PULMONARY AND SYSTEMIC FAT EMBOLIZATION AFTER MEDULLARY CANAL PRESSURIZATION - A HEMODYNAMIC AND HISTOLOGIC INVESTIGATION IN THE DOG

Background: The potential to produce fat embolism may be important in determining the ideal method and timing of fracture treatment in patie nts with preexisting lung injury. Methods: Four dogs underwent femoral and tibial canal reaming and pressurization. Blood gas samples were a nalyzed, and pulmonary arterial pressure was monitored at 1 and 72 hou rs. Animals were killed 72 hours postoperatively, and the lungs, kidne ys, and brain were examined histologically and compared with equivalen t specimens from four control dogs that had not undergone femoral and tibial canal reaming and pressurization. Results: Postmortem, intravas cular fat persisted for 72 hours after induction of pulmonary fat embo lism. Mean Pao(2) was unchanged from baseline at 72 hours after canal pressurization. Canal pressurization caused a sustained increase in pu lmonary arterial pressure (p = 0.02) for 1 hour after canal pressuriza tion. The mean pulmonary edema score at 72 hours was 29 +/- 3, Only a scant polymorph infiltrate (zero to two polymorphs per high-power fiel d) was present at any time. No hyaline membranes were seen at any time . The percentage area occupied by intravascular fat in the lungs was 0 .0214 +/- 0.0058 at 72 hours. No signs of ischemia or inflammation wer e seen in either the cerebral or the renal specimens, Conclusion: This study is the first to show that intravascular fat persists in the lun gs, kidneys, and brain for 72 hours after canal pressurization and, by itself, does not cause pathologic evidence of acute inflammation.