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1
Q

TRACHEAL/BRONCHIAL NARROWING,
MASS OR OCCLUSION
In the lumen

A
  1. Mucous plug—e.g. asthma, cystic fibrosis, ABPA. Low density, usually contains gas bubbles.
  2. Foreign body—air trapping is more common than atelectasis.
    Most frequently affects the lower lobes. The foreign body may be opaque. The column of air within the bronchus may be discontinuous (‘interrupted bronchus sign’).
  3. Misplaced endotracheal tube.
  4. Broncholithiasis—usually caused by a calcified lymph node (e.g.
    from previous TB or histoplasmosis) eroding into the adjacent bronchus
2
Q

Tracheal MASS

Arising from the wall

A
  1. Tracheal/bronchial tumours.
    (a) Squamous cell carcinoma—commonest tumour in the
    trachea and bronchi, associated with smoking. Irregular
    polypoid mass or focal wall thickening and narrowing. Small
    cell lung cancer can also be endobronchial.
    (b) Carcinoid tumour—second most common bronchial tumour.
    Usually a smooth, rounded enhancing mass ± calcification.
    Main tumour bulk may lie outside the lumen.
    (c) Adenoid cystic carcinoma—second most common tracheal
    tumour. Low grade, usually in young adults. Focal or diffuse
    mass, often extending beyond the tracheal wall. Typically
    extends longitudinally along the submucosa of the trachea.
    (d) Metastasis—e.g. from melanoma, RCC, colon, breast. Rare.
    (e) Mucoepidermoid carcinoma—rare, usually in lobar or
    segmental bronchi, most common in young adults.
    Indistinguishable from carcinoid.
    (f) Endobronchial hamartoma—often contains fat and
    calcification.
    (g) Tracheobronchial papillomatosis—due to HPV infection.
    Multiple small polyps in the larynx > trachea > bronchi ±
    cavitating lung nodules.
    (h) Other rare tumours—e.g. inflammatory myofibroblastic
    tumour (especially in children), lymphoma/PTLD, sarcomas,
    lipoma, leiomyoma, haemangioma, fibroma, granular cell
    tumour.
  2. Inflammation/infiltration/fibrosis
    (a) Wegener’s granulomatosis—typically causes focal subglottic
    stenosis, usually with concurrent lung involvement.
    (b) Infection—e.g. previous TB (look for calcified granulomas and
    nodes), fungal infection (in immunocompromised patients)
    and rhinoscleroma (tropical granulomatous infection, typically
    involves the nasal passages, but can spread to larynx and
    trachea).
    (c) Amyloidosis—irregular focal or circumferential tracheal
    thickening ± calcification, does not spare the posterior wall.
    (d) Relapsing polychondritis—diffuse smooth tracheal thickening,
    narrowing ± calcification, spares the posterior (noncartilaginous)
    tracheal wall. Also involves cartilage of ears, nose and larynx.Chest 63
    5
    (e) Tracheobronchopathia osteochondroplastica—diffuse
    nodular tracheal thickening + coarse calcification, spares the
    posterior tracheal wall.
    (f) Sarcoidosis
    —tracheal involvement rare, usually in the
    presence of lung and nodal disease.
    (g) Inflammatory bowel disease*—can rarely cause tracheal
    inflammation and narrowing. Ulcerative colitis > Crohn’s.
  3. Bronchial atresia—most commonly in the apicoposterior segment
    of the left upper lobe. Surrounding hyperlucent lung; mucus plug
    often seen distal to the atretic bronchus.
  4. Tracheobronchomalacia—manifests as a normal/dilated trachea
    on inspiration with excessive dynamic airway collapse (EDAC) on
    expiration—AP diameter of trachea reduced by >50%. Most
    common causes are ageing, COPD and prolonged intubation;
    others include connective tissue diseases, chronic inflammation
    and Mounier-Kuhn syndrome.
  5. Tracheobronchial injury—e.g. due to prolonged intubation,
    tracheostomy, inhaled toxins, burns, radiotherapy or trauma.
    Results in a smooth stenosis.
  6. Congenital tracheal stenosis—due to complete cartilage rings (as
    opposed to normal C-shaped cartilage). Usually presents in
    childhood.
3
Q

