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.

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.

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.

A physician workforce planning model applied to Canadian anesthesiology: assessment of needs.

PURPOSE: A human resource planning model for anesthesiology is described. METHODS: The model uses 'per capita' expenditure for anesthesiologists in Quebec, as a measure of clinical services provided to different age/gender groups. The future demand for anesthesia services is calculated as the product of 'per capita' expenditure and the population projections to a future date. Future demand was converted into full-time equivalent (FTE) providers required, by dividing by the annual 'units of service' optimally delivered by one FTE anesthesiologist. The pattern of age/gender (demographic) consumption of anesthesia services in Quebec was compared with data from Ontario to validate its use in a planning model. The model was then applied to all provinces and territories. RESULTS: The 'per capita' expenditures on anesthesia services in Quebec and Ontario showed a regular pattern. Using the model, the estimated 1999 demand for FTE anesthesiologists to provide clinical services in Quebec is 546 and 669 for 2016. When non-clinical demands were included, we estimated that Quebec's total demand will increase to approximately 730 FTEs in 2016. Similar estimates are made for all provinces. The population increase anticipated is 17.9% but the increase in FTE demand in Canada is 30.9%. CONCLUSION: The model showed that the cause of the increased FTE demand for anesthesiologists is a combination of increased population and its demographic composition. The relative impact of each of these factors varies in different provinces. Effective specialty-specific planning models can be designed but they need ongoing committed resources and personnel for their usefulness to be maximized.

Dynamic characteristics of cerebral lipid microemboli: videomicroscopy studies in rats.

UNLABELLED: Cerebral lipid microemboli (LME) may cause postoperative cognitive dysfunction after orthopedic and cardiovascular surgery. In 13 anesthetized rats, we created a cranial window to study LME using orthogonal polarization spectral imaging videomicroscopy. All rats received 0.2 mL of human marrow fat, obtained from surgical waste during arthroplasty, injected into the superior vena cava. Five rats died within seconds of this injection, despite resuscitation efforts. Seven minutes later, we injected an additional 0.1 mL in 6 of the 8 surviving rats. We observed the videomicroscopy for 1 h in all 8 rats. Arterial blood pressure (BP) was continuously measured. No LME were observed in the first 7 min (n = 8); however, within seconds of the additional 0.1 mL injection, mean BP decreased from 79 +/- 31 mm Hg to 28 +/- 12 mm Hg (n = 6; P < 0.02). Epinephrine and crystalloid infusion increased BP to 161 +/- 9 mm Hg and 20-100 LME were seen within 5 min. LME changed shape and fragmentation, erosion, and streaming patterns were noted, with transient arteriolar occlusion (10-220 s). Increasing BP resulted in reperfusion of occluded arterioles. No venous LME were noted. Postmortem, brain and lung LME were found with no patent foramen ovale. This model may be useful in studying cerebral LME. IMPLICATIONS: Marrow lipid may pass through the lung during orthopedic surgery, creating cerebral lipid microemboli (LME). We created a cranial window in rats to study LME flowing through pial-cortical vessels. Cerebral LME appeared after resuscitation from hypotension and vessel occlusion was transient. This model may be useful in studying cerebral LME.