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RADIATION-INDUCED ENDOBRONCHIAL INJURY: A PROPOSED SPECTRUM OF DISEASE
October 2008, Vol 134, No. 4_MeetingAbstracts Abstract: Poster Presentations | October 2008
RADIATION-INDUCED ENDOBRONCHIAL INJURY: A PROPOSED SPECTRUM OF DISEASE Jonathan Puchalski, MD*; Andrew Haas, MD; Colin Gillespie, MD; Steven Leh, MD; Daniel Sterman, MD Hospital of the University of Pennsylvania, Philadelphia, PA Chest. 2008;134(4_MeetingAbstracts):p12002. doi:10.1378/chest.134.4_MeetingAbstracts.p12002
Abstract PURPOSE: Radiation therapy is an integral component of therapy for many thoracic malignancies. Thoracic irradiation can damage the pulmonary parenchyma leading to radiation pneumonitis and fibrosis. We report four representative cases of endobronchial injury that depict the proposed spectrum of airway damage induced by radiation: superficial mucosal necrosis, full-thickness bronchial necrosis, bronchiectasis and bronchial stenosis. METHODS: Bronchoscopy was performed in patients for complaints of dyspnea or hemoptysis following thoracic radiation therapy for non-small cell and small cell lung cancer. Informed consent for the procedure was obtained, and findings were photo-documented. RESULTS: The first patient complained of hemoptysis and dyspnea. Superficial mucosal injury was confirmed by removing the necrotic debris and demonstrating either tumor or mucosa underneath. There was sharp demarcation between the area of normal mucosa in the non-irradiated field and superficial necrotic mucosa in the radiated field. In the second patient, also with hemoptysis, extensive necrotic debris was visualized bronchoscopically in the airways receiving radiation therapy but not in the contralateral airways that were not irradiated. Even with aspiration of the superficial debris, extensive underlying necrosis was evident. Radiographic evidence of broncho-pleural fistulae was present, indicating full thickness airway disruption. She soon experienced massive, fatal hemoptysis, confirming the extensive radiation-induced necrosis. The third patient had massive hemoptysis on two occasions, both requiring bronchial artery embolization. His CT demonstrated significant bronchiectasis in the radiation field. The fourth patient complained of slowly progressive dyspnea following radiation treatment. Chest CT demonstrated left upper lobar atelectasis prompting bronchoscopic evaluation. Complete stenosis of the lobe was identified and endoscopically treated. CONCLUSION: In addition to parenchymal lung injury, radiation therapy may induce a spectrum of endobronchial damage, ranging from superficial mucosal necrosis to complete bronchial necrosis, bronchiectasis and bronchial stenosis.
CLINICAL IMPLICATIONS: It is likely that the same macromolecular DNA damage and lipid peroxidation that occurs in alveolar epithelial cells occurs in bronchial injury. Future research investigating the molecular changes of the mucosa may provide insight into this spectrum of radiation-induced endobronchial injury. DISCLOSURE: Jonathan Puchalski, No Financial Disclosure Information; No Product/Research Disclosure Information Tuesday, October 28, 2008 1:00 PM - 2:15 PM
RADIATION-INDUCED ENDOBRONCHIAL INJURY: A PROPOSED SPECTRUM OF DISEASE Jonathan Puchalski, MD*; Andrew Haas, MD; Colin Gillespie, MD; Steven Leh, MD; Daniel Sterman, MD Hospital of the University of Pennsylvania, Philadelphia, PA Chest. 2008;134(4_MeetingAbstracts):p12002. doi:10.1378/chest.134.4_MeetingAbstracts.p12002
Abstract PURPOSE: Radiation therapy is an integral component of therapy for many thoracic malignancies. Thoracic irradiation can damage the pulmonary parenchyma leading to radiation pneumonitis and fibrosis. We report four representative cases of endobronchial injury that depict the proposed spectrum of airway damage induced by radiation: superficial mucosal necrosis, full-thickness bronchial necrosis, bronchiectasis and bronchial stenosis. METHODS: Bronchoscopy was performed in patients for complaints of dyspnea or hemoptysis following thoracic radiation therapy for non-small cell and small cell lung cancer. Informed consent for the procedure was obtained, and findings were photo-documented. RESULTS: The first patient complained of hemoptysis and dyspnea. Superficial mucosal injury was confirmed by removing the necrotic debris and demonstrating either tumor or mucosa underneath. There was sharp demarcation between the area of normal mucosa in the non-irradiated field and superficial necrotic mucosa in the radiated field. In the second patient, also with hemoptysis, extensive necrotic debris was visualized bronchoscopically in the airways receiving radiation therapy but not in the contralateral airways that were not irradiated. Even with aspiration of the superficial debris, extensive underlying necrosis was evident. Radiographic evidence of broncho-pleural fistulae was present, indicating full thickness airway disruption. She soon experienced massive, fatal hemoptysis, confirming the extensive radiation-induced necrosis. The third patient had massive hemoptysis on two occasions, both requiring bronchial artery embolization. His CT demonstrated significant bronchiectasis in the radiation field. The fourth patient complained of slowly progressive dyspnea following radiation treatment. Chest CT demonstrated left upper lobar atelectasis prompting bronchoscopic evaluation. Complete stenosis of the lobe was identified and endoscopically treated. CONCLUSION: In addition to parenchymal lung injury, radiation therapy may induce a spectrum of endobronchial damage, ranging from superficial mucosal necrosis to complete bronchial necrosis, bronchiectasis and bronchial stenosis.
CLINICAL IMPLICATIONS: It is likely that the same macromolecular DNA damage and lipid peroxidation that occurs in alveolar epithelial cells occurs in bronchial injury. Future research investigating the molecular changes of the mucosa may provide insight into this spectrum of radiation-induced endobronchial injury. DISCLOSURE: Jonathan Puchalski, No Financial Disclosure Information; No Product/Research Disclosure Information Tuesday, October 28, 2008 1:00 PM - 2:15 PM