A preliminary study of platelet activation after embolization of marrow contents.

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.

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.

Posttraumatic lung injury after pulmonary contusion and fat embolism: factors determining abnormal gas exchange.

BACKGROUND: The objective was to investigate changes in pulmonary blood flow after lung contusion and fat embolism. METHODS: Eighteen mongrel dogs were randomly assigned to three groups: fat embolism alone (n = 7); moderate unilateral pulmonary contusion followed by fat embolism (n = 6); and severe unilateral pulmonary contusion followed by fat embolism (n = 5). Fat embolism was produced by intramedullary reaming of left femur and tibia followed by canal pressurization using bone cement. Outcome measures were systemic blood pressure, pulmonary artery pressure, pulmonary artery occluded pressure, cardiac output (CO), and partial pressures of arterial and mixed venous oxygen (Pao2, PvO2). Samples were taken from contused and noncontused contralateral lung to calculate regional pulmonary blood flow. RESULTS: After the fat embolism, pulmonary artery pressure and pulmonary vascular resistance increased significantly (p < 0.05) in all groups, whereas Pao2 decreased in groups 2 and 3 and at 30 minutes in group 1. CO decreased significantly in group 3. Group 3 also demonstrated a greater initial decrease in Pao2 and PvO2 from baseline and a larger increase in pulmonary vascular resistance. In those animals that underwent contusion, regional pulmonary blood flow was not found to be different between contused and noncontused lung segments. After contusion, flow decreased significantly in contused and noncontused segments in group 3 only. CONCLUSIONS: Gas exchange deteriorates because of decreased CO. For any preexisting intrapulmonary shunt, the decrease of PvO2 will cause worsening of Pao2.

Amplified inflammatory response to sequential hemorrhage, resuscitation, and pulmonary fat embolism: an animal study.

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.

Case report: acute postoperative neurological impairment from fat embolism syndrome.

PURPOSE: To describe a case of fat embolism syndrome (FES) following elective tendon contracture release in a patient with myotonic dystrophy, to highlight the importance of considering this entity in the differential diagnosis of acute postoperative neurocognitive dysfunction. CLINICAL FEATURES: A 34-yr-old man with myotonic dystrophy underwent uneventful tendon contracture release under regional anesthesia. In the immediate postoperative period, neurological and respiratory complications developed, requiring intensive care support. The patient showed the classical clinical triad of hypoxemia, neurological impairment and a petechial rash associated with the FES. A diagnosis of FES was made and, despite therapy including fluid and inotropic support, the patient succumbed to the condition. There was no demonstrated intracardiac shunt, suggesting a physiological intrapulmonary shunt was responsible for the development of systemic manifestations of FES. CONCLUSIONS: Postoperative neurological dysfunction is a difficult condition with numerous possible causes. All possible etiologies, including FES, need to be considered in the differential diagnosis and postoperative management of patients developing acute postoperative neurological impairment and hypoxemia.

Intubation of SARS patients: infection and perspectives of healthcare workers.

PURPOSE: The outbreak of severe acute respiratory syndrome (SARS) in 2003 presented major challenges to the safety of anesthesiologists and other healthcare workers (HCWs). This study determined the incidence of SARS transmission to HCWs who intubated patients and analyzed the concerns of HCWs regarding personal and patient safety. METHODS: Healthcare workers who performed tracheal intubation in 10 Toronto hospitals were identified using the Ontario Public Health database. A questionnaire was used to collect information from the HCWs. To determine if the patterns of personal protection or concerns changed over time, data were analyzed according to whether the intubation occurred during SARS 1 (February 23 to April 21) or SARS 2 (April 22 to July 1). RESULTS: Thirty-three HCWs who performed 39 intubations on 35 SARS patients were interviewed. Three of 23 HCWs (13%) acquired SARS during SARS 1 whereas none (0/10) acquired SARS during SARS 2. Personal protection increased from SARS 1 to SARS 2 and HCWs' concerns changed over time. During SARS 1, concerns focused on the need for personal protective equipment whereas during SARS 2, concerns focused on the need for strict training and patient care protocols. HCWs perceived that their experiences were ineffectively integrated into risk management protocols. CONCLUSIONS: Protection guidelines failed to completely prevent the transmission of SARS to HCWs. Nine percent of the interviewed HCWs who intubated patients contracted SARS. A Risk Analysis Framework is presented to facilitate the rapid integration of HCWs' experiences into practice guidelines.