No abstract

Fat embolism (FE) occurs frequently after trauma and during orthopaedic procedures involving manipulation of intramedullary contents. Classically characterized as a triad of pulmonary distress, neurologic symptoms, and petechial rash, the clinical entity of FE syndrome is much less common. Both mechanical and biochemical pathophysiologic theories have been proposed with contributions of vascular obstruction and the inflammatory response to embolized fat and trauma. Recent studies have described the relationship of embolized marrow fat with deep venous thrombosis and postsurgical cognitive decline, but without clear treatment strategies. Because treatment is primarily supportive, our focus must be on prevention. In trauma, early fracture stabilization decreases the rate of FE syndrome; however, questions remain regarding the effect of reaming and management of bilateral femur fractures. In arthroplasty, computer navigation and alternative cementation techniques decrease fat embolization, although the clinical implications of these techniques are currently unclear, illustrating the need for ongoing education and research with an aim toward prevention.

Objectives: To identify the incidence and risk factors for development of tibial plafond nonunion. Design: Retrospective comparative study. Setting: Two Level 1 academic trauma centers. Patients/Participants: Seven hundred forty tibial plafond fractures (OTA/AO 43B3 and 43C) treated January 2006 to December 2015. Intervention: Open reduction and internal fixation. Main Outcome Measurement: Nonunion. Results: Five hundred eighteen patients with a mean age of 43 years (range, 18–81 years) and mean follow-up of 27 months (range, 12–115 months) were involved. Seventy-two patients (72/518, 14%) were identified as having a nonunion. Surgical approach was not associated with nonunion in univariate analysis. Multiple regression model 1 identified OTA/AO 43C [odds ratio (OR) = 4.43; 95% confidence interval (CI), 1.01–19.41; P = 0.048], tobacco use (OR = 2.02; 95% CI, 1.10–3.71; P = 0.024), both minimal and substantial bone loss (P = 0.006 and P < 0.001, respectively), and open fracture (OR = 1.96; 95% CI, 1.10–3.48; P = 0.022) as risk factors for tibial plafond nonunion. Model 2 identified locking plate (OR = 1.97; 95% CI, 1.13–3.40; P = 0.016) and failure to treat the medial column (vs. screw P = 0.047, or plate P = 0.038) as risk factors. Conclusions: The tibial plafond nonunion rate was 14%. Bone loss, open fracture, failure to treat the medial column, locking plates, and tobacco use were all significant risk factors for developing tibial plafond nonunion. Equally important, surgical approach was not significantly associated with plafond nonunion. Level of Evidence: Therapeutic Level IV. See Instructions for Authors for a complete description of levels of evidence.

Diagnostic Level III. See Instructions for Authors for a complete description of levels of evidence.