Respiratory tract

Published on 12/06/2015 by admin

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4

Respiratory tract

4.1

Unilateral hypertransradiant hemithorax

A paucity or decrease in the number of vessels on one side indicates an abnormal lung. An approximately equal number and/or calibre of vessels in both lungs suggests that the contralateral hemithorax is of increased density (e.g. caused by a pleural effusion in a supine patient or pleural thickening).

Lung

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 vessels

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.

4.2

Bilateral hypertransradiant hemithoraces

4.3

Tracheal/bronchial narrowing, stenosis or occlusion

Airway narrowing may occur at any site from below the level of the vocal cords down to the segmental/subsegmental airways.

4.4

Increased density of one hemithorax

With an undisplaced mediastinum

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.)

4.5

Pulmonary air cysts

A pulmonary air cyst is defined as a rounded parenchymal lucency or low-attenuation focus with a well-defined wall; the walls of cysts are generally thin (< 2 mm thickness). Cysts may contain solid material or fluid.

Diffuse lung diseases

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.

4.6

Non-resolving or recurrent consolidation

4.7

Consolidation with an enlarged hilum

Hilar lymph-node enlargement may be secondary to pneumonia, or pneumonia may be secondary to bronchial obstruction caused by a hilar mass. Signs suggestive of a secondary pneumonia include segmental or lobar consolidation, slow resolution, recurrent consolidation in the same part of the lung and associated volume loss/lobar collapse.

Secondary pneumonias

See 4.3, but note particularly lung cancer/other tumours.

4.8

Pneumonia involving part or the whole of one lobe

Consolidation involving the air spaces of an anatomically recognizable lobe is most often caused by the following organisms. (NB. The entire lobe may not be involved and there may be a degree of associated collapse.)

1. Streptococcal pneumonia – the commonest cause. Usually unilobar. Cavitation is rare. Pleural effusion is uncommon. Little or no collapse.

2. Klebsiella pneumonia – often multilobar involvement. High propensity for cavitation and lobar enlargement.

3. Staphylococcal pneumonia – especially in children. 40–60% of children develop pneumatocoeles. Effusion (empyema) and pneumothorax are also common. Bronchopleural fistula may develop. No lobar predilection.

4. Tuberculosis – in primary or postprimary tuberculosis, but more common in the former. Associated collapse is common. The right lung is affected more often than the left, and primary tuberculosis has a predilection for the anterior segment of the upper lobes or the medial segment of the middle lobe.

5. Streptococcus pyogenes pneumonia – affects the lower lobes predominantly. Often associated with pleural effusion/empyema.

4.10

Bronchiectasis

Bronchiectasis is the permanent (localized or diffuse) dilatation of airways. Signs of bronchiectasis are more reliably identified on CT than CXR, particularly with mild disease. Volumetric thin-section high-resolution images, using multidetector CT, are superior to interspaced HRCT for diagnosis of bronchiectasis. On CT, dilated bronchi manifest as either non-tapering airways (‘tramlines’ – airways which are imaged in longitudinal section) or ‘signet-ring’ opacities (i.e. a dilated bronchus in comparison with the homologous pulmonary artery branch). In severe disease, large cystic spaces ± air–fluid levels may be present. The ancillary (i.e. not diagnostic) signs of bronchiectasis include volume loss, plugging of small airways (tree-in-bud pattern) and large airways and mosaic attenuation.

Causes of bronchiectasis

Less frequent

1. Following childhood infections – e.g. secondary to measles and pertussis. Less common cause in the antibiotic era in developed countries but continues to be an important factor in developing countries.

2. Secondary to bronchial obstruction – foreign body, neoplasm, broncholithiasis or bronchial stenosis.

3. Chronic aspiration.

4. Congenital/genetic anomalies

5. Collagen vascular diseases – particularly rheumatoid arthritis, Sjögren’s syndrome.

6. Gastrointestinal disorders – ulcerative colitis, coeliac disease.

7. Immunological – allergic bronchopulmonary aspergillosis, following solid-organ (heart/lung) or bone marrow transplantation.

4.11

Air-space opacification

Sometimes termed ‘alveolar shadowing’, but this is incorrect because the lung opacification is due to displacement of air from anatomically larger acini. Instead, the general term ‘air-space’ consolidation or opacification is recommended. The signs of air-space disease are increased parenchymal density, which obscures visibility of vessels and bronchial walls. Air bronchograms/bronchiolograms may or may not be visible.

Causes of air-space opacification

Note that any of the following may be unilateral and, in some instances, confined to a single lobe.

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).

4.12

Pulmonary oedema

Defined as an increase in extravascular lung water and traditionally regarded as being secondary to cardiogenic or non-cardiogenic causes.

Non-cardiogenic pulmonary oedema

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.

4.13

Unilateral pulmonary oedema

4.14

Septal (Kerley B) lines

Pulmonary lobules are the smallest lung units bounded by interlobular septa. Each lobule is supplied by a lobular airway and arterial branch. The interlobular septa contain lymphatics, venous radicals and interstitium. Any pathological process involving the lymphatics, veins or interstitium might render interlobular septa visible. On chest radiography abnormal thickening of interlobular septa is best seen in the costophrenic angles, but thickened interlobular septa are more readily visible on CT (NB. A few normal interlobular septa are commonly seen on CT).

Lymphatic/interstitial infiltration

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.

4.15

Reticular pattern (with or without honeycombing)

A reticular pattern (or reticulation) is defined as a lacework of innumerable small linear opacities which on CXR become summated and produce an appearance resembling a ‘net’. The characteristics of a reticular pattern are better appreciated on CT. A reticular pattern generally indicates established interstitial lung disease. (NB. A reticular pattern may also be caused by thickening of interlobular septa, perilobular infiltration or another cause of parenchymal destruction which spares the septa; see below.) There may or may not be associated honeycombing (characterized on CT by clustered cystic air spaces usually in the subpleural lung). The distribution of a reticular pattern (i.e. upper zone versus lower zone or central versus peripheral) is of diagnostic value.

Reticular pattern – diffuse interstitial lung diseases

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

4.16a

Multiple small (‘pin-point’) micronodules

Must be of very high atomic number to be rendered visible on plain chest radiography.

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