LipidRescue™ Resuscitation

Case just occuring today:

57 yo for shoulder manip under interscalene block and brief GA. PMHx of HTN, no cardiac history, though ECG showed (chronic) RBBB.

ISB performed in SDS after versed 2 mg. IV. Block was done under direct visualization with ultrasound and nerve stimulator. U/S view showed classic LA fill around brachial plexus, and total 30 cc 0.2% Ropivicaine injected in divided doses with repeated negative aspiration. Dense block setup identified after removal of needle and patient had no complaints. Approximately 15 minutes later the patient began to complain of "strange feelings," and nausea. She became slightly combative, stating that she "needed to get up." Patient was placed supine and vitals showed a heart rate of 38, and BP of 68/35. O2 on, Iv opened up, and robinol 0.2 mg administered. Atropine drawn up and, due to suspicion of LA toxicity, intralipid called for. After approximately 2 minutes the HR was 42, and BP 77/45. Intralipid bolus begun with a very rapid (less than two minutes) resolution of dysphoria and combativeness. HR rose to 68, and BP 108/65. Infusion continued for 10 minutes after bolus, and total volume infused was approximately 200 cc. Patient was alert, cooperative, and recalled having "an out of body experience" at the time of the event. She was found to have a very dense blockade of her entire left arm. After 20 minutes of observation, decision was made to proceed with shoulder manipulation as planned, using only diprivan as anesthetic, and surgeon agreed to inject only celestone in the joint, forgoing his norm of adding 10 cc Ropivicaine. Patient was extremely comfortable in the recovery room.

Certainly appeared to me to be LA toxicity, though source/cause less obvious due to delay, and succesful block under direct U/S guidance. Some might argue for vagal response, but the CNS symptoms, and duration made this seem quite unlikely.

Full disclosure: I gave a talk for our department on Intralipid, and the evolving treatment of LA toxicity just 6 months ago, so perhaps I "jumped the gun" on its use in this case with relatively minor symptoms. Also, of course, one could opine that my observations are biased. Nonetheless, the patient rapid clearnce of symptoms were truly remarkable to all in attendance.

Comments?

Hard to believe that 30mls o f 0.2% Ropivacaine (60mg) is a toxic dose (assuming normal size individual for age) unless directly injected into a vessel. What antihypertensives was he/she taking? It can still be a vasovagal event and slower onset but improved conditions after glycopyrolate may be explained by slower circulation time, and not associated with lipid treatment. In any case, with USGRA, as little as 10-15mls may be sufficient.

Patient was on no meds, though diagnosed with "borderline" htn.

Agree with all that is said above, though I can imagine vagal reaction more easily than neuraxial spread. If you were there I believe you would have been convinced of LA toxicity: the rapid and pronounced dysphoria, mild combativeness ("squirrely"), along with hypotension and bradycardia. Had the CNS symptoms not been present, I would have given atropine and expected the usual response to vagal reaction (however delayed). But I will tell you without hesitation the CNS resolution was dramatic, preceded the CV correction, and was within minutes of administration of intralipid. Also, the patient's first comments after resolution were "what was THAT all about." Her overwhelming sensation at the time was a profound desire to "get out of her body."

Am I absolutely sure it was LA toxicity with resolution via intralipids? No
Does anything else even remotely make sense to me. No

One last note. We do a very large number of RA procedures, mostly for post-op pain management. The "tradition" of giving 30 cc has survived, despite addition of U/S, which does indeed suggest that less would be suffice. Anyone routinely using less in RA under U/S guidance and not seeing unwanted changes (i.e. shortened duration)?

I have cut down from 30 to <20mls for USG infraclavicular brachial plexus block. I see no clinical difference in duration. Initially with 30mls, I see diffuse spread of LA away from nerve...likely wasted. Only LA in close proximity to the nerve is doing the job. The rest that is further away is not. I am sure there is enough scientific evidence for this observation.

Don't forget about the Bezold-Jarrisch Reflex which is well documented in patients receiving interscalene blocks. The resultant bradycardia could also explain her other symptoms (e.g. N/V). Don't get me wrong - I'm a firm believer in the use of intralipid. Just remember, not all cardiac events are related to LA toxicity. Nevertheless, lipid rescue is pretty inocuous and I probably would have done the same.