fat embolism syndrome


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fat embolism syndrome

Emboli composed of fat are common, relatively innocuous and may occur in alcoholism, BM biopsy, cardiopulmonary bypass, compression injury, DM, lymphangiography, pancreatitis, sickle cell anemia, corticosteroid therapy; contrarily, the FES is neither common nor trivial; clinically significant FE may be endogenous or exogenous in origin; most are due to major fractures, especially of long bones, and trauma to parenchymal organs–eg, the liver–most deaths in the immediate post-trauma period have significant fat embolism, burns, blast injury, severe infections, especially α-toxin-producing Clostridium spp Clinical Hypoxia–50% of femoral shaft fractures have ↓ arterial PO2 within the first few days, acute onset of dyspnea, tachypnea, cyanosis, tachycardia with sudden onset of right-sided cardiac failure, showers of petechiae, thrombocytopenia, cerebral embolism–with changes in personality, confusion, drowsiness, weakness, agitation, spasticity, defects of the visual field, and rarely, extreme pyrexia Diagnosis It had been reported that fat droplets in a BAL was indicative of fat embolism, a finding which in one small–34 group of Pts proved to have a low specificity of 26.5%; > 3% oil red O positive macrophages in the BAL are often found in trauma Pts, and may indicate FES or silent FE Treatment No therapy is effective. See Embolism.
References in periodicals archive ?
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.