1 Acta Ortopédica Brasileira 2005 Vol: 13(4):. DOI: 10.1590/S1413-78522005000400010

Embolia gordurosa: uma revisão para a prática ortopédica atual

Fat embolism (FE) is the occlusion of small blood vessels by fat droplets originated mainly from femur, tibia and pelvis fractures, as well as from knee and hip arthroplasty. It usually does not cause damage to the involved organs, unless when it is massive. In a few cases, FE evolves to the 'fat embolism syndrome' (FES), affecting most often the lungs and the brain, although any organ or structure of the body can be damaged. Fat embolisms are hydrolyzed by lipase, forming free fatty acids (FFA), which cause a toxic effect to capillary endothelium, intensifying integrins activity, which, in turn, intensify neutrophils' adherence to endothelial cells, making easier the activity of the proteolytic enzymes of such neutrophils' lysosomes on the endothelium. The result of those reactions is the capillary meshwork rupture, followed by hemorrhage and edema on affected organs. The FES presents many conditions, ranging from respiratory failure and variable neurological changes, to convulsions and deep coma. The diagnosis of FES is essentially made on clinical basis only, since there are no laboratory tests to validate it. Among imaging tests, only brain magnetic resonance clearly shows the perivascular edema and infarction areas. FE treatment with uncountable drugs did not present positive results; however, the most required measure to FES is mechanical ventilation. Mortality rate is almost 100% in fulminant forms; approximately 20% in the sub acute forms, and there is no mortality in a sub clinical form. In order to prevent FES is crucial to avoid shock and hypoxia from the accident scenery, and to proceed to the early fixation of fractures, which reduces the incidence of SARA and post-trauma mortality.

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