DISCUSSION: The chronology of events and symptoms in present case, along with laboratory findings has been instrumental in diagnosis of fat embolism syndrome.
Both these criteria are not gold standard for diagnosis of fat embolism syndrome, but since diagnosis of FES is made clinically not chemically, we arrived at diagnosis of FES, even in absence of any evidence of bony or intra- abdominal injury.
Differential diagnosis in our case, included thromboembolism, heart failure, lung contusion, pulmonary hemorrhage and fat embolism syndrome.
Systemic corticosteroid could be of help in prevention, if used prophylactically, (9) but it was of doubtful role in our case of established fat embolism syndrome.
CONCLUSION: Without validated clinical criteria, diagnosis of fat embolism syndrome is quite challenging for a clinician, who should have high index of suspicion for fat embolism syndrome, particularly in breathless patients with history of trauma, even in absence of any evidence of bony or soft tissue injuries.
Neurological Manifestations of Fat Embolism Syndrome.
As opposed to computed tomography (CT) findings in other forms of ARDS, radiological features have only been described occasionally in severe fat embolism syndrome.
In this report, we present a case of severe fat embolism syndrome with unique CT findings including subpleural and centrilobular nodules.
Fat embolism syndrome is an infrequent clinical consequence of fat embolism, which is characterized by the release of fat droplets into the systemic circulation following trauma, particularly pelvic or long bone fractures.
Fat embolism syndrome is initiated by the release of bone marrow and fat into the circulation, which mechanically blocks the vasculature of the lungs and other vascular sites (skin, brain and kidney) (5).
In the prevention of fat embolism syndrome, the early splinting and early fixation of fractures are emphasized.
The description of CT findings in severe fat embolism syndrome is however virtually non-existent.