Pathophysiology
The pathophysiology of fat embolisms is still controversial and many theories have been proposed. Why some patients develop fat embolism while others don’t is not exactly understood and no single theory explains all the pathophysiological features of FES. The mechanical and biochemical theory are most accepted. The mechanical, or “infloating” theory, proposed by Gauss in 1924 states that as pressure increases in the intramedullary space, during trauma or surgical manipulation, yellow fat is forced out and enters the venous circulation through breaks in the vessel walls, where it can clump and form thrombotic masses.12 Limitations of the mechanical theory are that is does not explain the 24 to 72 hour interval until symptoms occur and it does not explain nontraumatic FES. The biochemical theory, also known as the free fatty acid and lipase theory, was proposed by Lehmann in 1927. This theory suggests that an inflammatory cascade occurs when fat embolisms are degraded into free fatty acids, which are known to injure pneumocytes and capillaries resulting in pulmonary inflammation.13 The combination of the mechanical and the biochemical theory, thus initiation of the symptoms by fat globules followed by the inflammatory cascade, is also described.