A 48-year-old man with dilated cardiomyopathy was referred to our hospital because of dyspnoea, haemoptysis and fever. Two months earlier, he suffered from bilateral pneumonia and was treated with antibiotics. On physical examination, respiratory crackles were heard over both lung fields. Chest film showed cardiac enlargement and diffuse air space opacities. Computed tomography (CT) scan of the chest (fig 1A) revealed areas of patchy ground glass opacities involving both lungs and associated with lobular areas of reduced attenuation indicating mosaic perfusion. The differential diagnosis includes pulmonary oedema, pneumonia (viral or bacterial infection), hypersensitivity pneumonitis and bronchiolitis obliterans organising pneumonia (BOOP) (idiopathic or post-infection).

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Figure 1 Transverse thin section computed tomography (CT) scan, coronal and sagittal reconstruction images (A) showing areas of patchy ground glass opacities involving both lungs and associated with lobular areas of reduced attenuation indicating mosaic perfusion.

Open lung biopsy specimen (B) showing organising granulation tissue involving bronchioles, alveolar ducts and alveoli with infiltration of mononuclear cells and foamy macrophages, consistent with the diagnosis of bronchiolitis obliterans organising pneumonia (BOOP).

Diuretics and antibiotics were not helpful. Five days later he developed severe respiratory failure; mechanical ventilation was initiated and he was transferred to the intensive care unit. The results of a microbiological examination of tracheobronchial aspirates were negative for any organism. Serologic tests for common agents of atypical pneumonia were negative. The exact diagnosis was crucial for the patient’s management, and consequently he underwent open lung biopsy. Histopathologic findings were consistent with the diagnosis of BOOP (fig 1B). Pulse therapy with methylprednisolone followed by maintenance therapy with prednisone resulted in a dramatic response and the patient was removed from the ventilator a few days later. A chest radiograph obtained 3 weeks later showed near complete resolution of the pulmonary infiltrates.

Rapidly progressive BOOP is a deadly form that occurs in <10% of patients with BOOP. Recently, Chakravorty et al1 described a case of progressive BOOP that presented with pneumothorax and developed multi-organ dysfunction. Similarly to our case, the diagnosis was confirmed on open lung biopsy and the patient responded well to treatment with corticosteroids. Corticosteroid resistance in patients with BOOP is reported to be rare.2 The typical radiographic appearances of organising pneumonia are multiple, usually bilateral, foci of consolidation. CT often demonstrates consolidation involving subpleural or peribronchial areas, ground glass opacities and parenchymal nodules.3 We do believe that early diagnosis of rapidly progressive BOOP based on CT and histological findings and initiation of corticosteroid therapy might improve survival in these patients.