Cicatrization Atelectasis: Corresponding to Radiation Therapy Portal for Lymphoma

Radiologic Findings PA (Fig. 1A) and lateral (Fig. 1B) chest radiographs demonstrate well-defined rather geometrically symmetric opacities with sharp borders involving the superior mediastinum and paramediastinal lung zones that follow a non-anatomic distribution. The bronchi within the affected lung are distorted and dilated. Note the hilar retraction, diaphragmatic elevation, and compensatory over-inflation of the uninvolved lower lungs.     Diagnosis: Cicatrization Atelectasis: Corresponding to Radiation Therapy Portal for Lymphoma

Differential Diagnosis

None

Discussion

Localized cicatrization atelectasis is a fibrotic process associated with irreversible volume loss (Fig. 1A-1B). The prototypical example is fibrosis secondary to chronic infection (e.g., long-standing tuberculosis) and necrotizing pneumonia. Idiopathic pulmonary fibrosis (IPF) and other chronic infiltrative lung diseases are associated with a more generalized but also irreversible form of cicatrization atelectasis.

Clinical Findings

Chronic radiation damage begins 3-4 months following initiation of therapy. The fibrosis and volume loss develops gradually and stabilizes 9-12 months following completion of therapy. Many patients are asymptomatic. Symptoms, when present, may be insidious and include cough and dyspnea. The associated lung fibrosis on imaging correlates with the expected location of the radiation therapy port (Fig. 1A-1B). For example, paramediastinal cicatrization atelectasis occurs in patients who have received mantle radiation (e.g., lymphoma and other mediastinal malignancies) whereas the cicatrization atelectasis and bronchovascular reorientation occurs in the peripheral upper and middle lobes in patients receiving chest wall radiation (e.g. breast cancer).

Imaging Findings

• Parenchymal opacity with loss of lung volume (Fig. 1A-1B).
• Parenchymal opacity conforming to the radiation port (Fig. 1A-1B).
• Affected lung occupies a smaller volume than normal, appears dense and heterogeneous because of architectural distortion, dilated bronchi, and bronchioles (Fig. 1A-1B).
• Compensatory signs of chronic volume loss are usually evident (e.g., localized mediastinal shift, compensatory overinflation of unaffected lung) (Fig. 1A-1B).

Treatment for Symptomatic Patients

• Supportive with supplemental oxygen
• Corticosteroids in select cases

Prognosis

• Irreversible
• Dependent on the underlying disease process

Caveats

• Cicatrization atelectasis is the only form of pulmonary atelectasis that is irreversible

Suggested Readings

1. Fraser RS, Müller NL, Colman N, Pare', PD. Atelectasis In: Fraser and Pare's Diagnosis of Diseases of the Chest, 4th ed. Philadelphia: Saunders, 1999:522-525.
2. Fraser RS, Müller NL, Colman N, Pare', PD. Irradiation. In: Fraser and Pare's Diagnosis of Diseases of the Chest, 4th ed. Philadelphia: Saunders, 1999; 2595-2606.
3. Parker MS, Rosado-de-Christenson ML, Abbott GF.  Cicatrization Atelectasis. In: Teaching Atlas of Chest Imaging 2006, Thieme, New York pp.164-165.
4. Westcott JL, Cole SR. Traction Bronchiectasis in End-Stage Pulmonary Fibrosis. Radiology 1986; 161(3): 665-669.
5. Woodring JH, Reed JC. Types and Mechanisms of Pulmonary Atelectasis. J Thorac Imaging 1996; 11:92-108.