Fat Embolism Syndrome Following Bone Fracture May Be Exacerbated By LPS

Abstract

Fat embolism (FES) after major bone fracture may lead to acute respiratory distress but little clinical evidence of lung injury remains. However, a study of patients with severe fractures showed reduced pulmonary function many years post‐injury. In rats modeling FES by i.v. triolein, we saw that despite an apparent full recovery, modest fibrotic damage persisted up to 6 weeks. We tested whether at that time an additional insult could exacerbate the lung effects. The model was established with 0.2 mL triolein i.v. to 18 rats and saline to 18 controls. Six weeks later, each group received (i.p.) lipopolysaccharide (LPS) n=9 or saline n=9. At necropsy 48 hr later BALs, lungs and organs were harvested for study. Lung parenchymal, vascular and bronchial damage was scored by 3 pathologists. Saline controls receiving LPS showed pulmonary arterial medial diameters wider than those of animals given triolein before LPS (p<0.04). Adventitia of lung vessels from triolein treated rats showed a significant difference between saline vs. LPS administration (p<0.02). LPS produced a threefold increase in PMN in BAL. At 6 weeks triolein droplets remained in rat lungs localizing to the subpleural septa, smaller and more widespread when LPS was given. Thus, LPS, a “second hit”, administered after triolein FES model produces a more severe lung damage to pulmonary arteries than does LPS following saline.Funded: Gelmacher Foundation