TITLE:
Intralipid for Amniotic Fluid Embolism (AFE)?
AUTHORS:
Joseph Eldor, Vladimir Kotlovker
KEYWORDS:
Intralipid; Bupivacaine Toxicity; Amniotic Fluid Embolism
JOURNAL NAME:
Open Journal of Anesthesiology,
Vol.2 No.4,
September
5,
2012
ABSTRACT: In 1998 it was first showed that intravenous Intralipid could prevent or improve resuscitation from cardiovascular collapse by severe bupivacaine overdose in rats. Since then published examples now include toxicities related to verapamil, diltiazem, amlodipine, quetiapine and sertraline, haldoperidol, lamotrigine, olanzapine, propranolol, atenolol, nevibolol, doxepin, dosulepin, imipramine, amitriptyline, glyosphate herbicide, flecainide, venlafaxine, moxidectin, and others. Amniotic fluid embolism (AFE) is a rare but potentially catastrophic obstetric emergency. Despite earlier recognition and aggressive treatment, morbidity and mortality rates remain high. An estimated 5% - 15% of all maternal deaths in Western countries are due to AFE. The pathophysiology of AFE is not completely understood. AFE most commonly occurs during labor, delivery, or the immediate postpartum period. However, it has been reported to occur up to 48 h postpartum. Pulmonary hypertension and right heart strain/failure may be the result of physical amniotic fluid debris in the pulmonary vasculature or, perhaps more likely, result from circulating pulmonary vasoconstrictive mediators. Therapy with Intralipid in male rats resulted in 100% survival and prevented Pulmonary arterial hypertension-induced right ventricular failure by preserving right ventricular pressure and right ventricular ejection fraction and preventing right ventricular hypertrophy and lung remodeling. In preexisting severe Pulmonary arterial hypertension, Intralipid attenu-ated most lung and right ventricular abnormalities. The beneficial effects of Intralipid in Pulmonary arterial hypertension seem to result from the interplay of various factors, among which preservation and/or stimulation of angiogenesis, suppression and/or reversal of inflammation, fibrosis and hypertrophy, in both lung and right ventricular, appear to be major contributors. In conclusion, Intralipid not only prevents the development of Pulmonary arterial hypertension and right ventricular failure but also rescues preexisting severe Pulmonary arterial hypertension. Intralipid treatment is a new treatment for AFE (amniotic fluid embolism) which was never suggested before. Animal studies should be done in order to evaluate this new treatment modality.