1. Mastectomy – absent breast ± absent pectoral muscle shadows.

2. Poliomyelitis – atrophy of pectoral muscles ± atrophic changes in the shoulder girdle and humerus.

3. Poland’s syndrome – unilateral congenital absence of pectoral muscles ± rib defects. Occurs in 10% of patients with syndactyly.

Pneumothorax – note the visceral pleural edge and absent vessels peripherally.

1. Compensatory hyperexpansion – e.g. following lobectomy (look for rib defects/bronchial sutures indicating previous surgery) or lobar collapse.

2. Airway obstruction – air trapping on expiration results in increased lung volume and shift of the mediastinum to the contralateral side.

3. Unilateral bullae – vessels are absent rather than attenuated. May mimic pneumothorax.

4. Swyer–James (McLeod) syndrome – the late sequela of bronchiolitis in childhood (usually viral but non-viral organisms also implicated). Lung volume on affected side is either normal or slightly reduced but, importantly, there is air trapping on expiration. Ipsilateral hilar vessels are small. CT not infrequently shows bilateral disease with mosaic attenuation and bronchiectasis.

5. Congenital lobar emphysema – one-third present at birth. Marked overinflation of a lobe (most commonly left upper lobe followed by right upper lobe or right middle lobe). The ipsilateral lobes are compressed and there may be mediastinal displacement to the contralateral side.

Pulmonary embolus (see Pulmonary embolic disease*) – to a major pulmonary artery (at least lobar in size). The pulmonary artery is dilated proximally and the affected lung shows moderate loss of volume. NB. Small pulmonary emboli are unlikely to result in any disparity.

1. Emphysema – with large central pulmonary arteries and peripheral arterial pruning ± bullae; centrilobular emphysema typically in mid/upper zones whereas panacinar emphysema commonly affects lower zones.

2. Asthma – during an acute episode or with chronic disease with ‘fixed’ airflow obstruction due to airway remodelling.

3. Acute bronchiolitis – particularly affects children in the first year of life. Overexpansion is due to small airways (bronchiolar) obstruction. May be associated with large airway mucosal thickening leading to bronchial wall thickening on plain radiography. Collapse and consolidation are not primary features of bronchiolitis.

4. Tracheal, laryngeal or bilateral bronchial stenoses (see 4.3).

Engelke, C., Schaefer-Prokop, C., Schirg, E., et al. High-resolution CT and CT angiography of peripheral pulmonary vascular disorders. RadioGraphics. 2002; 22:739–764.

Frazier, A. A., Galvin, J. R., Franks, T. J., et al. Pulmonary vasculature: hypertension and infarction. RadioGraphics. 2000; 20:491–524.

1. Foreign body – air trapping is more common than atelectasis. The lower lobe is most frequently affected. The foreign body may be opaque. The column of air within the bronchus may be discontinuous (the ‘interrupted bronchus sign’).

2. Mucus plug – e.g. allergic bronchopulmonary aspergillosis, asthma.

3. Misplaced endotracheal tube.

4. Broncholithiasis.

1. Tracheal/lung cancer – narrowing ± irregularity.

2. Other tumours – e.g. carcinoid tumour – usually a smooth, rounded filling defect. Main bulk of tumour may lie outside the lumen of the airway.

3. Inflammation/fibrosis – e.g. sarcoidosis, Wegener’s granulomatosis, post-tuberculous, relapsing polychondritis.

4. Bronchial atresia – most commonly affecting the apicoposterior segment of the left upper lobe.

5. Tracheobronchomalacia – excessive reduction (> 70% luminal calibre) in the calibre of the trachea/central airways at end-expiration. Diagnosis made on CT performed at residual volume or during dynamic expiration.

6. Fractured bronchus.

1. Lymph nodes.

2. Mediastinal tumours – smooth, eccentric narrowing.

3. Enlarged left atrium.

4. Aortic aneurysm.

5. Anomalous origin of left pulmonary artery from right pulmonary artery – producing compression of the right main bronchus as it passes over it, between the trachea and oesophagus to reach the left hilum. PA CXR shows the right side of the trachea to be indented and the vessel is seen end-on between the trachea and oesophagus on the lateral view.

