This Article Full Text Full Text (PDF) All Versions of this Article: chest.07-2076v1 133/3/722    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Add to My Personal Article Archive Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Huang, K.-L. Articles by Wu, C.-P. Search for Related Content PubMed PubMed Citation Articles by Huang, K.-L. Articles by Wu, C.-P.

Systemic Inflammation Caused by White Smoke Inhalation in a Combat Exercise^*

^* From the Department of Critical Care Medicine (Drs. Chen, Perng, and Wu) and Department of Emergency Medicine (Dr. Chu), Tri-Service General Hospital, Taipei, Taiwan, Republic of China; and Institute of Undersea and Hyperbaric Medicine (Dr. Huang), National Defense Medical Center, Taipei, Taiwan, Republic of China.

Correspondence to: Chin-Pyng Wu, MD, PhD, Department of Critical Care Medicine, Tri-Service General Hospital, 325 Cheng-Kung Rd, Sec. 2, Neihu, Taipei 114, Taiwan, Republic of China; e-mail: chinpyng{at}ndmctsgh.edu.tw

Abstract

Background: White smoke inhalation is an uncommon but potentially deadly cause of acute lung injury. No clinical spectrum or treatment protocol have been developed.

Methods: Twenty patients accidentally been exposed to white smoke during military training were the subjects of this study. We analyzed clinical manifestations, cytokine changes, and treatment outcomes.

Results: All patients initially presented with fever, dry cough, chest tightness, and shortness of breath. Twenty-five percent of these patients had severe acute lung injury requiring artificial ventilation support. Elevation of serum tumor necrosis factor- was observed before treatment with antibiotics and glucocorticoids, but the elevation of transforming growth factor-β₁ was delayed for 2 to 4 weeks after the accident. All the patients had leukocytosis, which correlated positively to disease severity and negatively to intensive treatments. Ninety-five percent of patients had varying degrees of restrictive ventilation impairment, and 85% of these patients had a significantly reduced diffusion capacity in the lungs. Seventy percent of these patients had transient impairment of liver function, which did not correlate to disease severity. The respiratory sequela of restrictive ventilation impairment developed in the most severely affected patients, whereas other tissue toxicities were mostly transient. Treatment included glucocorticoids, antibiotics, and respiratory therapy. All of the patients survived.

Conclusion: A proper ventilation strategy, early pharmacologic therapy including glucocorticoids, and complication prevention may contribute to good treatment outcomes after white smoke inhalation.

Key Words: cytokine • inhalation injury • pulmonary function • smoke bomb • zinc chloride