Through mechanical obstruction and inflammation, fat embolism syndrome (FES) cause respiratory failure, petechiae, altered consciousness and fall in blood pressure. Inflammation secondary to fat embolization is of major pathophysiological significance, although the exact mechanism by which fat emboli cause severe inflammation remains to be elucidated. Fat emboli gain access to the venous system most frequently after long bone or pelvic fractures or during orthopedic surgery.
FES is characterized by fat unintentionally entering the venous circulation, causing mechanical occlusion of smaller blood vessels leading to pulmonary, and – in traveling into the arterial circulation – myocardial and cerebral infarction. It is established that right-to-left shunt occurs even in the absence of a persistent foramen ovale, as in our case. Fat embolism has also been observed in medical conditions such as pancreatitis, hemoglobinopathies and fatty liver disease.
In the present project we will study the effect of fat and bone marrow on the inflammatory and hemostatic systems both in in vivo whole blood models, in pig studies and in clinical studies. We suggest it is necessary to better understand the inflammatory interplay in order to describe the pathophysiology of fat embolism. It can lead to improved preventive and diagnostic measures and could identify targets and substances for clinical therapeutic intervention.