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Leopoldo C Cancio - One of the best experts on this subject based on the ideXlab platform.
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dynamic changes in shunt and ventilation perfusion mismatch following experimental Pulmonary Contusion
Shock, 2010Co-Authors: Andriy I Batchinsky, Corina Necsoiu, Bryan S. Jordan, Michael A Dubick, Leopoldo C CancioAbstract:ABSTRACT The objective of this study was to investigate early changes in oxygenation by means of the multiple inert gas elimination technique and in coagulation by means of thromboelastography (TEG) after right-sided Pulmonary Contusion (PC) in swine. Anesthetized swine (group 1; n = 8) sustained a right-chest PC by a captive-bolt stunner. Multiple inert gas elimination technique, TEG, and thoracic computed tomography (CT) scans were performed before and 10, 30, 60, and 120 min after injury. Three-dimensional CT scan reconstruction enabled measurement of volumes of poorly (VolPoor) and nonaerated (VolNon) lung. Eight animals (group 0) were used as uninjured controls. Pulmonary Contusion led to sustained tachycardia and transient hypotension. Partial pressure of arterial oxygen (PaO2) decreased from 83.9 ± 4.2 mmHg at baseline to 51.3 ± 2.8 mmHg 10 min after PC (P
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dynamic changes in shunt and ventilation perfusion mismatch following experimental Pulmonary Contusion
Shock, 2010Co-Authors: Andriy I Batchinsky, Corina Necsoiu, Bryan S. Jordan, Michael A Dubick, Leopoldo C CancioAbstract:The objective of this study was to investigate early changes in oxygenation by means of the multiple inert gas elimination technique and in coagulation by means of thromboelastography (TEG) after right-sided Pulmonary Contusion (PC) in swine. Anesthetized swine (group 1; n = 8) sustained a right-chest PC by a captive-bolt stunner. Multiple inert gas elimination technique, TEG, and thoracic computed tomography (CT) scans were performed before and 10, 30, 60, and 120 min after injury. Three-dimensional CT scan reconstruction enabled measurement of volumes of poorly (Vol(Poor)) and nonaerated (Vol(Non)) lung. Eight animals (group 0) were used as uninjured controls. Pulmonary Contusion led to sustained tachycardia and transient hypotension. Partial pressure of arterial oxygen (PaO2) decreased from 83.9 +/- 4.2 mmHg at baseline to 51.3 +/- 2.8 mmHg 10 min after PC (P < 0.001). Vol(Poor) and Vol(Non) on the right increased significantly after PC, followed by gradual progression in injury marked by decreased Vol(Poor) and increased Vol(Non). By the multiple inert gas elimination technique, blood flow to the true shunt compartment increased from 4.4% +/- 1.0% at baseline to 21.2% +/- 4.9% 10 min after PC, P < 0.001, peaked at 33.2% +/- 7.5% 30 min after PC, P < 0.001, and remained significantly higher compared with controls. Transient increase in blood flow to low and very low ventilation-perfusion (V/Q) compartments was also seen. Clot reaction time and formation rate by TEG increased at 2 h after PC. True shunt is the major cause of hypoxemia after PC, but V/Q mismatch also contributes significantly early after injury. By CT, PC leads to significant loss of functional lung volume on the side of injury. A mild hypocoagulable state was identified 2 h after injury.
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ventilation perfusion relationships following experimental Pulmonary Contusion
Journal of Applied Physiology, 2007Co-Authors: Andriy I Batchinsky, Bryan S. Jordan, William B Weiss, Edward J Dick, David A Cancelada, Leopoldo C CancioAbstract:Ventilation-perfusion changes after right-sided Pulmonary Contusion (PC) in swine were investigated by means of the multiple inert gas elimination technique (MIGET). Anesthetized swine (injury, n =...
