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Just a clarification...
Certainly propofol would not work as a rescue drug due to the volume needed and cardiac depressant effects. My question is however, is the lipid emulsion in propofol indeed the same as Intralipid?
Thanks
Mark
Certainly propofol would not work as a rescue drug due to the volume needed and cardiac depressant effects. My question is however, is the lipid emulsion in propofol indeed the same as Intralipid?
Thanks
Mark
June 23, 2008 |
mark manley
the standard formulation of propofol contains 10% intralipid, or the equivalent. BUT
as you point out....propofol won't work in LA toxicity. the reason i try to emphasize this is that there is a tendency among clinicians to confuse lipid emulsion wiht propofol (it's all white, afterall). and it's not unusual (tho recently, far less common) for me to field the question, "so dr weinberg, how much propofol do we give for bupivacaine toxicity?". obviously, that drives me nuts!
as you point out....propofol won't work in LA toxicity. the reason i try to emphasize this is that there is a tendency among clinicians to confuse lipid emulsion wiht propofol (it's all white, afterall). and it's not unusual (tho recently, far less common) for me to field the question, "so dr weinberg, how much propofol do we give for bupivacaine toxicity?". obviously, that drives me nuts!
June 23, 2008 |
[Guy Weinberg]
Thanks for the info. I am an anesthesiologist preparing to give a "M & M" on LA toxicity. Though propofol doesn't play a role, I think it will take the "exotic treatment" notion out of it to know that the lipid emulsion is something we give (in small doses) every day.
Mark
Mark
June 23, 2008 |
mark
good point, mark.
btw, if the M&M is based on a case, don't forget to post it here, too.
if just a lecture, you can use any of the four cases in last month's AA as examples.
if you need any specific slides, i can probably help.
btw, don't miss the article comparing lipid to epi in May's Anesthesiology.
good luck
guy
btw, if the M&M is based on a case, don't forget to post it here, too.
if just a lecture, you can use any of the four cases in last month's AA as examples.
if you need any specific slides, i can probably help.
btw, don't miss the article comparing lipid to epi in May's Anesthesiology.
good luck
guy
June 24, 2008 |
[Guy Weinberg]
Presented today...went well. Thanks for your offer! We do a large number of regional anesthetics but have not had any cases of cardiac arrest (yet?). Nonetheless, we began stocking 20% Intralipid in our "block carts" and coded carts a few months ago.
One thing that came up today. We have accumulated four separate cases in two institutions of ISB for shoulder surgery with a familiar untoward event. In all 4 cases the surgery was delayed, and the patients experienced bradycardia and mild to severe hypotension 30-40 minutes after successful block. In all cases the bradycardia was extremely resistent to robinol, atropine and ephedrine. Induction of GA had not yet occurred. All resolved without sequelae. We are wondering/speculating about subtle insideous LA cardiotoxicity as a cause...any thoughts?
One thing that came up today. We have accumulated four separate cases in two institutions of ISB for shoulder surgery with a familiar untoward event. In all 4 cases the surgery was delayed, and the patients experienced bradycardia and mild to severe hypotension 30-40 minutes after successful block. In all cases the bradycardia was extremely resistent to robinol, atropine and ephedrine. Induction of GA had not yet occurred. All resolved without sequelae. We are wondering/speculating about subtle insideous LA cardiotoxicity as a cause...any thoughts?
June 25, 2008 |
mark manley
i view hypotention and bradycardia as strongly suggestive if not pathognomonic of LA toxicity. there is substantial interpatient variability wrt sensitivity to LA toxicity that some patients will exhibit these signs with normal doses, even in the absence of obvious intravascular injection - presumably a result of systemic absorbtion and i assume this is what you're seeing. if you wanted to get really fancy, you could get 12-lead ECGs during and after the events to follow QRS duration and possibly QTc. if a patient's ECG looks very threatening, or the BP is very low, you could also give a bolus of lipid and follow the ECG to see if reversal of the intervals correlates with improvement of BP, HR and presumably LA toxicity. But, in short, i think you're seeing some LA toxicity in those patients.
Guy
Guy
June 26, 2008 |
[Guy Weinberg]
Thanks
Mark