![]() the patient continues to be unstable or in cardiopulmonary arrest,. ![]() there are no further conventional therapy options,.appropriate high quality supportive care has been administered,.Lipid emulsion therapy can be considered as a last resort in drug toxicity when: When it comes to severe drug toxicity we are often dealing with a patient with unstable hemodynamic parameters and a poor prognosis. 5,6 Lipid Rescue () offers case reports for lipid emulsion use in a multitude of drug toxicities including tricyclic antidepressants, cocaine, and non-dihydropyridine calcium channel blockers. 2 Formal guidelines do exist for lipid emulsion use in local anesthetic toxicity and the best evidence is for bupivacaine toxicity. When should I use lipid emulsion therapy?Īt this point in time, there is no FDA approved indication for lipid emulsion therapy in drug toxicity. Enhanced cardiac metabolism theory: In situations of myocardial depression due to drug toxicity, it is thought that myocardial contractility might be improved by providing extra substrate in the form of fatty acids.Partitioning or “lipid sink” theory: Partitioning is thought to work by providing a “sink” for which lipophilic xenobiotics can reside thus removing them from accessibility to end organ receptors.There are two prevailing theories that are most often quoted: (Image courtesy of James Heilman, MD via Creative Commons license). 4įigure 2: 100mL bag of 20% lipid emulsion. 4–6 Case reports continue to be published highlighting lipid emulsion therapy for an ever-expanding number of drug toxicities including non-dihydropyridine calcium channel clockers, beta blockers, bupropion, lamotrigine, and tricyclic antidepressants. Since then, several other case reports have emerged and clinical guidelines have been developed for lipid emulsion therapy in severe local anesthetic toxicity. Following this treatment, the patient was successfully electrically cardioverted. Shortly before cardiopulmonary bypass was to be performed, 100 mL of 20% lipid emulsion was given intravenously, followed by 0.5 mL/kg/hr for 2 hours. Shortly after injection the patient had a generalized tonic-clonic seizure followed by a 20-minute cardiac arrest with various cardiac dysrhythmias. In 2006, the first case report was published in which an adult male patient was inadvertently injected intravenously with 20 mL of 0.5% bupivacaine and 20 mL of 1.5% mepivacaine in the context of a brachial plexus block for rotator cuff repair. 2 This led to further studies involving dogs and eventually humans. 2 Its use in toxicology dates to the late 1990s when rat models demonstrated a survival benefit in bupivacaine toxicity. Intravenous lipid emulsion has been around for a long time in the form of total parenteral nutrition and as a vehicle for lipophilic drugs most notably propofol. ![]() At the same time, you begin to think ahead to what vasoactive agent you might give, whether you will need antiarrhythmic agents, and what the evidence suggests for intravenous lipid emulsion in drug overdose. 1You gain intravenous access, initiate continuous cardiac monitoring, and begin administering intravenous sodium bicarbonate boluses. Figure 1: 12 lead ECG showing characteristic changes related to tricyclic antidepressant toxicity.
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