Radiation-Induced Lung Injury

In Brief Normal lung parenchyma is often unavoidably exposed to radiation during thoracic radiotherapy for bronchogenic and systemic neoplasms. Because the lung is extremely radiosensitive, radiation-induced lung injury occurs commonly. The cellular processes of radiation-induced injury begin within hours after irradiation, but the clinical and radiographic features may not be manifest for weeks to months after exposure. Radiation causes genetic and macromolecular cell injury through direct effects on DNA as well as indirect effects through lipid peroxidation and initiation of apoptotic pathways and inflammatory cascades. Often, the inflammation resolves with minimal parenchymal changes; however, the inflammatory process may progress to parenchymal fibrosis. The risk of radiation lung injury appears to be best predicted by the dose-volume histogram that is calculated from the total radiation dose delivered to a percentage of lung parenchyma. The clinical manifestations of radiation pneumonitis are generally not specific and must be distinguished from respiratory infections. Many patients present with a dry, hacking, usually nonproductive cough and dyspnea. The chest computed tomography scan is more sensitive than the chest radiograph in detecting radiation pneumonitis and usually demonstrates alveolar and interstitial opacifications in the radiation port. Steroids are frequently used to treat radiation pneumonitis. Although minimizing the amount of radiation and shielding are the principal methods to prevent radiation lung injury, amifostine has been demonstrated to reduce the incidence and severity of radiation pneumonitis. Inhaled corticosteroids and keratinocyte growth factor hold promise as future therapeutic agents for the prevention and treatment of radiation lung injury. The lung is one of the most radiosensitive organs. With increasing use of thoracic irradiation as well as the potential for pulmonary radiation exposure from nuclear and radiologic terrorism, normal lung parenchyma is at risk for radiation-induced lung injury. Radiation causes genetic and macromolecular cell injury through direct effects on DNA as well as indirect effects through lipid peroxidation. The risk of radiation lung injury appears to be best predicted by the dose-volume histogram. Most patients present with a dry, hacking, usually nonproductive cough and dyspnea. Although minimizing the amount of radiation and shielding are the principal methods to prevent radiation lung injury, amifostine reduces the incidence and severity of radiation pneumonitis. Corticosteroids are the principal treatment for radiation pneumonitis. Inhaled corticosteroids and keratinocyte growth factor are future therapeutic agents for the prevention and treatment of radiation lung injury.