Chest ImagingRadiation pneumonitis
the effects of radiation therapy on the lungs and
pleura. The severity and extent of damage to normal lung tissue depend on:
the volume of normal lung included in the field of radiation;
the total dose and the fraction of that dose;
individual susceptibility to radiation; and
previous or concomitant therapy that may influence the time and severity of the radiation changes.
The pathological changes occur in the initial 24-48 hours after radiation but those changes are undetectable clinically and radiologically. The phase of acute radiation pneumonitis develops 1-6 months after the therapy. The peak reaction occurs in 3-4 months. The subsequent fibrosis starts developing and continues to progress 12-18 months. In the acute phase, there is fibrinous alveolar exudation leading to hyaline membrane formation, endothelial cell damage and evidence of arteritis. A certain degree of alveolar and interstitial fibrosis may be present, depending on the severity of the radiation. At the peak of inflammatory changes, the regenerative phase occurs. Exudate and oedema disperse the alveolar lining cells and capillary endothelial cells regenerate. Fibrosis progresses, consolidates and contracts over the following weeks and months. Progressive sclerosis of the pulmonary vessels and bronchi frequently occur, leading to bronchiectasis and oligaemia of the affected areas.
Radiologically, the earliest changes appear 6-8 weeks after the beginning of the therapy. The most important observation is that radiation changes to the lung confined to the field of irradiation. As a result, the margins of the abnormal areas in the lung are sharp and correspond to the radiation ports. On the chest radiograph, the first phase is characterized by diffuse haze in the radiation areas with obscuration of the vessels and progressive appearance of areas of consolidation containing air bronchogram (Fig.1). Pleural effusions are usually present. During the regenerative fibrotic phase the lung infiltration becomes more linear or reticular. Fibrous contraction condenses the opacities and distorts adjacent structures, particularly the hilar vessels. On CT scans, at the phase of acute radiation pneumonitis, patchy and confluent areas of ground glass attenuation and airspace consolidation appear in the irradiated field (Fig.2). The geographic distribution of the changes is quite striking. At the fibrotic phase, shrinkage of vessels and bronchi and linear bands progressively appear. Contraction is seen as distorsion of adjacent structures. Traction bronchiectasis within the contracted portion of the lungs is frequently apparent.
MR imaging may be indicated when differential diagnosis between infection and recurrent tumour is considered (lymphoma recurrence thoracic). Radiation fibrosis has low signal intensity on both T1-weighted and T2-weighted sequences. Neoplasm has typically high signal intensity on T2-weighted images and can be distinguished from pure fibrosis. However, acute radiation pneumonitis, secondary infectious pneumonitis or haemorrhage may have a signal intensity similar to that of neoplasm, and as a result, may be confused with recurrent disease.
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PA chest radiograph performed 5 months after mantle radiation therapy of the mediastinum for treatment of Hodgkin's disease, shows typical consolidation and air bronchograms strictly confined to the areas corresponding to the radiation field.
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Radiation pneumonitis, Fig.1 | | Radiation pneumonitis, Fig.2 | |