Fat Embolism - Pathogenesis

Pathogenesis

The pathogenesis occurs due to both mechanical obstruction and biochemical injury. It is aggravated by local platelet and erythrocyte aggregation. The release of fatty acids from the fat globules also causes local toxic injury to endothelium. The vascular damage is aggravated by platelet activation and recruitment of granulocytes.

Several mechanisms have been proposed to explain the pathogenesis of fat embolism. They may be acting together or singly.

1. Mechanical. Mobilisation of fluid fat following trauma to bone and soft tissue.
2. Emulsion instability. Explains the pathogenesis of fat embolism in non traumatic cases. Fat embolus formed by aggregation of plasma lipids (chylomicrons and fatty acids) due to disturbances in emulsification of fat. Symptoms include fatty liver (hepatic steatosis).
3. Intravascular coagulation. May result from to disseminated intravascular coagulation (DIC).
4. Toxic injury. Blood vessels injured by high plasma levels of free fatty acid, results in increased vascular permeability and consequently pulmonary edema.