• J A Heinonen, M B Skrifvars, J Haasio, J T Backman, P H Rosenberg, and E Litonius.
• University of Helsinki, Helsinki, Finland.
• Anaesth Intensive Care. 2016 Mar 1; 44 (2): 270-7.

AbstractIntravenous lipid emulsion is, in some countries, the recommended treatment for local anaesthetic toxicity. Systemic local anaesthetic toxicity results in hypoxaemia and acidosis, and whether this influences the effects of lipid therapy on drug concentrations and cardiovascular recovery is currently unknown. Twenty anaesthetised pigs were given a 3-mg/kg bolus of levobupivacaine followed by a five minute phase of hypoventilation and 1 mmol/kg of lactic acid in one minute. After lactic acid infusion, pigs were treated, in randomised order, with either 20% lipid emulsion or Ringer's acetate for 30 min: a 1.5-ml/kg bolus followed by a 0.25-ml/kg/minute infusion. Haemodynamic parameters were recorded and blood samples were collected for pharmacokinetic analysis. There was no difference between the groups in the area under the plasma levobupivacaine concentration-time curve (AUC) or between that and AUC of unentrapped levobupivacaine in the Lipid group, or in the plasma half-lives. The cardiovascular outcome and normalisation of the electrocardiogram were similar in both groups. Five pigs developed marked hypotension: one in both groups died, while two in the Lipid group and one in the Ringer group needed adrenaline. Administration of lipid emulsion did not improve cardiovascular recovery from levobupivacaine toxicity exacerbated by acidosis and hypoxaemia. Lipid emulsion did not entrap levobupivacaine or affect levobupivacaine pharmacokinetics.

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