• Krishnan Raghavendran, Bruce A Davidson, Jadwiga D Helinski, Cristi J Marschke, Patricia Manderscheid, James A Woytash, Robert H Notter, and Paul R Knight.
• Departments of *Surgery, †Anesthesiology, and ‡Pathology, State University of New York (SUNY) at Buffalo, Buffalo; and §Department of Pediatrics, University of Rochester, Rochester, New York.
• Anesth. Analg. 2005 Nov 1; 101 (5): 1482-1489.

AbstractLung contusion affects 17%-25% of adult blunt trauma patients, and is the leading cause of death from blunt thoracic injury. A small animal model for isolated bilateral lung contusion has not been developed. We induced lung contusion in anesthetized rats by dropping a 0.3-kg weight onto a precordial protective shield to direct the impact force away from the heart and toward the lungs. Lung injury was characterized as a function of chest impact energy (1.8-2.7 J) by measurements of arterial oxygenation, bronchoalveolar lavage (BAL) albumin and cytology, pressure-volume mechanics, and histopathology. Histology confirmed bilateral lung contusion without substantial cardiac muscle trauma. Rats receiving 2.7 J of chest impact energy had 33% mortality that exceeded prospectively defined limits for sublethal injury. Hypoxemia in rats with maximal sublethal injury (2.45 J) met criteria for acute lung injury at < or =24 h, improving by 48 h. BAL albumin levels were highest at < or =24 h, and remained elevated along with increased BAL leukocytes and decreased lung volumes at 48 h. We concluded that an impact energy of 2.45 J induces isolated, bilateral lung contusion and provides a useful model for future mechanistic pathophysiological assessments.

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