Treatment with a higher dosage of corticosteroids at 1 mg/kg/day resulted in rapid clinical improvement over several days and considerable improvement of the chest x-ray (Figure 1, right).
Radiation-induced injury of the lung is common after irradiation for carcinoma of the thorax. Typically, both the pathological and radiological changes are confined to the outline of the radiation fields. There are two well-describe,d distinct clinical phases: acute pneumonitis occurring about four to 12 weeks after completion of radiotherapy, and pulmonary fibrosis occurring more than nine months after treatment. The exact mechanism remains controversial, but classic radiation pneumonitis results from a dose-related pulmonary toxicity, with the inflammatory and fibrotic processes being mediated by locally released cytokines and growth factors. This mechanism of lung injury involves direct tissue damage from radiotherapy, and is generally confined to the outline of the radiation field.
Bilateral pulmonary reactions in patients undergoing unilateral irradiation have also been reported, with BAL showing a picture predominantly of lymphocytic alveolitis of the CD4 type . This suggests that, other than direct dose-related toxicity, there must be another mechanism, likely immunologically mediated, that causes a picture similar to hypersensitivity pneumonitis postradiotherapy. Radiation might induce the activation of pulmonary lymphocytes that recognize autoantigens released and unmasked after the initially local lung tissue damage.
Figure 1) Left Right perihilar coarse streaky opacity and left mid-lung airspace and reticular opacities. Right Significant resolution of pulmonary infiltrates after five days of increased dose of prednisone