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ventilation perfusion relationships following experimental Pulmonary Contusion
Journal of Applied Physiology, 2007Co-Authors: Andriy I Batchinsky, Bryan S. Jordan, William B Weiss, Edward J Dick, David A Cancelada, Leopoldo C CancioAbstract:Ventilation-perfusion changes after right-sided Pulmonary Contusion (PC) in swine were investigated by means of the multiple inert gas elimination technique (MIGET). Anesthetized swine (injury, n = 8; control, n = 6) sustained a right-chest PC by a captive-bolt apparatus. This was followed by a 12-ml/kg hemorrhage, resuscitation, and reinfusion of shed blood. MIGET and thoracic computed tomography (CT) were performed before and 6 h after injury. Three-dimensional CT scan reconstruction enabled determination of the combined fractional volume of poorly aerated and non-aerated lung tissue (VOL), and the mean gray-scale density (MGSD). Six hours after PC in injured animals, PaO2 decreased from 234.9 ± 5.1 to 113.9 ± 13.0 mmHg. Shunt (QS) increased (2.7 ± 0.4 to 12.3 ± 2.2%) at the expense of blood flow to normal ventilation/perfusion compartments (97.1 ± 0.4 to 87.4 ± 2.2%). Dead space ventilation (VD/VT) increased (58.7 ± 1.7% to 67.2 ± 1.2%). MGSD increased (−696.7 ± 6.1 to −565.0 ± 24.3 Hounsfield units), ...
Jason J Hoth - One of the best experts on this subject based on the ideXlab platform.
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innate immune response to Pulmonary Contusion identification of cell type specific inflammatory responses
Shock, 2012Co-Authors: Jason J Hoth, Barbara K Yoza, Jonathan D Wells, Charles E. MccallAbstract:ABSTRACTLung injury from Pulmonary Contusion is a common traumatic injury, predominantly seen after blunt chest trauma, such as in vehicular accidents. The local and systemic inflammatory response to injury includes activation of innate immune receptors, elaboration of a variety of inflammatory medi
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innate immune response to Pulmonary Contusion identification of cell type specific inflammatory responses
Shock, 2012Co-Authors: Jason J Hoth, Barbara K Yoza, Jonathan D Wells, Charles E. MccallAbstract:Lung injury from Pulmonary Contusion is a common traumatic injury, predominantly seen after blunt chest trauma, such as in vehicular accidents. The local and systemic inflammatory response to injury includes activation of innate immune receptors, elaboration of a variety of inflammatory mediators, and recruitment of inflammatory cells to the injured lung. Using a mouse model of Pulmonary Contusion, we had previously shown that innate immune Toll-like receptors 2 and 4 (TLR2 and TLR4) mediate the inflammatory response to lung injury. In this study, we used chimeric mice generated by adoptive bone marrow transfer between TLR2 or TLR4 and wild-type mice. We found that, in the lung, both bone marrow-derived and nonmyeloid cells contribute to TLR-dependent inflammatory responses after injury in a cell type-specific manner. We also show a novel TLR2-dependent injury mechanism that is associated with enhanced airway epithelial cell apoptosis and increased Pulmonary FasL and Fas expression in the lungs from injured mice. Thus, in addition to cardioPulmonary physiological dysfunction, cell type-specific TLR and their differential response to injury may provide novel specific targets for management of patients with Pulmonary Contusion.
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mechanism of neutrophil recruitment to the lung after Pulmonary Contusion
Shock, 2011Co-Authors: Jason J Hoth, Elizabeth M Hiltbold, Jonathan D Wells, Charles E. Mccall, Barbara K YozaAbstract:Blunt chest trauma resulting in Pulmonary Contusion is a common but poorly understood injury. We previously demonstrated that lung Contusion activates localized and systemic innate immune mechanisms and recruits neutrophils to the injured lung. We hypothesized that the innate immune and inflammatory activation of neutrophils may figure prominently in the response to lung injury. To investigate this, we used a model of Pulmonary Contusion in the mouse that is similar to that observed clinically in humans and evaluated postinjury lung function and Pulmonary neutrophil recruitment. Comparisons were made between injured mice with and without neutrophil depletion. We further examined the role of chemokines and adhesion receptors in neutrophil recruitment to the injured lung. We found that lung injury and resultant physiological dysfunction after Contusion was dependent upon the presence of neutrophils in the alveolar space. We show that CXCL1, CXCL2/3, and CXCR2 are involved in neutrophil recruitment to the lung after injury, and that ICAM-1 is locally expressed and actively participates in this process. Injured gp91phox deficient mice showed improved lung function, indicating that oxidant production by neutrophil NADPH oxidase mediates lung dysfunction after Contusion. These data suggest that both neutrophil presence and function are required for lung injury after lung Contusion.
