IV FAT EMULSION INFUSION TRIAL

Increasing the intracellular myocardial fatty acid content, thereby replenishing tissue ATP stores (2, 3, 10, 12).There are proposed secondary modalities explaining the beneficial effects of ILE, including: This proposed modality states that, rather than a static lipid compartment, ILE acts as a scavenger of lipophilic toxins, removing the drug from sensitive organs and areas of high blood flow, such as the heart and brain, and redistributing them to other organs like the muscles for storage and the liver for detoxification (3, 4, 9). Research now supports the lipid shuttle theory, which builds on the lipid sink theory. It was postulated that this would subsequently remove the toxic drugs from the circulation (2, 3, 4, 7, 8, 9, 10, 11).Ĭritics have since stated that a static lipid reservoir would become saturated too quickly before removing sufficient toxin from circulation. This theory states that ILE creates an intravascular lipid layer, providing a binding surface for lipophilic toxins. Originally, the lipid sink theory was favoured.

Many different theories have been proposed with the partitioning theory gaining widespread acceptance. The mechanism of action of Intravenous Lipid Emulsion (ILE) is not well understood. ILE was trialed as a rescue therapy, resulting in ROSC shortly thereafter (6). She experienced refractory cardiac arrest for over 50 minutes. A 17 year old woman presented to the emergency department following an intentional overdose on her Lamotrigine and Bupropion. In 2007, the first clinical use of ILE outside of LAST was documented. This resulted in return of spontaneous circulation (ROSC) shortly thereafter (5).

IV FAT EMULSION INFUSION TRIAL

He exhibited refractory cardiac arrest, ongoing for 20 minutes, prompting a trial of ILE. A 58 year old male experienced local anesthetic systemic toxicity (LAST) following an uncomplicated interscalene nerve block. ILE was first used in human clinical therapy in 2006. In 2003, they repeated these experiments in dogs, and again found that ILE improved survival following bupivacaine induced arrest (3, 5). They also found that rats resuscitated with ILE following bupivacaine induced arrest had improved survival (2, 3, 4, 5). They discovered that rats pretreated with ILE required higher doses of bupivacaine to experience cardiac arrest. They injected intravenous lipids in animal models, as they believed this would mimic a carnitine deficient state. Weinberg and colleagues tested their hypothesis in animal models in 1998. They later discovered that this patient had a carnitine deficiency, leading to their theory that carnitine deficiency was associated with increased susceptibility to bupivacaine toxicity (2,3).ĭr. Weinberg and colleagues noted a case of unexplained ventricular arrhythmia following a sub-toxic dose of bupivacaine in a healthy 16 year old woman. The original intention of Intravenous Lipid Emulsion (ILE) was for total parenteral nutrition (TPN) (1). Intravenous lipids were originally created by Dr. We seek to review the available literature discussing ILE and provide you with some recommendations on its clinical application. The precise mechanism of action remains unknown, no definitive consensus exists regarding its clinical indications, and there are no high quality studies evaluating its potential benefits in humans. Much uncertainty still exists surrounding intravenous lipid emulsion (ILE) therapy.

Iv fat emulsion infusion