Shock. Author manuscript; available in PMC 2009 August 1.
Published in final edited form as: Shock. 2009 August ; 32(2): 122–130. doi:10.1097/SHK.0b013e31819c385c.
NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript
Lung Contusion: Inflammatory Mechanisms and Interaction with Other Injuries
Krishnan Raghavendran1, Robert H.Notter2, Bruce A. Davidson3, Jadwiga D. Helinski3, Steven L. Kunkel4, and Paul R. Knight3 1 Department of Surgery, University of Michigan, Ann Arbor, MI
4 2 3
Department of Pathology, University of Michigan, Ann Arbor, MI Department of Pediatrics, University of Rochester, Rochester, NY Department of Anesthesiology, University at Buffalo-State University of New York, Buffalo, NY
Thisarticle reviews current animal models and laboratory studies investigating the pathophysiology of lung contusion (LC), a common and severe condition in patients with blunt thoracic trauma. Emphasis is on studies elucidating cells, mediators, receptors and processes important in the innate pulmonary inflammatory response that contribute to LC injury. Surfactant dysfunction in the pathogenesis of LCis also discussed, as is the potential role of epithelial cell or neutrophil apoptosis. Studies examining combination injuries where LC is exacerbated by secondary insults like gastric aspiration in trauma patients are also noted. The need for continuing mechanism-based research to further clarify the pathophysiology of LC injury, and to define and test potential therapeutic interventionstargeting specific aspects of inflammation or surfactant dysfunction to improve clinical outcomes in patients with LC, is also emphasized.
Blunt chest trauma is involved in nearly one-third of acute trauma admissions to the hospital, and lung contusion (LC) is an independent risk factor for the development of acute lung injury (ALI), acute respiratory distress syndrome (ARDS), andventilator-associated pneumonia (VAP) (8,35). The lung is also the second commonest organ involved in blast trauma-induced LC, which often has a peri-hilar distribution and carries a high risk of mortality (11). When LC injury leads to hypoxemia severe enough to meet the definition of ALI/ARDS, the prognostic and economic impacts are significant. These clinical syndromes continue to have verysubstantial overall mortality and morbidity despite significant advances in cardiorespiratory intensive care over the past several decades (38). In a 2004 study of trauma patients, the incremental hospital cost per patient with ALI or ARDS ($36,713 or $59,633, respectively) was much higher than for patients without ALI/ARDS ($24,715) (54). The pathophysiology of pulmonary contusion and blunt chest traumaincludes inflammation, increased alveolocapillary permeability and pulmonary edema, ventilation/perfusion mismatching, increased intrapulmonary shunting, and a loss of compliance(9). A schematic showing selected pathophysiological aspects contributing to pulmonary contusion injury is given in Figure 1. Clinically, patients with pulmonary contusion display hypoxemia,
Please addresscorrespondence to: Krishnan Raghavendran, M.D., Department of Surgery (Division of Acute Care Surgery), University of Michigan, 1500 E.Medical center drive, 1C421-UH, Ann Arbor, MI-48109, E-Mail: E-mail: firstname.lastname@example.org.
Raghavendran et al.
hypercarbia, and increased work of breathing of varying severity and duration (8), which are treated with supplemental oxygen and mechanical ventilationas indicated. There is frequently an inconsistent correlation between the volume of lung that is grossly contused in patients and the severity of clinical respiratory failure, indicating that cellular and sub-cellular injury and inflammation, as well as interactions with other insults occurring at or near the time of trauma, may be involved. The current review focuses on acute inflammatory...