accurately attributes the event to systemic absorption rather than to a drug allergy.