Experimentally induced fat embolism syndrome: shift from obstruction to toxic effects

Abstract

Liposuction, which is widely performed in the field of plastic surgery, was recently identified as a necessary process for the harvesting of adipose-derived stem cells [1]. In liposuction, fat tissue is crushed and removed using physical force. An inevitable consequence of liposuction is damage to the small vessels, through which shredded pieces of fat (fat emboli) can then flow; this phenomenon is known as fat embolism. If a pathologic state results, it is called fat embolism syndrome (FES) [2]. In FES, fat emboli are not fat tissue fragments or fat cells; rather, they are lipid drops floating in the circulation [3]. FES was first reported by Zenker [4] in 1862. Both fulminantacute and sub-acute FES, which are caused by an abnormal influx of fat into the blood vessels, are associated with characteristic clinical symptoms, including petechiae, confusion, and acute respiratory failure. FES can have fatal complications. Fortunately, most instances of fat embolism are subclinical [5]. Fat, the causative agent of FES, can be divided into two types: transported fat, which is present in the blood; and stored fat, which is located outside the blood vessels. Transported fat is in the form of chylomicrons bound to apolipoprotein, whereas stored fat accumulates within adipocytes as triglycerides (TGs). TGs can be hydrolyzed to free fatty acids (FFAs) by lipase, and FFAs bound to alHong Il Kim, Seok Kyung In, Hyung Suk Yi, Hyo Young Kim, Yoon Soo Kim