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mechanism of neutrophil recruitment to the lung after Pulmonary Contusion
Shock, 2011Co-Authors: Jason J Hoth, Elizabeth M Hiltbold, Jonathan D Wells, Charles E. Mccall, Barbara K YozaAbstract:Blunt chest trauma resulting in Pulmonary Contusion is a common but poorly understood injury. We previously demonstrated that lung Contusion activates localized and systemic innate immune mechanisms and recruits neutrophils to the injured lung. We hypothesized that the innate immune and inflammatory activation of neutrophils may figure prominently in the response to lung injury. To investigate this, we used a model of Pulmonary Contusion in the mouse that is similar to that observed clinically in humans and evaluated postinjury lung function and Pulmonary neutrophil recruitment. Comparisons were made between injured mice with and without neutrophil depletion. We further examined the role of chemokines and adhesion receptors in neutrophil recruitment to the injured lung. We found that lung injury and resultant physiological dysfunction after Contusion were dependent on the presence of neutrophils in the alveolar space. We show that CXCL1, CXCL2/3, and CXCR2 are involved in neutrophil recruitment to the lung after injury and that intercellular adhesion molecule 1 is locally expressed and actively participates in this process. Injured gp91-deficient mice showed improved lung function, indicating that oxidant production by neutrophil NADPH oxidase mediates lung dysfunction after Contusion. These data suggest that both neutrophil presence and function are required for lung injury after lung Contusion.
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Pulmonary Contusion primes systemic innate immunity responses.
Journal of Trauma-injury Infection and Critical Care, 2009Co-Authors: Jason J Hoth, Barbara K Yoza, Jonathan D Wells, R. S. San-martin, J W Meredith, Charles E. MccallAbstract:Introduction: Traumatic injury may result in an exaggerated response to subsequent immune stimuli such as nosocomial infection. This "second hit" phenomenon and molecular mechanism(s) of immune priming by traumatic lung injury, specifically, Pulmonary Contusion, remain unknown. We used an animal model of Pulmonary Contusion to determine whether the injury resulted in priming of the innate immune response and to test the hypothesis that resuscitation fluids could attenuate the primed response to a second hit. Methods: Male, 8 to 9 weeks, C57/BL6 mice with a Pulmonary Contusion were challenged by a second hit of intratracheal administration of the Toll-like receptor 4 agonist, lipopolysaccharide (LPS, 50 μg) 24 hours after injury (injury + LPS). Other experimental groups were injury + vehicle or LPS alone. A separate group was injured and resuscitated by 4 cc/kg of hypertonic saline (HTS) or Lactated Ringer's (LR) resuscitation before LPS challenge. Mice were killed 4 hours after LPS challenge and blood, bronchoalveolar lavage, and tissue were isolated and analyzed. Data were analyzed using one-way analysis of variance with Bonferroni multiple comparison posttest for significant differences ( * p ≤ 0.05). Results: Injury + LPS showed immune priming observed by lung injury histology and increased bronchoalveolar lavage neutrophilia, lung myeloperoxidase and serum IL-6, CXCL1, and MIP-2 levels when compared with injury + vehicle or LPS alone. After injury, resuscitation with HTS, but not Lactated Ringer's was more effective in attenuating the primed response to a second hit. Conclusion: Pulmonary Contusion primes innate immunity for an exaggerated response to a second hit with the Toll-like receptor 4 agonist, LPS. We observed synergistic increases in inflammatory mediator expression in the blood and a more severe lung injury in injured animals challenged with LPS. This priming effect was reduced when HTS was used to resuscitate the animal after lung Contusion.
Charles E. Mccall - One of the best experts on this subject based on the ideXlab platform.
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innate immune response to Pulmonary Contusion identification of cell type specific inflammatory responses
Shock, 2012Co-Authors: Jason J Hoth, Barbara K Yoza, Jonathan D Wells, Charles E. MccallAbstract:Lung injury from Pulmonary Contusion is a common traumatic injury, predominantly seen after blunt chest trauma, such as in vehicular accidents. The local and systemic inflammatory response to injury includes activation of innate immune receptors, elaboration of a variety of inflammatory mediators, and recruitment of inflammatory cells to the injured lung. Using a mouse model of Pulmonary Contusion, we had previously shown that innate immune Toll-like receptors 2 and 4 (TLR2 and TLR4) mediate the inflammatory response to lung injury. In this study, we used chimeric mice generated by adoptive bone marrow transfer between TLR2 or TLR4 and wild-type mice. We found that, in the lung, both bone marrow-derived and nonmyeloid cells contribute to TLR-dependent inflammatory responses after injury in a cell type-specific manner. We also show a novel TLR2-dependent injury mechanism that is associated with enhanced airway epithelial cell apoptosis and increased Pulmonary FasL and Fas expression in the lungs from injured mice. Thus, in addition to cardioPulmonary physiological dysfunction, cell type-specific TLR and their differential response to injury may provide novel specific targets for management of patients with Pulmonary Contusion.