Outside the wall

A

Lymphadenopathy—e.g. due to malignancy, sarcoidosis, TB.
2. Mediastinal masses—e.g. retrosternal goitre, primary tumours,
duplication cysts, mediastinal invasion by lung cancers. Smooth,
eccentric airway narrowing due to extrinsic compression.
Narrowing may be irregular if the airway is directly invaded by
tumour.
3. Fibrosing mediastinitis—idiopathic or resulting from
histoplasmosis, radiotherapy, autoimmune diseases, etc.
4. Enlarged left atrium or grossly enlarged pulmonary
arteries—e.g. in Eisenmenger’s syndrome or absent pulmonary
valve.
5. Aortic aneurysm—indents left side of distal trachea.
6. Left pulmonary artery sling—due to the anomalous origin of the
left pulmonary artery (LPA) from the right pulmonary artery (RPA),
compressing the right main bronchus as it passes between the
trachea and oesophagus to reach the left hilum. PA CXR shows
right-sided tracheal indentation, and the vessel is seen end-on
between the trachea and oesophagus on the lateral view. LPA sling
is often associated with complete cartilage rings, causing further
narrowing. Other vascular rings and slings (e.g. double aortic arch)
can also cause tracheal narrowing

4
Q

BRONCHIECTASIS

Causes of bronchiectasis

A
  1. Postinfective
    (a) TB*—upper lobes, look for calcified granulomas and nodes.
    (b) Mycobacterium avium complex—middle lobe and lingula,
    usually in older women (Lady Windermere syndrome).
    (c) Chronic aspiration—typically in lower lobes.
    (d) Swyer-James syndrome—secondary to childhood infection, e.g. measles, pertussis. Affected lung is hyperlucent with a paucity of vessels and may be small.
    (e) Immunodeficiency—e.g. HIV, post transplant, hypogammaglobulinaemia, severe combined immunodeficiency, common variable immunodeficiency,
    Chédiak-Higashi syndrome.
  2. Traction bronchiectasis—in areas of lung fibrosis.
  3. Cystic fibrosis*—widespread bronchiectasis.
  4. Idiopathic—no apparent cause in up to one-third of patients.
  5. Secondary to bronchial obstruction—foreign body, neoplasm, broncholithiasis or bronchial stenosis.
  6. Congenital/genetic anomalies
    (a) Primary ciliary dyskinesia—results in poor mucociliary
    clearance, recurrent infection and bronchiectasis (especially
    lower lobes). Associated chronic sinusitis, recurrent otitis media
    and fertility problems. ∼50% have situs abnormalities, hence
    the classical triad of Kartagener syndrome (bronchiectasis,
    dextrocardia, chronic sinusitis).
    (b) Mounier-Kuhn syndrome—also known as tracheobronchomegaly. Grossly dilated trachea (often >3 cm) and bronchi with diverticulosis between cartilage rings.
    (c) Williams-Campbell syndrome—bronchial cartilage deficiency.
    Similar appearance to Mounier-Kuhn except trachea and proximal bronchi are spared.
    (d) Alpha-1 antitrypsin deficiency*—basal predominant panlobular emphysema is characteristic.
  7. Immunological—ABPA (focal central bronchiectasis in an asthmatic
    patient, usually mucous-filled), obliterative bronchiolitis (look for
    mosaic attenuation due to air trapping).
  8. Collagen vascular diseases—especially rheumatoid arthritis, Sjögren’s syndrome.
  9. Gastrointestinal disorders—ulcerative colitis, coeliac disease.

