Fat Emboli Syndrome in association with trauma most commonly
occurs secondary to long bone and pelvic fractures. The rate of developing FES
with a single long bone fracture is between 1-3% and higher depending on the
number of fractures. Fat globules can enter the bloodstream from bone marrow
following a traumatic injury. Once in the arterial circulation, the fat
droplets can lodge into small vessels and also release chemical mediators
causing inflammation and ischemia leading to multiorgan dysfunction.
FES usually presents 1-3 days after the initial injury. Hypoxemia
with tachypnea and dyspnea are usually the earliest findings and many patients
will require mechanical ventilation. Neurological changes are also common and
may include confusion, depressed consciousness, seizures and focal deficits. A
petechial rash can also develop but is not as common as the other symptoms.
Fever, coagulation abnormalities and myocardial depression may also occur.
FES is a clinical diagnosis as it cannot be confirmed or
excluded using any currently available diagnostic tests. Chest XR may show
diffuse bilateral pulmonary infiltrates and increased pulmonary markings. Chest
CT might demonstrate focal areas of ground glass opacifications. Brain MRI can
display areas of high intensity T2 signal and head CT may show petechial
hemorrhages or can appear completely normal.
The risk of FES can be reduced by early immobilization and
surgical repair of fractures. Currently treatment includes only supportive
care. Some studies have shown that use of prophylactic corticosteroids may
reduce the incidence of FES but this treatment is still controversial as there
is limited evidence in its routine use. Most patients who suffered from FES
have a complete recovery, however, some may develop residual long-term neurological
deficits. Mortality rates have been reported between 5-15%.
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