Radiological studies showed a ventricular septal defect alongside cardiac and arterial anomalies (heart silhouette enlargement, elevation of the cardiac apex, presence of a right aortic arch, enlargement affecting the main pulmonary arteries and their major branches, high pulmonary artery vascularity, and ventricular septal defect). See also
Tricuspid atresia
Mitral regurgitation


== References ==
Pattern of opacities
ConsolidationAcute: Alveolar hemorrhage syndromes, acute eosinophilic pneumonia, acute interstitial pneumonia, cryptogenic organizing pneumonia
Chronic: Chronic eosinophilic pneumonia, cryptogenic organizing pneumonia, lymphoproliferative disorders, pulmonary alveolar proteinosis, sarcoidosis

Linear or reticular opacitiesAcute: Pulmonary edema
Chronic: Idiopathic pulmonary fibrosis, connective tissue-associated interstitial lung diseases, asbestosis, sarcoidosis, hypersensitivity pneumonitis, drug-induced lung disease

Small nodulesAcute: Hypersensitivity pneumonitis
Chronic: Hypersensitivity pneumonitis, sarcoidosis, silicosis, coal workers pneumoconiosis, respiratory bronchiolitis, alveolar microlithiasis

Cystic airspacesChronic: Pulmonary langerhans cell histiocytosis, pulmonary lymphangioleiomyomatosis, honeycomb lung caused by IPF or other diseases
Ground glass opacities
Acute: Alveolar hemorrhage syndromes, pulmonary edema, hypersensitivity pneumonitis, acute inhalational exposures, drug-induced lung diseases, acute interstitial pneumonia
Chronic:  Nonspecific interstitial pneumonia, respiratory bronchiolitis associated interstitial lung disease, desquamative interstitial pneumonia, drug-induced lung diseases, pulmonary alveolar proteinosis

Thickened alveolar septaAcute: Pulmonary edema
Chronic: Lymphangitic carcinomatosis, pulmonary alveolar proteinosis, sarcoidosis, pulmonary veno occlusive disease

Distribution
Upper lung predominancePulmonary Langerhans cell histiocytosis, silicosis, coal workers pneumoconiosis, carmustine related pulmonary fibrosis,  respiratory broncholitis associated with interstitial lung disease. Lower lung predominanceIdiopathic pulmonary fibrosis, pulmonary fibrosis associated with connective tissue diseases, asbestosis, chronic aspiration

Central predominance (perihilar)Sarcoidosis, berylliosis

Peripheral predominanceIdiopathic pulmonary fibrosis, chronic eosinophilic pneumonia, cryptogenic organizing pneumonia

Associated findings
Pleural effusion or thickeningPulmonary edema, connective tissue diseases, asbestosis, lymphangitic carcinomatosis, lymphoma, lymphangioleiomyomatosis, drug-induced lung diseases

LymphadenopathySarcoidosis, silicosis, berylliosis, lymphangitic carcinomatosis, lymphoma, lymphocytic interstitial pneumonia

Genetic testing
For some types of paediatric ILDs and few forms adult ILDs, genetic causes have been identified. These may be identified by blood tests. For a limited number of cases, this is a definite advantage, as a precise molecular diagnosis can be done; frequently then there is no need for a lung biopsy.