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.