OBJECTIVES:Intravasation of bone marrow contents into venous circulation and pulmonary embolization after intramedullary nailing may be coupled with the activation of coagulation and fibrinolytic ...cascades. The objective of this study was to assess hemostatic response to pulmonary extravasated marrow contents. We hypothesize that activation of platelet activity and the coagulation cascade may occur after embolization of marrow contents in an experimental animal model of intramedullary nailing.
METHODS:Fifteen New Zealand white male rabbits were randomly assigned to control or fat embolism (FE) groups. In the FE group (n = 8), femurs were surgically instrumented with retrograde intramedullary nails and pressurized with bone cement. In the control group (n = 7), a sham knee incision was made that was immediately closed without drilling, reaming, or pressurization. Fibrinogen, D-dimer latex screen assay, 1 stage prothrombin time, and activated partial thromboplastin time were analyzed.
RESULTS:As the main platelet activation indicators, the marker Annexin-V percent binding increased in the FE group at 2 hours (P = 0.04) and 4 hours (P = 0.04), and the marker CD62P percent expression increased in the FE group at 2 hours (P = 0.04).
CONCLUSIONS:This preliminary study showed that pressurization of marrow and intravasation of fat and marrow products cause activation of platelets and the coagulation cascade, with or without tissue trauma. This may be relevant to the treatment of multiply injured patients with prior respiratory and coagulation abnormalities. A future larger study may be needed.
Pathophysiology of Fat Embolism: A Rabbit Model Blankstein, Michael; Byrick, Robert J; Richards, Robin R ...
Journal of orthopaedic trauma,
2011-November, Letnik:
25, Številka:
11
Journal Article
Recenzirano
OBJECTIVES:The objective of this study was to assess the effects of fat embolism on rabbit physiology.
METHODS: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.
RESULTS: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.
CONCLUSIONS: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.
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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