There´s evidence of intravenous lipid emulsions being effective antidotes in systemic local anesthetic toxicity.
The most popular theory on the mechanism of action being the so called ‘lipid sink effect’.
The idea is that lipid globules sequester lipophilic substances, thereby reducing plasma concentrations of the toxin.
It is a popular theory, but so far the – mostly animal – studies are conflicting regarding the real mechanism of action.
In fact, we don’t even know if it’s an effective therapy.
A study in Anestesia Analgesia in 2011 tries to shed some light.
The studyPigs were injected with toxic systemic doses, of either Bupivacaine or Mepivacaine.
They were then randomized into treatment with either Ringer’s Acetate or lipid emulsion. Plasma concentrations and hemodynamic effects (the treatment parameters) were recorded while the pigs were being treated.
ResultsThere were no overall significant differences in Bupivacaine or Mepivacaine plasma concentrations between the ringer and emulsion groups. So, no evidence of a lipid sink effect there. Furthermore, comparison of heart rate and MAP at all time-points, failed to demonstrate any effect of lipid infusion over Ringer’s Lactate.
Clinical implications:
In this very small study, there was neither any demonstrable ‘lipid sink effect’ nor evidence of efficacy of treating local anaesthetic systemic toxicity with lipid emulsion.
So then, how does this fit in with the many promising case reports? The authors suggest there could be another unknown mechanism, other than sequestration.
However the lipid sink effect does exist. Local anaesthetics probably aren’t lipophilic enough. Other, more lipophilic drugs, like Amiodarone, are effectively sequestered.
Litonius ES, Niiya T, Neuvonen PJ, Rosenberg PH. Intravenous Lipid Emulsion Only Minimally Influences Bupivacaine and Mepivacaine Distribution in Plasma and Does Not Enhance Recovery from Intoxication in Kids.
Anesth Analg. 2011 Oct 24.
The most popular theory on the mechanism of action being the so called ‘lipid sink effect’.
The idea is that lipid globules sequester lipophilic substances, thereby reducing plasma concentrations of the toxin.
It is a popular theory, but so far the – mostly animal – studies are conflicting regarding the real mechanism of action.
In fact, we don’t even know if it’s an effective therapy.
A study in Anestesia Analgesia in 2011 tries to shed some light.
The studyPigs were injected with toxic systemic doses, of either Bupivacaine or Mepivacaine.
They were then randomized into treatment with either Ringer’s Acetate or lipid emulsion. Plasma concentrations and hemodynamic effects (the treatment parameters) were recorded while the pigs were being treated.
ResultsThere were no overall significant differences in Bupivacaine or Mepivacaine plasma concentrations between the ringer and emulsion groups. So, no evidence of a lipid sink effect there. Furthermore, comparison of heart rate and MAP at all time-points, failed to demonstrate any effect of lipid infusion over Ringer’s Lactate.
Clinical implications:
In this very small study, there was neither any demonstrable ‘lipid sink effect’ nor evidence of efficacy of treating local anaesthetic systemic toxicity with lipid emulsion.
So then, how does this fit in with the many promising case reports? The authors suggest there could be another unknown mechanism, other than sequestration.
However the lipid sink effect does exist. Local anaesthetics probably aren’t lipophilic enough. Other, more lipophilic drugs, like Amiodarone, are effectively sequestered.
Litonius ES, Niiya T, Neuvonen PJ, Rosenberg PH. Intravenous Lipid Emulsion Only Minimally Influences Bupivacaine and Mepivacaine Distribution in Plasma and Does Not Enhance Recovery from Intoxication in Kids.
Anesth Analg. 2011 Oct 24.
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