LipidRescue™ Resuscitation

This is an admittedly ill-informed crazy idea. Could lipid rescue do any good in a catastrophic amniotic fluid embolism? As far as I can tell, the pathogenesis of this condition is still unclear. Perhaps there is a lipid-soluble mediator that could be kept from causing so much trouble. Does anyone have any thoughts on this?

Again, this is just speculation, but one possible mediator could be platelet-activating factor. PAF is found in amniotic fluid, and in much greater amounts after labor starts. Perhaps amniotic fluid embolism causes its damage by being, in essence, an IV bolus of PAF. PAF is lipid soluble, so perhaps lipid rescue could lessen the damage.

Intralipid for Amniotic Fluid Embolism (AFE)?
http://www.csen.com/oja.pdf

Lipid Emulsion Rescue of Amniotic Fluid Embolism Induced Cardiac Arrest: A Case Report
http://www.csen.com/AFE.pdf

"As a last resort, IV lipid 20% emulsion (1.5mL/kg) was administered as a bolus. Within 30 to 90 seconds, the patient had return of spontaneous circulation, normal sinus rhythm, and dramatic improvement in left and right ventricular function, shown clearly by TEE. After several minutes, the patient’s condition slowly deteriorated once again to asystole, at which time CPR was once again started and a second lipid emulsion bolus (1.5mL/kg) was administered and followed with an infusion at 0.25mL/kg/min. Within 30 to 60 seconds, the patient again had a return of spontaneous circulation with normal sinus rhythm. In addition, she also exhibited spontaneous movements of her extremities."

"Although Eldor and Kotlovker (13) were the first to suggest a possible benefit of lipid emulsion therapy in the treatment of AFE, this is the first published instance in which a patient received intravenous lipid emulsion temporally related to the recovery from cardiovascular collapse associated with amniotic fluid embolism. The main limitation is the fact that AFE is a diagnosis of exclusion; however, other differential diagnoses are less likely. There is TEE evidence that shows overall improvement of cardiac function temporally related to administration of lipid emulsion. The patient had return of spontaneous circulation occurring shortly after the administration of lipid emulsion on 2 different occasions after exhausting all other ACLS options, suggesting that lipid emulsion may have been responsible for the successful resuscitation. In addition, after the initial improvement, a relapse occurred, which was treated with a second bolus of lipid emulsion after which the same improvement in clinical and cardiac function occurred. Full neurologic recovery was noted after significantly prolonged cardiovascular collapse with chest compressions (40 minutes) and exhaustion of other standard ACLS medications. The excellent neurologic recovery emphasizes the importance of high quality and sustained CPR. Furthermore, a possible physiologic mechanism for the cardiopulmonary recovery is presented and is based on scientific models from previous research on the effects of lipid emulsion and its components. This report suggests a possible benefit of lipid emulsion therapy in the treatment of cardiovascular collapse caused by AFE, and further research will be required to elucidate the role of lipid emulsion therapy in the setting of AFE."