Chronic airspace disease: Review of the causes and key computed tomography findings

Table 1 Clinical, laboratory and imaging findings, and prognosis/treatment of inflammatory causes of chronic airspace disease

Causes of chronic airspace disease/ General category	Clinical information	Laboratory findings	Imaging findings	Prognosis and treatment
Alveolar sarcoidosis/ Inflammatory	History of sarcoidosis	Elevated ACE	Infiltrative and consolidative opacities with ill-defined margins and sometimes air bronchograms; Typical findings of sarcoidosis may or may not be present (perilymphatic nodules, enlarged lymph nodes in the right paratracheal region and bilateral hila)	Corticosteroids only given for active disease; Presence of alveolar sarcoidosis is more suggestive of active disease; Relatively rapid response to treatment; May recur
Chronic eosinophilic pneumonia/ Inflammatory	History of asthma in 50% of cases; Middle-aged women	Chronic eosinophilic pneumonia; Increased eosinophils in bronchoalveolar lavage; Elevated IgE	Middle/upper and peripheral lung predominant chronic airspace opacity and consolidations; Opacities may show subtle or major changes in appearance (migratory); GGO and interlobular septal thickening (crazy-paving)	Good prognosis; Often require long-term low-dose oral corticosteroid therapy in order to prevent relapse
Organizing pneumonia/ Inflammatory	No obvious cause in most of the cases (therefore cryptogenic organizing pneumonia); History of vasculitis or connective tissue disorder may be present; History of anticancer treatment may be present		Classic findings: Bilateral peribronchovascular and/or subpleural consolidations with mid-lower lung zone preference; Less common findings: Small, ill-defined peribronchial or peribronchiolar nodules large nodules or masses; Halo sign; Reverse halo sign; Crazy paving arcade-like or polygonal opacities; Opacities may show subtle changes in appearance overtime (migratory)	Most (especially cryptogenic forms) respond very well to corticosteroid treatment; A small percentage of patients many develop progressive fibrosis
EGPA (Churg-Strauss syndrome)/ Inflammatory	Small to medium vessel necrotizing pulmonary vasculitis; History of asthma is usually present; May have extrapulmonary findings (sinusitis, diarrhea, skin purpura, arthralgias)	Eosinophilia; ANCA (+)	More common: Peripheral or random parenchymal opacification either consolidation or ground glass; Opacities can be transient and change in appearance and distribution in the follow-up imaging; Less common: Centrilobular nodules and bronchial wall thickening; Cavitation is rare	Corticosteroids; May need addition immunosuppression with cyclosporine, azathioprine if there is cardiac, renal, GI or CNS involvement; Low mortality rate; Cardiac involvement is a major contributor to death
Granulomatosis with polyangiitis (Wegner granulomatosis)/ Inflammatory	Multisystem necrotizing non-caseating granulomatous vasculitis affecting small to medium; May involve sinuses and kidneys	ANCA (+)	Chronic airspace opacity and consolidation; Nodules and masses which may cavitate in 50% of cases; Halo or reverse halo sign may be present due to hemorrhage and associated ground-glass appearance	Immunosuppression with cyclophosphamide, methotrexate and/or corticosteroids; Rapidly fatal if not treated
Treatment and drug-related/ Inflammatory	History of cancer treatment; Respiratory symptoms related to pneumonitis including dyspnea and fever		Can have the following appearances; Organizing pneumonia; Nonspecific interstitial pneumonia; ARDS; Eosinophilic pneumonia; Pulmonary hemorrhage	Supportive treatment; Withholding treatment. May or may not recur after reintroduction of treatment

ACE: Angiotensin-converting enzyme; ANCA: Antineutrophil cytoplasmic antibody; ARDS: Acute respiratory distress syndrome; CNS: Central nervous system; EGPA: Eosinophilic granulomatosis with polyangiitis; GGP: Ground glass opacity; GI: Gastrointestinal.