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innate immune response to Pulmonary Contusion identification of cell type specific inflammatory responses
Shock, 2012Co-Authors: Jason J Hoth, Barbara K Yoza, Jonathan D Wells, Charles E. MccallAbstract:ABSTRACTLung injury from Pulmonary Contusion is a common traumatic injury, predominantly seen after blunt chest trauma, such as in vehicular accidents. The local and systemic inflammatory response to injury includes activation of innate immune receptors, elaboration of a variety of inflammatory medi
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mechanism of neutrophil recruitment to the lung after Pulmonary Contusion
Shock, 2011Co-Authors: Jason J Hoth, Elizabeth M Hiltbold, Jonathan D Wells, Charles E. Mccall, Barbara K YozaAbstract:Blunt chest trauma resulting in Pulmonary Contusion is a common but poorly understood injury. We previously demonstrated that lung Contusion activates localized and systemic innate immune mechanisms and recruits neutrophils to the injured lung. We hypothesized that the innate immune and inflammatory activation of neutrophils may figure prominently in the response to lung injury. To investigate this, we used a model of Pulmonary Contusion in the mouse that is similar to that observed clinically in humans and evaluated postinjury lung function and Pulmonary neutrophil recruitment. Comparisons were made between injured mice with and without neutrophil depletion. We further examined the role of chemokines and adhesion receptors in neutrophil recruitment to the injured lung. We found that lung injury and resultant physiological dysfunction after Contusion was dependent upon the presence of neutrophils in the alveolar space. We show that CXCL1, CXCL2/3, and CXCR2 are involved in neutrophil recruitment to the lung after injury, and that ICAM-1 is locally expressed and actively participates in this process. Injured gp91phox deficient mice showed improved lung function, indicating that oxidant production by neutrophil NADPH oxidase mediates lung dysfunction after Contusion. These data suggest that both neutrophil presence and function are required for lung injury after lung Contusion.
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mechanism of neutrophil recruitment to the lung after Pulmonary Contusion
Shock, 2011Co-Authors: Jason J Hoth, Elizabeth M Hiltbold, Jonathan D Wells, Charles E. Mccall, Barbara K YozaAbstract:Blunt chest trauma resulting in Pulmonary Contusion is a common but poorly understood injury. We previously demonstrated that lung Contusion activates localized and systemic innate immune mechanisms and recruits neutrophils to the injured lung. We hypothesized that the innate immune and inflammatory activation of neutrophils may figure prominently in the response to lung injury. To investigate this, we used a model of Pulmonary Contusion in the mouse that is similar to that observed clinically in humans and evaluated postinjury lung function and Pulmonary neutrophil recruitment. Comparisons were made between injured mice with and without neutrophil depletion. We further examined the role of chemokines and adhesion receptors in neutrophil recruitment to the injured lung. We found that lung injury and resultant physiological dysfunction after Contusion were dependent on the presence of neutrophils in the alveolar space. We show that CXCL1, CXCL2/3, and CXCR2 are involved in neutrophil recruitment to the lung after injury and that intercellular adhesion molecule 1 is locally expressed and actively participates in this process. Injured gp91-deficient mice showed improved lung function, indicating that oxidant production by neutrophil NADPH oxidase mediates lung dysfunction after Contusion. These data suggest that both neutrophil presence and function are required for lung injury after lung Contusion.
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Pulmonary Contusion primes systemic innate immunity responses.