Chung, J. H., Kanne, J. P., Gilman, M. D. Structured review article – CT of diffuse tracheal diseases. AJR Am J Roentgenol. 2011; 196:W240–W246.

Prince, J. S., Duhamel, D. R., Levin, D. L., et al, Non-neoplastic lesions of the tracheobronchial wall: radiologic findings with bronchoscopic correlation. RadioGraphics. 2002;(Suppl):S215–S230.

1. Consolidation/air-space opacification – indicating the replacement of air from the air spaces by exudate or other disease process (e.g. tumour, blood, oedema). An air bronchogram/bronchiologram may be present. Vascular margins and airway wall are obscured.

2. Pleural effusion – in the supine position, an uncomplicated effusion gravitates to the dependent part of the chest, producing a generalized increased density ± an apical ‘cap’ of fluid on CXR. Note that pulmonary vessels will be visible through the increased density (cf. Consolidation/air-space opacification). Erect or decubitus CXRs may confirm the diagnosis.

3. Malignant pleural mesothelioma – often associated with a pleural effusion which obscures the tumour ± calcified pleural plaques (more commonly demonstrated at CT). Encasement of the lung limits mediastinal shift. (NB. Affected hemithorax may even be smaller.)

1. Large pleural effusion (q.v.) – NB. A large effusion with no mediastinal shift indicates significant lung collapse (and, hence, central obstruction) or relative ‘fixation’ of the mediastinum (e.g. caused by malignant pleural mesothelioma).

2. Diaphragmatic hernia – on the right side with herniated liver; on the left side the hemithorax is not usually opaque because of air within the herniated bowel. The left hemithorax may be opaque in the early neonatal period when air has not yet had time to reach the herniated bowel.

1. Lung collapse.

2. Postpneumonectomy.

3. Lymphangitis carcinomatosa – bilateral and symmetrical infiltration is most common; unilateral lymphangitis occurs more often in patients with lung cancer. Linear and nodular opacities ± ipsilateral hilar and mediastinal lymph-node enlargement. Septal lines. Pleural effusions are common.

4. Pulmonary agenesis and hypoplasia – usually asymptomatic. Absent or hypoplastic pulmonary artery.

5. Malignant pleural mesothelioma – see above.

Youngberg, A. S. Unilateral diffuse lung opacity. Radiology. 1977; 123:277–282.

1. Staphylococcus aureus – a characteristic feature of childhood staphylococcal pneumonia, developing in 40–60% of cases.

2. Streptococcus pneumoniae.

3. Escherichia coli.

4. Klebsiella pneumoniae.

5. Haemophilus influenzae.

6. Pneumocystis jiroveci – usually multiple and in the upper parts of the lungs. Patients with cysts are more likely to develop pneumothoraces.

7. Legionella pneumophila.

8. Hydatid.

Lung laceration – cysts measuring up to 5 cm in diameter. Resolution over time.

1. Congenital pulmonary adenomatoid malformation/sequestration.

2. Intrapulmonary bronchogenic cyst.

1. Following treatment of pulmonary metastases – bladder cancer and germ cell tumours. May be visible only on CT.

2. Hyalinizing granulomas – rare disorder of unknown aetiology but possible association with infection and autoimmunity. Multiple ill-defined/well-defined nodules and cysts.

3. Metastatic epithelioid sarcoma.

1. Langerhans’ cell histiocytosis (LCH) – cysts, sometimes with bizarre (i.e. non-circular) outlines, in mid/upper zones. In ‘early’ disease multiple nodules, which then cavitate. Relative sparing of lower zones and medial tips of middle lobe and lingula. Pulmonary LCH (but not other forms of LCH) is strongly linked to cigarette smoking.

2. Lymphangioleiomyomatosis (LAM) – exclusively in female subjects of child-bearing age and related to mutation of TSC1 (chromosome 9). Smooth-muscle proliferation around vessels, lymphatics and airways. Cysts are a characteristic finding and more uniform in size than in LCH. No zonal predilection (cf. LCH).

3. Tuberose sclerosis (TSC) – neurocutaneous disorder associated with mutations of TSC1 and TSC2 genes. Pathology of lung disease in TSC almost identical to LAM.

