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Acute Respiratory Distress Syndrome Secondary to Inhalation of Chlorine Gas in Sheep

Batchinsky, Andriy I. MD; Martini, David K. MS; Jordan, Bryan S. MS, RN; Dick, Edward J. DVM; Fudge, James DVM; Baird, Candace A. RVT; Hardin, Denise E. AT; Cancio, Leopoldo C. MD

Journal of Trauma and Acute Care Surgery: May 2006 - Volume 60 - Issue 5 - p 944-957
doi: 10.1097/01.ta.0000205862.57701.48
Original Articles

Background: Toxic industrial chemicals (TICs) are potential terrorist weapons. Several TICs, such as chlorine, act primarily on the respiratory tract, but knowledge of the pathophysiology and treatment of these injuries is inadequate. This study aims to characterize the acute respiratory distress syndrome (ARDS) caused by chlorine gas (Cl2) inhalation in a large-animal model.

Methods: Anesthetized female sheep were ventilated with 300 L of a Cl2/air/oxygen mixture for 30 minutes. In phase 1 (n = 35), doses were 0 ppm (Group 1, n = 6); 120 ppm (Group 2, n = 6); 240 to 350 ppm (Group 3, n = 11); and 400 to 500 ppm (Group 4, n = 12). In phase 2 (n = 17), doses were 0 ppm (Group 5, n = 5); 60 ppm (Group 6, n = 5); and 90 ppm (Group 7, n = 7), and the multiple inert gas elimination technique (MIGET) was used to characterize the etiology of hypoxemia. Computed tomography (CT) scans were performed daily for all animals.

Results: In Phase 1, lung function was well maintained in Group 1; Cl2 caused immediate and sustained acute lung injury (Pao2-to-FiO2 ratio, PFR<3.0) in Group 2 and ARDS (PFR<2.0) in Groups 3 and 4. All animals in Groups 1 and 2 survived 96 hours. Kaplan-Meier analysis showed dose-related differences in survival (log-rank test, p < 0.0001). Logistic regression identified 280 ppm as the lethal dose 50%. CT and histopathology demonstrated lesions of both small airways and alveoli. In Phase 2, MIGET showed diversion of blood flow from normal to true-shunt lung compartments and, transiently, to poorly ventilated compartments.

Conclusions: Cl2 causes severe, dose-related lung injury, with features seen in both smoke inhalation and in ARDS secondary to systemic disease. This model will be used to test new therapeutic modalities.

From the US Army Institute of Surgical Research, Fort Sam Houston, Texas.

Submitted for publication November 1, 2005.

Accepted for publication January 6, 2006.

The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

Funded by the Peer-Reviewed Medical Research Program, US Army Medical Research and Materiel Command, Ft. Detrick, Maryland (DAMD 17–03-2–0016).

Presented at the 64th Annual Meeting of the American Association for the Surgery of Trauma, September 22–24, 2005, Atlanta, Georgia.

Address for reprints: Library Branch, US Army Institute of Surgical Research, 3400 Rawley E. Chambers Avenue, Fort Sam Houston, TX 78234-6315; email:

© 2006 Lippincott Williams & Wilkins, Inc.