Local anaesthetic systemic toxicity during interscalene block

This is local anaesthetic systemic toxicity with progression from prodromal neurological symptoms through seizure to cardiovascular collapse, and it is treated as an emergency with a fixed sequence.

1. Call for help and stop the injection. Note that 150 mg of bupivacaine is a high dose; toxicity is dose-related and the adrenaline does not prevent it.
2. Airway and oxygenation: 100% oxygen by mask, jaw thrust, and intubate if ventilation is inadequate. Hypoxia, hypercarbia and acidosis all worsen cardiotoxicity and reduce the effectiveness of lipid rescue, so oxygenation is not secondary.
3. Start lipid emulsion immediately (21.5 mL... see next answer for exact dosing), even before the rhythm deteriorates further.
4. Terminate the seizure: midazolam 2-4 mg intravenously is preferable to propofol in a hypotensive patient; the 100 mg of propofol already given is contributing to the current hypotension and should not be repeated.
5. Treat the bradycardia and hypotension with small boluses of epinephrine (10-20 mcg initially, up to 1 mcg/kg) and intravenous fluid; start chest compressions if there is no pulse.
6. Prepare for a prolonged resuscitation: lipid rescue can take more than an hour. Consider cardiopulmonary bypass or extracorporeal membrane oxygenation if available and the patient does not respond.
7. After return of circulation, monitor for at least 4-6 hours because toxicity can recur as lipid stores redistribute.

Use 20% lipid emulsion, dosed on lean body weight (about 70 kg here):

• Bolus: 1.5 mL/kg over one minute, which is about 105 mL.
• Infusion: 0.25 mL/kg/min, which is about 17.5 mL/min, started immediately after the bolus and continued for at least 15 minutes after circulatory stability is restored.

If the patient remains unstable (persistent hypotension, recurrent arrhythmia or cardiac arrest):

• Repeat the bolus once or twice at 5-minute intervals, and
• Double the infusion rate to 0.5 mL/kg/min (about 35 mL/min).

The recommended maximum is approximately 10-12 mL/kg over the first 30 minutes, which for this patient is roughly 700-840 mL. If the patient is still in arrest at that point, the resuscitation should continue with extracorporeal support rather than further escalation of lipid.

Practical points: propofol is not a substitute for lipid emulsion, and because propofol is formulated in lipid, the propofol already given counts towards the lipid load and also causes myocardial depression. The infusion should be continued and the patient watched closely after any apparent recovery, because a second peak of toxicity can occur.

Several drugs that are routine in other resuscitation settings are harmful in local anaesthetic toxicity.

• Further local anaesthetic of any type, including lidocaine for arrhythmia: it adds to the sodium channel blockade and competes with lipid binding, worsening toxicity.
• Beta-blockers and calcium channel blockers: they deepen bradycardia and myocardial depression, are difficult to reverse, and have been associated with worse outcomes in lipid rescue models. Amiodarone is preferred for ventricular arrhythmia.
• Vasopressin: it is not recommended in lipid-based resuscitation and may worsen outcomes.
• Large or repeated doses of propofol: it causes myocardial depression and adds a lipid load, and should be limited to a small dose for seizure control in a haemodynamically stable patient.
• High-dose epinephrine: doses above about 1 mcg/kg impair the effect of lipid emulsion in animal models and increase mortality. Use small titrated boluses instead of the standard 1 mg arrest dose where a pulse is present.

It is also important not to stop resuscitation early: patients with bupivacaine-induced cardiac arrest may require prolonged CPR, and survival with good neurological outcome has been reported after more than an hour of resuscitation with lipid therapy.