Journal of Trauma-injury Infection and Critical Care, 2009Co-Authors: Jason J Hoth, Barbara K Yoza, Jonathan D Wells, R. S. San-martin, J W Meredith, Charles E. MccallAbstract:Introduction: Traumatic injury may result in an exaggerated response to subsequent immune stimuli such as nosocomial infection. This "second hit" phenomenon and molecular mechanism(s) of immune priming by traumatic lung injury, specifically, Pulmonary Contusion, remain unknown. We used an animal model of Pulmonary Contusion to determine whether the injury resulted in priming of the innate immune response and to test the hypothesis that resuscitation fluids could attenuate the primed response to a second hit. Methods: Male, 8 to 9 weeks, C57/BL6 mice with a Pulmonary Contusion were challenged by a second hit of intratracheal administration of the Toll-like receptor 4 agonist, lipopolysaccharide (LPS, 50 μg) 24 hours after injury (injury + LPS). Other experimental groups were injury + vehicle or LPS alone. A separate group was injured and resuscitated by 4 cc/kg of hypertonic saline (HTS) or Lactated Ringer's (LR) resuscitation before LPS challenge. Mice were killed 4 hours after LPS challenge and blood, bronchoalveolar lavage, and tissue were isolated and analyzed. Data were analyzed using one-way analysis of variance with Bonferroni multiple comparison posttest for significant differences ( * p ≤ 0.05). Results: Injury + LPS showed immune priming observed by lung injury histology and increased bronchoalveolar lavage neutrophilia, lung myeloperoxidase and serum IL-6, CXCL1, and MIP-2 levels when compared with injury + vehicle or LPS alone. After injury, resuscitation with HTS, but not Lactated Ringer's was more effective in attenuating the primed response to a second hit. Conclusion: Pulmonary Contusion primes innate immunity for an exaggerated response to a second hit with the Toll-like receptor 4 agonist, LPS. We observed synergistic increases in inflammatory mediator expression in the blood and a more severe lung injury in injured animals challenged with LPS. This priming effect was reduced when HTS was used to resuscitate the animal after lung Contusion.
Andriy I Batchinsky - One of the best experts on this subject based on the ideXlab platform.
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dynamic changes in shunt and ventilation perfusion mismatch following experimental Pulmonary Contusion
Shock, 2010Co-Authors: Andriy I Batchinsky, Corina Necsoiu, Bryan S. Jordan, Michael A Dubick, Leopoldo C CancioAbstract:ABSTRACT The objective of this study was to investigate early changes in oxygenation by means of the multiple inert gas elimination technique and in coagulation by means of thromboelastography (TEG) after right-sided Pulmonary Contusion (PC) in swine. Anesthetized swine (group 1; n = 8) sustained a right-chest PC by a captive-bolt stunner. Multiple inert gas elimination technique, TEG, and thoracic computed tomography (CT) scans were performed before and 10, 30, 60, and 120 min after injury. Three-dimensional CT scan reconstruction enabled measurement of volumes of poorly (VolPoor) and nonaerated (VolNon) lung. Eight animals (group 0) were used as uninjured controls. Pulmonary Contusion led to sustained tachycardia and transient hypotension. Partial pressure of arterial oxygen (PaO2) decreased from 83.9 ± 4.2 mmHg at baseline to 51.3 ± 2.8 mmHg 10 min after PC (P
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dynamic changes in shunt and ventilation perfusion mismatch following experimental Pulmonary Contusion
Shock, 2010Co-Authors: Andriy I Batchinsky, Corina Necsoiu, Bryan S. Jordan, Michael A Dubick, Leopoldo C CancioAbstract:The objective of this study was to investigate early changes in oxygenation by means of the multiple inert gas elimination technique and in coagulation by means of thromboelastography (TEG) after right-sided Pulmonary Contusion (PC) in swine. Anesthetized swine (group 1; n = 8) sustained a right-chest PC by a captive-bolt stunner. Multiple inert gas elimination technique, TEG, and thoracic computed tomography (CT) scans were performed before and 10, 30, 60, and 120 min after injury. Three-dimensional CT scan reconstruction enabled measurement of volumes of poorly (Vol(Poor)) and nonaerated (Vol(Non)) lung. Eight animals (group 0) were used as uninjured controls. Pulmonary Contusion led to sustained tachycardia and transient hypotension. Partial pressure of arterial oxygen (PaO2) decreased from 83.9 +/- 4.2 mmHg at baseline to 51.3 +/- 2.8 mmHg 10 min after PC (P < 0.001). Vol(Poor) and Vol(Non) on the right increased significantly after PC, followed by gradual progression in injury marked by decreased Vol(Poor) and increased Vol(Non). By the multiple inert gas elimination technique, blood flow to the true shunt compartment increased from 4.4% +/- 1.0% at baseline to 21.2% +/- 4.9% 10 min after PC, P < 0.001, peaked at 33.2% +/- 7.5% 30 min after PC, P < 0.001, and remained significantly higher compared with controls. Transient increase in blood flow to low and very low ventilation-perfusion (V/Q) compartments was also seen. Clot reaction time and formation rate by TEG increased at 2 h after PC. True shunt is the major cause of hypoxemia after PC, but V/Q mismatch also contributes significantly early after injury. By CT, PC leads to significant loss of functional lung volume on the side of injury. A mild hypocoagulable state was identified 2 h after injury.