Upper zone predominant
• Cystic fibrosis
• Post TB
• Sarcoidosis

Middle zone predominant
• ABPA
• Mycobacterium avium complex infection

Lower zone predominant
•	 Postinfective—staphyloccocal, whooping cough, measles, influenza, chronic aspiration, immunodeficiency
•	 Primary ciliary dyskinesia
•	 Alpha-1 antitrypsin deficiency
•	 Obliterative bronchiolitis
5
Q
UNILATERAL HYPERTRANSRADIANT 
HEMITHORAX
chest wall 3
pleura 1
lung 5
vessels 1
A

Chest wall
1. Mastectomy—absent breast ± absent pectoral muscle shadows.
2. Poliomyelitis—atrophy of pectoral muscles ± atrophic changes
in the shoulder girdle and humerus.
3. Poland syndrome—unilateral congenital absence of pectoral
muscles ± rib defects. Seen in 10% of patients with syndactyly.

Pleura
Pneumothorax—note the visceral pleural edge and absent vessels
peripherally. In supine patients look for the deep sulcus sign or
abnormally well-defined mediastinal and diaphragmatic contours.

Lung
1. Compensatory hyperexpansion—e.g. following lobectomy (look
for rib defects and sutures indicating previous surgery) or lobar
collapse.
2. Airway obstruction—air trapping on expiration results in
increased lung volume and contralateral mediastinal shift.
3. Unilateral bullae—vessels are absent rather than attenuated. May
mimic pneumothorax.
4. Swyer-James syndrome—the late sequela of bronchiolitis in
childhood (usually viral). Normal or reduced lung volume with
air trapping on expiration. Ipsilateral hilar vessels are small. CT
often shows bilateral disease with mosaic attenuation and
bronchiectasis.
5. Congenital lobar overinflation—previously known as congenital
lobar emphysema. One-third present clinically at birth, the
remainder later in life. Marked overinflation of a lobe (left upper >
right middle > right upper). The ipsilateral lobes are compressed ±
contralateral mediastinal shift.

Pulmonary vessels
Pulmonary embolus—to a main/lobar pulmonary artery. In
addition to the area of hyperlucency (Westermark sign), the
pulmonary artery is dilated proximally ± ipsilateral loss of volume.
NB: this sign is only present in 2% of PEs, and small emboli are
unlikely to result in any disparity

6
Q

BILATERAL HYPERTRANSRADIANT
HEMITHORACES
With overexpansion of the lungs

A
  1. Emphysema—± bullae; centrilobular emphysema typically in mid/
    upper zones, whereas panlobular emphysema commonly affects
    lower zones.
  2. Asthma—during an acute episode or in chronic disease with
    ‘fixed’ airflow obstruction due to airway remodelling.
  3. Acute bronchiolitis—particularly in infants. Overexpansion is due
    to small airways (bronchiolar) obstruction. May be associated with
    bronchial wall thickening on CXR. Collapse and consolidation are
    not primary features of bronchiolitis.
  4. Tracheal, laryngeal or bilateral bronchial stenoses—
7
Q

BILATERAL HYPERTRANSRADIANT
HEMITHORACES
With normal or small lungs

A
  1. Bilateral anterior pneumothoraces—seen in postoperative
    patients imaged supine, most commonly neonates/infants.
  2. Pulmonary oligaemia—due to cyanotic heart disease
8
Q

INCREASED DENSITY OF
ONE HEMITHORAX
With an undisplaced mediastinum

A
  1. Consolidation
  2. Pleural effusion—on a supine CXR, an uncomplicated effusion
    gravitates to the dependent part of the chest, producing a
    generalized increased density ± an apical ‘cap’ of fluid. Note that
    pulmonary vessels will be visible through the increased density
    (cf. consolidation). Erect or decubitus CXRs or US may confirm
    the diagnosis.
  3. Malignant pleural mesothelioma—often associated with a pleural
    effusion that obscures the tumour ± calcified pleural plaques
    (better seen on CT). Encasement of the lung limits mediastinal
    shift; the affected hemithorax may even be smaller
9
Q

INCREASED DENSITY OF
ONE HEMITHORAX
With mediastinal displacement away from the
dense hemithorax

