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Scientific Articles   |    
Amplified Inflammatory Response to Sequential Hemorrhage, Resuscitation, and Pulmonary Fat EmbolismAn Animal Study
Michael Blankstein, MD1; Robert J. Byrick, MD2; Masaki Nakane, MD2; K.W. Annie Bang, PhD3; John Freedman, MD2; Robin R. Richards, MD, FRCS(C)2; Osamu Kajikawa, PhD4; Rad Zdero, PhD5; David Bell, MD2; Emil H. Schemitsch, MD, FRCS(C)1
1 St. Michael's Hospital, 55 Queen Street East, Suite 800, Toronto, M5C 1R6 ON, Canada. E-mail address for E.H. Schemitsch: schemitsche@smh.toronto.on.ca
2 Department of Anesthesia (R.J.B., M.N., R.R.R., and D.B.) and Department of Medicine, Haematology and Platelet Research Laboratory (J.F.), St. Michael's Hospital, 30 Bond Street, Toronto, M5B 1W8 ON, Canada
3 Pathology and Laboratory Medicine, Mt. Sinai Hospital, 600 University Avenue, Toronto, M5G 1X5 ON, Canada
4 Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington, 325 Ninth Avenue, Seattle, WA 98104-2499
5 Department of Mechanical and Industrial Engineering, Ryerson University, 350 Victoria Street, Toronto, M5B 2K3 ON, Canada
View Disclosures and Other Information
Disclosure: The authors did not receive any outside funding or grants in support of their research for or preparation of this work. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity.

Investigation performed at St. Michael's Hospital, Toronto, Ontario, Canada

Copyright ©2010 American Society for Journal of Bone and Joint Surgery, Inc.
J Bone Joint Surg Am, 2010 Jan 01;92(1):149-161. doi: 10.2106/JBJS.H.01141
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Abstract

Background: 

The objective of this study was to assess the role of pulmonary fat embolism caused by intramedullary pressurization of the femoral canal in the development of acute lung injury in the setting of acute hemorrhagic shock and resuscitation.

Methods: 

Thirty New Zealand White rabbits were randomly assigned to one of four groups: (1) nine animals in which hemorrhagic shock was induced by carotid bleeding, resuscitation was performed, and the femoral canal was reamed and pressurized with bone cement to induce fat embolism (hemorrhagic shock and resuscitation/fat embolism [HR/FE] group); (2) six animals in which shock was induced by carotid bleeding, resuscitation was performed, and a sham knee incision was made and closed without drilling, reaming, or pressurization (hemorrhagic shock and resuscitation [HR] group); (3) eight animals in which no hemorrhage or shock was induced but the femoral canal was reamed and pressurized with bone cement to induce fat embolism (fat embolism [FE] group); and (4) seven animals that had a three-hour ventilation period followed by a sham knee incision (control group). The animals were ventilated for four hours following closure. Flow cytometry with use of antibodies against CD45 and CD11b was performed to test neutrophil activation in whole blood. Histological examination of lung specimens was also performed. Plasma and bronchoalveolar lavage fluid were analyzed for monocyte chemotactic peptide-1 and interleukin-8 levels with use of the ELISA (enzyme-linked immunosorbent assay) method.

Results: 

Three animals in the HR/FE group died immediately after canal pressurization and were excluded. CD11b mean channel fluorescence was significantly elevated, as compared with baseline, only in the HR/FE group at two hours (p = 0.025) and four hours (p = 0.024) after knee closure. Histological analysis showed that only the HR/FE (p < 0.001) and HR (p = 0.010) groups had significantly greater infiltration of alveoli by polymorphonuclear leukocytes as compared with that in the controls. No significant differences in plasma cytokine levels were found between the groups. Only the HR/FE group had significantly higher interleukin-8 (p = 0.020) and monocyte chemotactic peptide-1 (p = 0.004) levels in the bronchoalveolar lavage fluid as compared with those in the controls.

Conclusions: 

Fat embolism from canal pressurization alone did not activate a pulmonary inflammatory response. The combination of hemorrhagic shock, resuscitation, and fat embolism elicited neutrophil activation, infiltration of alveoli by polymorphonuclear leukocytes, and inflammatory cytokine expression in bronchoalveolar lavage fluid.

Clinical Relevance: 

The parameters measured may be early indicators of an inflammatory response leading to fat embolism syndrome.

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    Accreditation Statement
    These activities have been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint sponsorship of the American Academy of Orthopaedic Surgeons and The Journal of Bone and Joint Surgery, Inc. The American Academy of Orthopaedic Surgeons is accredited by the ACCME to provide continuing medical education for physicians.
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