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ventilation perfusion relationships following experimental Pulmonary Contusion
Journal of Applied Physiology, 2007Co-Authors: Andriy I Batchinsky, Bryan S. Jordan, William B Weiss, Edward J Dick, David A Cancelada, Leopoldo C CancioAbstract:Ventilation-perfusion changes after right-sided Pulmonary Contusion (PC) in swine were investigated by means of the multiple inert gas elimination technique (MIGET). Anesthetized swine (injury, n =...
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ventilation perfusion relationships following experimental Pulmonary Contusion
Journal of Applied Physiology, 2007Co-Authors: Andriy I Batchinsky, Bryan S. Jordan, William B Weiss, Edward J Dick, David A Cancelada, Leopoldo C CancioAbstract:Ventilation-perfusion changes after right-sided Pulmonary Contusion (PC) in swine were investigated by means of the multiple inert gas elimination technique (MIGET). Anesthetized swine (injury, n = 8; control, n = 6) sustained a right-chest PC by a captive-bolt apparatus. This was followed by a 12-ml/kg hemorrhage, resuscitation, and reinfusion of shed blood. MIGET and thoracic computed tomography (CT) were performed before and 6 h after injury. Three-dimensional CT scan reconstruction enabled determination of the combined fractional volume of poorly aerated and non-aerated lung tissue (VOL), and the mean gray-scale density (MGSD). Six hours after PC in injured animals, PaO2 decreased from 234.9 ± 5.1 to 113.9 ± 13.0 mmHg. Shunt (QS) increased (2.7 ± 0.4 to 12.3 ± 2.2%) at the expense of blood flow to normal ventilation/perfusion compartments (97.1 ± 0.4 to 87.4 ± 2.2%). Dead space ventilation (VD/VT) increased (58.7 ± 1.7% to 67.2 ± 1.2%). MGSD increased (−696.7 ± 6.1 to −565.0 ± 24.3 Hounsfield units), ...
Joel D. Stitzel - One of the best experts on this subject based on the ideXlab platform.
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finite element model prediction of Pulmonary Contusion in vehicle to vehicle simulations of real world crashes
Traffic Injury Prevention, 2015Co-Authors: Kerry A. Danelson, Joel D. StitzelAbstract:Objective: Pulmonary Contusion (PC) is a common chest injury following motor vehicle crash (MVC). Because this injury has an inflammatory component, studying PC in living subjects is essential. Medical and vehicle data from the Crash Injury Research and Engineering Network (CIREN) database were utilized to examine Pulmonary Contusion in case occupants with known crash parameters.Method: The selected CIREN cases were simulated with vehicle finite element models (FEMs) with the Total HUman Model for Safety (THUMS) version 4 as the occupant. To match the CIREN crash parameters, vehicle simulations were iteratively improved to optimize maximum crush location and depth. Fifteen cases were successfully modeled with the simulated maximum crush matching the CIREN crush to within 10%. Following the simulations, stress and strain metrics for the elements within the lungs were calculated. These injury metrics were compared to patient imaging data to determine the best finite element predictor of Pulmonary Contusion....