A
  1. Large pleural effusion—NB: a large effusion with no mediastinal
    shift indicates significant lung collapse (and central obstruction) or
    relative ‘fixation’ of the mediastinum (e.g. caused by malignant
    pleural mesothelioma).
  2. Very large intrathoracic tumour—e.g. solitary fibrous tumour of
    pleura (older adults), Ewing sarcoma of chest wall (children and
    young adults). These can be large enough to fill the entire
    hemithorax.
  3. 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 (except in the early neonatal period
    when air may not yet have reached the herniated bowel)
10
Q

INCREASED DENSITY OF
ONE HEMITHORAX
With mediastinal displacement towards the
dense hemithorax 5

A
  1. Lung collapse.
  2. Post pneumonectomy—look for surgical clips and rib defects.
  3. Lymphangitis carcinomatosa—bilateral and symmetrical infiltration is most common; unilateral lymphangitis occurs more often with lung cancer. Linear and nodular opacities + septal lines ± ipsilateral hilar and mediastinal lymphadenopathy. Pleural effusions are common.
  4. Pulmonary agenesis, aplasia or hypoplasia—usually
    asymptomatic. Absent or hypoplastic pulmonary artery. Agenesis is
    the absence of lung and bronchus; aplasia is absence of lung with
    rudimentary bronchus, and hypoplasia is the presence of a
    bronchial tree with variable underdevelopment of lung volume.
  5. Malignant pleural mesothelioma
11
Q

AIR-SPACE OPACIFICATION/ CONSOLIDATION 8

A
  1. Oedema—air spaces filled with fluid.
  2. Infection—air spaces filled with pus.
  3. Diffuse pulmonary haemorrhage—e.g. Goodpasture’s syndrome,
    Wegener’s granulomatosis, idiopathic pulmonary haemosiderosis,
    microscopic polyangiitis, SLE, Behçet’s disease, contusion, bleeding
    diatheses, pulmonary infarction.
4. Malignancy—adenocarcinoma and lymphoma can both appear as 
an area (or areas) of consolidation.
  1. Sarcoidosis*—an ‘air-space’ pattern can be seen in up to 20%,
    due to filling of air spaces by macrophages and granulomatous
    infiltration.
  2. Chronic eosinophilic pneumonia—characteristically
    nonsegmental, upper zone predominant and peripheral, paralleling
    the chest wall.
  3. Organizing pneumonia—may be cryptogenic or as a response to
    another ‘insult’, e.g. infection, drug toxicity, connective tissue
    disease. Typically there are multifocal air-space opacities in the
    periphery of mid/lower zones. Occasionally unifocal. A
    characteristic perilobular distribution may be seen. Another pattern
    is the ‘reverse halo’ or atoll sign (a ring of consolidation
    surrounding a central area of GGO).
  4. Lipoid pneumonia—due to aspiration of ingested or inhaled oils.
    Consolidation tends to be basal and has an attenuation close to fat
    on CT
12
Q

NONRESOLVING OR RECURRENT

CONSOLIDATION 9

A
  1. Bronchial obstruction—e.g. caused by a tumour or foreign body.
  2. Inappropriate antimicrobial therapy—e.g. in unsuspected TB, Klebsiella or fungal infection.
  3. Malignancy—adenocarcinoma, lymphoma.
  4. Recurrent aspiration—due to a pharyngeal pouch/cleft, achalasia,
    systemic sclerosis, hiatus hernia, paralytic/neuromuscular disorders,
    chronic sinusitis or ‘H’ type tracheooesophageal fistula (in infants).
  5. Preexisting lung pathology—e.g. bronchiectasis.
  6. Impaired immunity—e.g. prolonged steroid or other
    immunosuppressive therapy, immunoglobulin deficiency, diabetes,
    cachexia, HIV.
  7. Organizing pneumonia.
  8. Sarcoidosis
  9. Vasculitis—e.g. Wegener’s, Churg-Strauss
13
Q

