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-alpha was observed before treatment with antibiotics and glucocorticoids, but the elevation of transforming growth factor-beta(1) 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.
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-alpha was observed before treatment with antibiotics and glucocorticoids, but the elevation of transforming growth factor-beta(1) 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.