Back to INTERNAL MEDICINEOther forms of trauma that rarely result in fat embolism include massive soft tissue injury, severe burns and liposuction. Nontraumatic settings occasionally lead to fat embolism. These include conditions associated with fatty liver, prolonged corticosteroids therapy, acute pancreatitis, osteomyelits, and conditions causing bone infarcts, such as sickle cell disease.
The principal clinical features of fat embolism syndrome are: Respiratory failure, Cerebral dysfunction and Petechiae
The source of fat droplets can be from disrupeted fat-containing tissues, or as a result from the release of some substance that alters fat emulsion in the plasma. As support for the last explanation, is the observation that intravascular coagulation occurs coincident with thrombocytopenia.
It is also clear that the syndrome is not simply a consequence of mechanical obstruction of small vessels by fat droplets. An important aspect of the pathogenesis of FES appears to be endothelial injury caused by fatty acids released from impacted fat droplets by lipoprotein lipase, with ensuring increased microvascular permeability and fluid leakage into interstitial spaces.
The onset of FES is sudden, with Restlessness and vague pain in the chest. Fever occurs, often in excess of 38,3 C (101 F), with a disproportionatelly pulse rate. Drowsiness with oliguria is almost pathognomonic; but the clinical diagnosis is definite if all the three following criteria are present within 72 hours after traumatic fracture.
1) Otherwise unexplained dyspnea, tachypnea, arterial hypoxemia with cyanosis and diffuse alveolar infiltrates on chest X-ray
2) Otherwise unexplained signs of cerebral dysfunction, such as confusion, delirium or coma.
3) Petechiae over the upper half of the body, conjunctive, oral mucosa and retinae.
Search for fat droplets in the urine, blood or CSF are occasionally helpful. In a recent study, large fat droplets were formed in brochoalveolar lavage cells of patients with definite fat embolism syndrome.
Other laboratories tests can be helpful are:platelet count, red blood cell count lipase and calcium serum dosage(which can be elevated and decrease respectively).
Management of fat embolism syndrome is supportive and consists primarily of ensuring good arterial oxygenation. Supplemental oxygen is given to maintain the arterial oxygen tension in the normal range. Restriction of fluid intake and the use of diuretics can be done (if systemic perfusion can be maintained), to minimize fluid accumulation in the lungs .
Prompt surgical stabilization of long bones fractures and correcting or preventing decreased systemic perfusion, reduce the risk of the syndrome.
The mortality rate from fat embolism syndrome is 10 percent or less and thus is clearly much lower then the 50 percent or greater mortality rate for most causes of the adult respiratory distress syndrome. Even severe respiratory failure associated with fat embolism seldom leads to death.
Zollinger-Ellison syndrome. InWynngaarden JB, Smith LH, Bennet JC(eds): CecilTextbook of Medicine, 20th edition. W B SaundersCompany, 1996.
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