[Basic studies on the pathogenesis and treatment of fat embolism. I. Fracture mechanism and fat embolism]

We examined the amount of fat that can be forced into the circulation by compression of femora and of heads of the tibia in the very moment of injury. By fractures of diaphyses no considerable reduction of the intraosseous space was achieved and no fat was expelled through the foramina nutritia before the hard cortical bone was splintered. However, considerable amounts of fat were expelled into veins, when the epiphyses of the femora or when the head of the tibia was compressed from medially and from laterally. Even by a purely manual compression some fat was forced to leave the spongiosa by the foramina nutritia. This is explained by the higher elasticity of the spongious bone, permitting a marked space reduction by compression even before a fracture sets in. The mechanism resembles the procedure of opacification of veins by contrast media, injected into the bone cavity under pressure. The significance of these findings for the pathogenesis of clinical fat embolism is discussed.