Pathophysiology of fat embolism: A rabbit model.

Blankstein M, Byrick RJ, Richards RR, Mullen JB, Zdero R, Schemitsch EH. Pathophysiology of fat embolism: A rabbit model. J Orthop Trauma. 2011;25:674-80.



The objective of this study was to assess the effects of fat embolism on rabbit physiology.


After anesthetic administration, both femoral condyles of the right knee only of 23 New Zealand white rabbits were exposed through a medial parapatellar approach to the knee. In the pulmonary fat embolism group (n = 15), the femoral canal was drilled in a retrograde fashion and then reamed and pressurized with a 1- to 1.5-mL cement injection. In the no-pressurization group (n = 4), after reaming, no cement was injected. In the control group (n = 4), the knee incision was immediately closed. Animals were then observed for 5 hours. Hemodynamics and blood gases were recorded at standard intervals. Postmortem, the lungs were removed en bloc and fixed for histologic assessment and quantitative histomorphometry.



Four intraoperative deaths occurred in the pulmonary fat embolism group immediately after pressurization and may have been associated with hypotension and cardiac arrest. In the pulmonary fat embolism group, pulmonary artery pressure increased, and both mean arterial pressure and PaO2 decreased after pressurization. Approximately 2% of lung volume was occupied by intravascular fat and there were no signs of perivascular inflammation. Control and no-pressurization animals remained stable throughout the experiment.



This model simulates pulmonary fat embolism after long-bone fractures. Despite cardiorespiratory dysfunction, there was no evidence of fat initiating pulmonary inflammation based on histologic data within the timeframe of the investigation.