LipidRescue™ Resuscitation

Guy, like so many contributors before let me first express our gratitude to you and your co-workers for the seminal observations and work you have done and continue to do including co-ordinating this website. Thanks also to Meg Rosenblatt for her initial clinical report which resulted in us storing Intralipid 20% in every OR in July 2006.

We now report yet another apparent miraculous save using lipid emulsion therapy in the face of systemic bupivacaine toxicity. We believe our case is significant in that it may be the first case in which lipid emulsion (Intralipid 20%) was the first and only line of intravenous intervention used and needed to rapidly reverse the neuro and cardio toxic effects of presumed bupivacaine toxicity.

On December 18, 2007 a 17 yr old otherwise healthy male presented for repair of his medial patello-femoral ligament. Spinal anesthesia with femoral nerve block was agreed to.

The patient was taken to the OR at 1041hrs, an IV started and the standard monitors attached. He was given 2mg of midazolam and 50ug of fentanyl. The block was performed using a 22g Pro-block needle attached to a digistim 3 nerve stimulator. The femoral nerve was identified via quadriceps twitches down to a current of 0.6mA (0.1ms duration, 1Hz). Initial aspiration was negative. A total of 30ml of 0.5% bupivacaine was injected in 5ml increments with aspiration between each injection. The patient was awake and conversant but drowsy through the performance of the block. As the needle was withdrawn the patient began seizing. A presumptive diagnosis of bupivacaine toxicity was made and a code called at 1050hrs.

Mask ventilation with 100% oxygen was immediately initiated. A number of additional anesthesiologists arrived in the room. 3 mg of additional midazolam was given and almost immediately lipid therapy was initiated by syringe bolus injection and manual pressure to the Intralipid bag.

The patient was determined to be pulseless and the EKG appeared to indicate Vfib. Vigorous chest compressions were started with pulses palpable at the femoral artery.
Intubation was achieved at 1051hrs. CO2 waveforms remained present during CPR.

The most available defibrillator happened to be a Philips Heartstart AED. Pads were applied and all patient contact was terminated. The AED determined a Vfib rhythm and advised shocking. A shock was delivered. The patient's rhythm immediately converted to a narrow complex sinus tachycardia. He was noted to have bounding pulses and a BP of 183/83. A susequent AED analysis at 1100hrs advised no further shock therapy.

The medics arrived at 1105hrs and we transferred an essentially stable, intubated patient to the hospital. Within hours he was extubated with no complaints, not even a tender chest!

The rapidity and apparent specificity of our lipid only intervention prior to administration of more "traditional" resuscitative medications may add further momentum to the notion that lipid emulsion therapy is a "crucial antidote" in the treatment of systemic bupivacaine toxicity. In all a total of 500ml of 20% Intralipid was administered.


One further interesting observation worth noting I think, relates to the occurrence of seizure activity. Initial seizure activity occurred at the end of the block and then ceased when circulatory arrest occurred (pulseless). Seizure activity resumed with chest compressions and then ended when compressions ceased briefly for intubation. Seizures recurred with the resumption of compressions and ceased during AED analysis. There was one further burst of seizure activity when circulation was restablished after the shock was delivered. No further seizure activity was observed.

Viva lipid therapy!