LipidRescue™ Resuscitation

This was a case of a 60 yo man with a history of COPD, HTN, Hep C, DJD, and Depression for which he was taking Bupropion. Patient was 188cm (6'2") tall and weighed 90kg.

This patient was scheduled for a right total knee arthroplasty. In these patients, we generally perform a single injection lumbar plexus block and a single injection sciatic nerve block for surgical anesthesia and post operative analgesia.

In our dedicated block area, monitors were placed on the patient. The patient was premedicated with midazolam 1mg IV. The patient was placed in the lateral decubitus position. A lumbar plexus block was done using a 4 inch insulated needle with quadriceps contractions disappearing at 0.47mA. After negative aspiration, 30ml of a 1:1 mixture of 0.5% Bupivacaine and 1.5% Mepivacaine with 1:200,000 epinephrine was injected. The patient continued to be alert and was conversing with us after the block. A posterior approach to the sciatic nerve was performed next with gastrocnemius contractions disappearing at 0.45mA. After negative aspiration, 20ml of the same 1:1 local anesthetic solution with epinephrine was injected. Within a minute, the patient began experiencing myoclonic activity in his upper extremities. The patient also became stuporous but was responding to verbal stimuli. The patient was returned to supine position. Immediately, the possibility of systemic local anesthetic toxicity precipitating seizures was considered. The patient maintained his airway throughout this episode and never showed signs of adverse cardiovascular effects. Four milligrams of midazolam and 100 milligrams of propofol were urgently given to treat a possible seizure. Of note, vital signs never changed. Heart rate remained in the 80s Blood pressure was consistently 130s/80s. ECG morphology never changed. Oxygen saturation never fell below 97% on 2L nasal canula. After midazolam and prolofol were administered, the patient remained stuporous but was no longer exhibiting any myoclonic or posturing activity. The patient continued to respond to verbal stimuli. The patient's stuporous mental status was concerning for possible continuation of partial seizures or a post-ictal state. However, we also had to consider that the midazolam and propofol could be contributing to the patient's altered metal state. A total of flumazenil 0.3mg was administered intravenously in divided doses. We did this with caution as we were cognizant that this could lower the seizure threshold and precipitate further seizures. We also administered intralipid as therapy for systemic local anesthetic toxicity. We gave 50ml of the 20% solution as a bolus and continued therapy with a 150ml infusion given over 30 minutes. After the intralipid was administered, the patient returned to his normal baseline mental state. The patient was observed closely for 20 minutes. Since there was no evidence of adverse cardiovascular effects from this episode and his neurologic state had returned to his normal baseline, we decided to proceed with the surgery.

The patient was taken to the operating room. On transfer to the operating table, it was noted that patient's right leg was successfully blocked. Patient underwent right total knee arthoplasty under general anesthesia without any complications. Of note, the patient initially required very little anesthetic during surgery. However, after one hour, the patient's blood pressure began increasing and he required higher doses of inhalational agent and fentanyl suggesting that the nerve blocks were wearing off. The surgery took four hours to complete. The patient emerged from general anesthesia in good condition. In the recovery room, the patient complained of some knee pain but was otherwise stable.

Some questions to consider:
After the intralipid was administered, the patient immediately returned to his baseline mental state. Was this all due to the effect on the local anesthetic? Did the intralipid also reverse the effects of the propofol?

The dose of local anesthestic does not seem excessive considering the patient weighed 90kg. Negative aspiration and rare occurrence of intravascular injection with sciatic nerve blocks also suggests that there was no direct inravascular injection of LA. However, this patient was taking buproprion. Does buproprion increase the risk of systemic local anesthetic toxicity? If so, what measures should be taken to reduce this risk?

The nerve block continued to be effective after intralipid therapy. However, the block duration was noticeably shorter than would be expected. What effect does intralipid therapy have on plexus blocks?

Hi Phil,
Thanks for posting, and allowing me to help in this patient's management (I arrived shortly after the midazolam and propofol were given).
Your questions are excellent and probably require some degree of laboratory investigation to answer rigorously. HOwever, after seeing this case, I would recommend reducing total LA dose in patients taking drugs that can block sodium channels or have some cardiotoxic profile. It is hard not to think that the bupropion made some contribution to the patients symtpoms. Regarding the effect of lipid infusion on the block's duration or kinetics of other drugs......this is an area for further study; start writing the IRB proposal!