4. Neurofibromatosis – cystic lung disease and interstitial fibrosis are reported but some doubt exists and changes maybe simply represent smoking-related interstitial lung disease.

5. Birt–Hogg–Dubé syndrome – autosomal dominant multisystem disorder characterized by pulmonary cysts, cutaneous fibrofolliculomas and increased risk of renal tumours. Recurrent pneumothoraces due to lung involvement.

6. Lymphoid interstitial pneumonia – rarely idiopathic; usually occurs in context of dysproteinaemias, HIV infection and connective tissue disorders (in particular rheumatoid arthritis, Sjögren’s syndrome). Mechanism of cyst formation is uncertain but may be caused by partial obstruction of small airways.

7. Hypersensitivity pneumonitis – possibly related to lymphocytic interstitial pulmonary infiltrate in subacute phase.

8. End-stage fibrotic diffuse interstitial lung diseases – e.g. idiopathic pulmonary fibrosis, sarcoidosis, chronic hypersensitivity pneumonitis.

Biyyam, D. R., Chapman, T., Ferguson, M. R., et al. Congenital lung abnormalities: embryologic features, prenatal diagnosis, and postnatal radiologic–pathologic correlation. RadioGraphics. 2010; 30:1721–1738.

Seaman, D. M., Meyer, C. A., Gilman, M. D., McCormack, F. X. Pictorial essay: diffuse cystic lung disease at high-resolution CT. AJR Am J Roentgenol. 2011; 196:1305–1311.

Silva, C. I. Diffuse lung cysts in lymphoid interstitial pneumonias: high-resolution CT and pathologic findings. J Thorac Imaging. 2006; 21:241–244.

Franquet, T., Gimenez, A., Roson, N., et al. Aspiration diseases: findings, pitfalls and differential diagnosis. RadioGraphics. 2000; 20:673–685.

Parameswaran, G. I. Infection in high-risk populations. Infect Dis Clin North Am. 2007; 21:673–695.

1. Primary tuberculosis – lymph-node enlargement is unilateral in 80% and involves the hilar (60%), or combined hilar and paratracheal (40%) nodes.

2. Viral pneumonias.

3. Mycoplasma pneumonia – lymph-node enlargement is common in children but rare in adults. May be unilateral or bilateral.

4. Primary histoplasmosis – in endemic areas. Hilar lymph-node enlargement is common, particularly in children. During healing, lymph nodes calcify and may cause bronchial obstruction, thereby initiating distal infection.

5. Coccidioidomycosis – in endemic areas. The pneumonic type consists of predominantly lower lobe consolidation that is frequently associated with hilar lymph-node enlargement.

More frequent

Less frequent

Dodd, J. D., Souza, C. A., Müller, N. L. Conventional high-resolution CT versus helical high-resolution MDCT in the detection of bronchiectasis. AJR Am J Roentgenol. 2006; 187:414–420.

Hansell, D. M., Lynch, D. A., McAdams, H. P., Bankier, A. A., Diseases of the airways diseases. Imaging of diseases of the chest. 5th ed. Elsevier Mosby, Philadelphia, PA, 2010.

McGuinness, G., Naidich, D. P. CT of airways disease and bronchiectasis. Radiol Clin North Am. 2002; 40(1):1–19.

1. Oedema – see 4.12.

2. Infection – see also 4.7–4.9

3. Diffuse pulmonary haemorrhage – e.g. idiopathic pulmonary haemosiderosis, anti-glomerular basement disease, microscopic polyangiitis, systemic lupus erythematosus, Behçet’s syndrome, Wegener’s granulomatosis, contusion, bleeding diatheses, Goodpasture’s syndrome, idiopathic pulmonary haemosiderosis (in the acute stage), pulmonary infarction.

4. Malignancy – adenocarcinoma, lymphoma.

5. Sarcoidosis* – called ‘air-space’ sarcoidosis and occurring in up to 20%. Air-space pattern is due to thickened interstitium and filling of air spaces by macrophages and granulomatous infiltration.

6. Eosinophilic lung disease – chronic eosinophilic pneumonia is characteristically non-segmental, in the upper zones and paralleling the chest wall.

