Non-specific interstitial pneumonitis
Patient with known membranous glomerulonephritis and antiphospholipid syndrome with multiple previous pulmonary emboli who is on immunosuppressive treatment was investigated for shortness of breath with a CT pulmonary angiogram
A CTPA was obtained
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There are bilateral, widespread patchy areas of ground glass opacities slightly more marked within both lower lobes, with very mild central bronchial dilatation. There is no evidence of reticular interlobular septal thickening, pulmonary nodules or fibrosis. The intervening lung demonstrates a normal architecture, and there is no volume loss. There is no pleural effusion. No confluent areas of consolidation are seen. No evidence of air trapping. There are no filling defects within the main, lobar or segmental pulmonary arteries to suggest pulmonary emboli.
These are indicative of inflammatory foci of non-specific interstitial pneumonitis.
A biopsy of 4 specimens was obtained for further evaluation.
Microscopic report: Sections of these four specimens of lung tissue demonstrate broadly similar appearances. All include pleural surface and underlying lung parenchyma. Bronchial, vascular and alveolar architecture are generally preserved. Bronchial, vascular and alveolar architecture are generally preserved. In most areas, there appears to be normal alveolar expansion, except for one apparently collapsed lobule. Mild patchy subpleural emphysematous change is noted.
Predominantly within subpleural alveoli, there is a mild patchy increase in lightly pigmented macrophages, in a minority of areas imparting a desquamative interstitial pneumonia-like picture. In other areas of lung there is irregular, at most mild thickening of alveolar walls accompanied by a patchy inflammatory infiltrate consisting predominantly of mononuclear cells. Eosinophils are not seen. Very occasional multinucleate cells are seen within the infiltrate. No areas of granulomatous inflammation, infarction or suppurative inflammation are seen. Special stains for microorganisms are negative.
Most pulmonary artery branches show normal thickness of the arterial wall. There are occasional arteries that appear recanalised, suggesting previous thrombosis with repair. There is no evidence of vasculitis. Prussian blue stains demonstrate small quantities of granular iron within alveolar macrophages, in a predominantly subpleural location. Bronchi appear generally normal, with no evidence of peribronchial inflammation, bronchial wall thickening or bronchial epithelial metaplasia or dysplasia.
COMMENT: These lung biopsies demonstrate a mild irregular predominantly chronic interstitial inflammatory process, the overall pattern favouring non-specific interstitial pneumonia. There are focal changes consistent with the history of previous pulmonary embolism and the patchy old alveolar haemorrhage would appear most likely to be secondary to this. The appearances do not suggest current infection, usual interstitial pneumonia, Wegener's granulomatosis or other pulmonary vasculitis.