Fat embolism is usually diagnosed on the basis of clinical findings[1]–[3]. According to the literature, Gurd’s criteria[1], consisting of major and minor clinical features, is the most commonly used diagnostic tool. Up to now, the diagnosis of FES has remained clinical[3] without a reference gold standard system. Our patient showed the pathognomonic triad of petechiae, hypoxia, and confusion. Radiological and CT findings confirmed the diagnosis.
Reamed intramedullary nailing continues to be the gold standard for stabilizing femoral and tibial shaft fractures. Reaming of the femoral or tibial canal allows insertion of a larger-diameter nail, optimizing the mechanical environment. Also, with the release of the products of reaming (endogenous growth factors and reaming debris), it provides an osteogenic stimulus. It is known, however, that reaming the medullary canal stimulates the immunoinflammatory system, leading to a “second hit” phenomenon. This is especially true in patients with a high ISS and associated chest injuries[13, 14].
In an attempt to reduce the incidence of fat embolism during reaming and nailing of long bone fractures, the reamer/irrigator/aspirator (RIA) system was developed (Synthes, Paoli, PA, USA). Experimental data suggest that the RIA device prevents fat embolism, although clinical evidence is lacking[15].
From a pathological point of view, fat emboli occur in nearly all patients after long bone fractures, although in most patients they are benign and without clinical consequences[2]. The reason for the development of FES in some individuals and not others remains unclear.
Based on the ISS, Pape et al.[16] categorized patients with femoral fractures as being stable, borderline, unstable, or in extremis. Because our patient was clinically categorized as stable (ISS of 9, thoracic Abbreviated Injury Score of 0, NISS of 9), we performed the nailing procedure. From an immunological point of view, our patient probably was not stable. He was likely borderline stable/unstable.