7. Organizing pneumonia – may be cryptogenic or as a response to other ‘insult’ (e.g. infection, drug toxicity, connective tissue disease). Typically, multifocal air-space opacities in periphery of mid/lower zones. Occasionally a single focus may be present. A characteristic perilobular distribution is seen in some patients. Another pattern is the so-called ‘reverse halo’ or Atoll sign (a ring of consolidation surrounding central ground-glass opacification).

1. Fluid overload – excess i.v. fluids, renal failure and excess hypertonic fluids, e.g. contrast media.

2. Cerebral disease – cerebrovascular accident, head injury or raised intracranial pressure.

3. Near drowning – radiologically no significant radiological differences between freshwater and seawater drowning.

4. Aspiration (Mendelson’s syndrome).

5. Radiotherapy – several weeks following treatment. Ultimately has a characteristic straight edge as fibrosis ensues.

6. Rapid re-expansion of lung following thoracocentesis.

7. Liver disease and other causes of hypoproteinaemia.

8. Transfusion-related acute lung injury (TRALI) – commonest cause of transfusion-related mortality in UK and USA. Onset of oedema is either during transfusion or within 1–2 hours.

9. Drug-induced

10. Poisons

11. Mediastinal tumours – producing venous or lymphatic obstruction.

12. Acute respiratory distress syndrome – may be primary (e.g. caused by severe pneumonia, aspiration) or secondary (e.g. following non-thoracic sepsis or trauma); CXR may be normal in first 24 hours but progressive widespread opacification with onset of interstitial and then frank intra-alveolar leak of oedema and haemorrhagic fluid.

13. High altitude (acute mountain sickness) – following rapid ascent to > 3000 metres.

Asrani, A. Urgent findings in portable chest radiography. AJR Am J Roentgenol. 2011; 196:WS37–WS46.

Gluecker, T., Capasso, P., Schnider, P., et al. Clinical and radiologic features of pulmonary edema. RadioGraphics. 1999; 19:1507–1531.

Desai, S. R., Wells, A. U., Suntharalingam, G., et al. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary injury: a comparative CT study. Radiology. 2001; 218:689–693.

Desai, S. R. Acute respiratory distress syndrome: imaging the injured lung. Clin Radiol. 2002; 57:8–17.

1. Prolonged lateral decubitus position.

2. Unilateral aspiration.

3. Pulmonary contusion.

4. Rapid thoracocentesis of air or fluid.

5. Bronchial obstruction.

6. Systemic artery to pulmonary artery shunts – e.g. Waterston (on the right side), Blalock–Taussig (left or right side) and Pott’s procedure (on the left side).

1. Congenital absence or hypoplasia of a pulmonary artery.

2. McLeod syndrome.

3. Thromboembolism.

4. Unilateral emphysema.

5. Lobectomy.

6. Pleural disease.

Calenoff, L., Kruglik, G. D., Woodruff, A. Unilateral pulmonary oedema. Radiology. 1978; 126:19–24.

1. Left ventricular failure.

2. Mitral stenosis.

3. Pulmonary veno-occlusive disease.

1. Lymphangitis carcinomatosa/lymphomatosa – most often caused by lymphatic infiltration in patients with cancer of the lung, breast, stomach and pancreas or lymphoma. Nodular thickening (typically bilateral) of interlobular septa is the characteristic finding on CT.

2. Pneumoconioses – surrounding tissues may contain a heavy metal, e.g. tin, which contributes to the density.

3. Sarcoidosis* – septal lines are uncommon.

4. Idiopathic bronchiectasis – thickened interlobular septa are a feature in around one-third of patients (see 4.10).

5. Erdeim–Chester disease – infiltration of pulmonary interstitium by histiocytes of non-Langerhans’ type. Primarily a bone disorder but extraskeletal involvement in around 50%. Lung involvement in around one-third of patients. On chest radiography, reticulonodular infiltrate in mid/upper zones. On CT, smooth thickening of interlobular septa is characteristic, associated with ground-glass opacification and centrilobular nodules.

6. Diffuse pulmonary haemorrhage – with recurrent episodes of bleeding, thickened interlobular septa may be seen on CT (see 4.11).

7. Diffuse pulmonary lymphangiomatosis – proliferation of lymphatic channels in pleura, interlobular septa and peribronchovascular connective tissue.