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finite element based injury metrics for Pulmonary Contusion from vehicle to vehicle crash simulations
ASME 2012 Summer Bioengineering Conference Parts A and B, 2012Co-Authors: Kerry A. Danelson, Joel D. StitzelAbstract:Motor Vehicle Crashes (MVCs) are a public health problem in the United States. In 2009, 33,808 Americans were killed in a MVC and 2.22 million more were injured.4 Pulmonary Contusion (PC) is a common injury following MVC with over 38% of the Abbreviated Injury Scale (AIS) 3+ thoracic injuries identified as some form of PC in a recent National Automotive Sampling System (NASS) study.5 Miller et al. correlated the percent injured lung to the possibility of developing Acute Respiratory Distress Syndrome (ARDS). The results indicated that if 20% of the lung was injured, the incidence of ARDS sharply increased with seventy-eight percent of those patients developing ARDS.2 The significance of these findings is that the volumetric measurement of PC can predict possible clinical outcomes.© 2012 ASME
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correlating the extent of Pulmonary Contusion to vehicle crash parameters in near side impacts
Annals of advances in automotive medicine Annual Scientific Conference ... Association for the Advancement of Automotive Medicine. Association for the, 2011Co-Authors: Kerry A. Danelson, Ashley A. Weaver, Caroline Chiles, Aaron B Thompson, Katherine Donadino, Joel D. StitzelAbstract:Pulmonary Contusion (PC) is the most common injury following blunt thoracic trauma with an associated mortality of 10% to 20%. The purpose of this study is to determine how crash parameters correlate to the volume of Pulmonary Contusion. The Crash Injury Research Engineering and Network (CIREN) database was queried to extract data on all occupants sustaining PC in a near-side crash. The selected CIREN data included all completed cases from 2005 through 2010. Cases involving a roll-over or without a thorax CT uploaded to the database were excluded. After all cases had been examined the study had 64 occupants with varying volumes of PC. Specific crash characteristics compiled included change in velocity due to the impact, energy, occupant characteristics, side airbag deployment, and crush profile measurements. Crush metrics quantifying the area of the crush profile and the location of the crush relative to the occupant were calculated. The thoracic CT scans from these cases were downloaded and segmented to determine the percent volume of high attenuation lung and PC as compared to the total volume of the lung. The results of the general linear model analysis suggest that maximum crush was the best predictor of high attenuation lung and lung location best predicted PC. An analysis of NASS and CIREN demonstrated that crashes with PC tended to have crash parameters that indicated higher severity. These correlations can be used in the future to develop an injury criterion for PC using finite element metrics.
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biomechanical analysis of Pulmonary Contusion in motor vehicle crash victims a crash injury research and engineering network ciren study
Biomedical sciences instrumentation, 2009Co-Authors: Ashley A. Weaver, Scott F Gayzik, Joel D. StitzelAbstract:Pulmonary Contusion is the most common thoracic soft tissue injury encountered in motor vehicle crashes and is seen in 10-17% of all trauma admissions. This study presents a biomechanical and radiological analysis with the goal of quantifying Pulmonary Contusion resulting from motor vehicle crashes in order to illustrate the relationships between crash characteristics, Contusion severity, and patient outcome. The 20 patients selected for this study were involved in motor vehicle crashes and subsequently enrolled in the Crash Injury and Research Engineering Network (CIREN) program at Wake Forest University Baptist Medical Center. Demographic data, sustained injuries, and crash characteristics were obtained through medical records and the CIREN database for all patients in the study. For each patient, the first chest computed tomography (CT) scan following the crash was segmented using a semi-automated approach to obtain volumes of trapped air, total lung, healthy lung, and high attenuation lung representing contused tissue. Three-dimensional models of the healthy and contused lung tissue were created for each patient. Rib fractures were present in 75% of patients and a substantial proportion of patients with Pulmonary Contusion injuries were involved in near side collisions. The near side door was identified as the most commonly involved component in Pulmonary Contusion injuries. The methodology and analysis presented in this study between crash characteristics, Pulmonary Contusion severity, and patient outcome are data that may contribute to future improvements in motor vehicle safety. Language: en
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a finite element based injury metric for Pulmonary Contusion investigation of candidate metrics through correlation with computed tomography
Stapp car crash journal, 2007Co-Authors: Scott F Gayzik, Jason J Hoth, Wayne J Meredith, Melissa Daly, Joel D. StitzelAbstract:This study (1) investigates the use of computed tomography (CT) to quantify the volume of pathologic lung tissue in a prospective study of Pulmonary Contusion and (2) uses a finite element model of the lung to investigate several mathematical predictors of Contusion to determine the injury metric that best matches the spatial distribution of Contusion obtained from the CT analysis. The study employs direct impact to the right lung of male rats.