8. Congenital lymphangiectasia – abnormal dilatation of lymphatic vessels. (NB. No increase in number of lymphatics; cf. lymphangiomatosis.) May be associated with extrathoracic congenital anomalies (e.g. renal, cardiac). Usually fatal.

9. Alveolar proteinosis – smooth thickening of interlobular (and intralobular) septa in geographical areas of ground-glass infiltration (i.e. the ‘crazy-paving’ pattern). Infiltration of air spaces and interstitium and air spaces by PAS-positive macrophages.

10. Alveolar microlithiasis.

11. Amyloidosis.

Hawtin, K. E., Roddie, M. E., Mauri, F. A., Copley, S. J. Pulmonary sarcoidosis: the ‘Great Pretender’. Clin Radiol. 2010; 65:642–650.

Webb, W. R. Thin-section CT of the secondary pulmonary lobule: anatomy and the image – the 2004 Fleischner Lecture. Radiology. 2006; 239:322–338.

1. Idiopathic pulmonary fibrosis (IPF) – most common idiopathic interstitial pneumonia. Associated with the histological/radiological pattern of UIP. Typical patient is male, aged 50–60 years and complaining of progressive dyspnoea. On CXR there is a reticular pattern in mid/lower zones. Predominant basal and subpleural reticular pattern with honeycombing is the characteristic finding on CT. Ancillary findings include ground-glass opacification (less extensive than reticular pattern), traction bronchiectasis/bronchiolectasis and mediastinal lymph-node enlargement. Atypical HRCT findings in around 30–50%. Coexistent emphysema in upper zones (associated with preserved lung volumes). Increased incidence of lung cancer.

2. Connective tissue diseases (CTDs) – fibrotic lung disease is common and most frequent cause of death. Variable patterns of interstitial lung disease including UIP, NSIP, lymphoid interstitial pneumonia (LIP; see also 4.5) and diffuse alveolar damage. Variable prevalence in different CTDs: UIP pattern more prevalent than NSIP in rheumatoid arthritis; NSIP pattern more prevalent in systemic sclerosis and polymyositis/dermatomyositis; LIP most prevalent in rheumatoid arthritis and Sjögren’s syndrome.

3. Occupational lung disease

4. Sarcoidosis* – archetypal granulomatous fibrotic diffuse interstitial lung disease. Typically associated with symmetrical, bronchocentric reticular pattern in upper zones. Calcified mediastinal and hilar lymph nodes.

5. Chronic hypersensitivity pneumonitis – secondary to repeated exposure to a potentially wide variety of particulate (1–5 µm diameter) organic antigens originating from animals, plants, drugs or bacteria/fungi. A reticular pattern ± honeycombing, ground-glass opacification ± traction bronchiectasis/bronchiolectasis and lobular areas of apparently ‘spared’ lung are characteristic on CT.

6. Cystic lung diseases – because of the effects of anatomical superimposition on chest radiographs, the multiple cysts in disorders such as Langerhans’ cell histiocytosis, lymphangioleiomyomatosis and tuberous sclerosis can manifest as a reticular pattern (see also 4.5). Relative preservation of lung volumes.

7. Drug-induced lung disease – e.g. caused by nitrofurantoin, busulphan, cyclophosphamide, bleomycin and melphalan.

8. Bone marrow transplantation – airways disease (constrictive obliterative bronchiolitis) and upper zone fibrosis associated with recurrent small pneumothoraces.

9. Miscellaneous causes of diffuse lung disease

Dixon, S., Benamore, R. The idiopathic interstitial pneumonias: understanding key radiological features. Clin Radiol. 2010; 65:823–831.

Raghu, G., Collard, H. R., Egan, J. J., et al. An official ATS/ERS/JRS/ALAT statement: idiopathic pulmonary fibrosis evidence-based guideline for diagnosis and management. Am J Respir Crit Care Med. 2011; 183:788–824.

Wells, A. U., Hirani, N. Interstitial lung disease guideline. Thorax. 2008; 63(Suppl V):v1–v58.

1. Miliary tuberculosis – widespread and secondary to haematogenous dissemination. Uniform size. Indistinct margins but discrete. No septal lines. Normal hila unless superimposed on primary tuberculosis.

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