MIGRATORY CONSOLIDATION 5

A
  1. Organizing pneumonia—peripheral mid-lower zone distribution.
  2. Recurrent aspiration—typically in lower zones.
  3. Pulmonary eosinophilia—both simple pulmonary eosinophilia (Löffler syndrome, resolves spontaneously within 1 month) and chronic eosinophilic pneumonia (persists for several months). Peripheral upper zone distribution.
  4. Pulmonary haemorrhage/infarcts/vasculitis.
  5. Alveolar proteinosis.
14
Q

CONSOLIDATION WITH AN

ENLARGED HILUM

A

Secondary pneumonias

Primary pneumonias
1. Primary TB*—lymphadenopathy is unilateral in 80% and involves
hilar ± paratracheal nodes.
2. Viral pneumonias.
3. Mycoplasma pneumonia—lymphadenopathy is common in
children but rare in adults. May be unilateral or bilateral.
4. Primary histoplasmosis—in endemic areas. Hilar lymphadenopathy is common, particularly in children. Upon healing lymph nodes calcify and may obstruct bronchi (broncholith) causing distal infection.
5. Coccidioidomycosis—in endemic areas. The pneumonic type
consists of predominantly lower lobe consolidation frequently
associated with hilar lymphadenopathy

15
Q

PNEUMONIA INVOLVING ALL OR PART

OF ONE LOBE 5

A
  1. Streptococcal pneumonia—most common cause. Usually unilobar. Cavitation is rare; pleural effusion uncommon. Little or no collapse.
  2. Klebsiella pneumonia – often multilobar. High propensity for
    cavitation and lobar enlargement (bulging the adjacent fissure).
  3. Staphylococcal pneumonia—especially in children, 40% to 60%
    of whom develop pneumatocoeles. Parapneumonic effusion, empyema and pneumothorax are common complications. Bronchopleural fistula may develop.
  4. TB*—primary > postprimary; right lung > left lung. Associated
    collapse is common. Primary TB has a predilection for the anterior
    segment of upper lobes or medial segment of the middle lobe.
  5. Streptococcus pyogenes pneumonia—mainly affects the lower
    lobes. Often associated with pleural effusion or empyema
16
Q

CONSOLIDATION WITH BULGING

OF FISSURES 3

A
  1. Infection with abundant exudates—pneumonia caused by
    Klebsiella pneumoniae, Streptococcus pneumoniae, Mycobacterium
    tuberculosis or Yersinia pestis (plague).
  2. Abscess—when an area of consolidation breaks down. Organisms
    that commonly produce abscesses include Staphylococcus aureus,
    Klebsiella spp. and other gram-negative organisms.
  3. Lung cancer—adenocarcinoma can fill and expand a lobe
17
Q

PULMONARY OEDEMA

Noncardiogenic pulmonary oedema 12

A
  1. Fluid overload—excess IV fluids, renal failure, excess hypertonic
    fluids (e.g. contrast media).
  2. Acute respiratory distress syndrome—may be primary (e.g. caused by severe pneumonia, aspiration) or secondary (e.g. following nonthoracic sepsis or trauma); CXR may be normal in the first 24 hours but shows progressive widespread opacification due to interstitial and then alveolar oedema and haemorrhagic fluid.
  3. Cerebral disease—stroke, head injury, raised intracranial pressure
    or large shunt (e.g. vein of Galen malformation).
  4. Near drowning—no significant radiological difference between
    freshwater and seawater drowning.
  5. Aspiration—of acidic gastric contents causing a chemical
    pneumonitis (Mendelson’s syndrome).
  6. Liver disease—and other causes of hypoproteinaemia.
  7. Transfusion-related acute lung injury (TRALI)—most common
    cause of transfusion-related mortality in the UK. Onset of oedema
    is either during transfusion or within 1–2 hours.
  8. Drug-induced—includes those which induce cardiac arrhythmias
    or depress myocardial contractility, and those which alter
    pulmonary capillary wall permeability, e.g. overdoses of heroine,
    morphine, methadone, cocaine, dextropropoxyphene and
    aspirin. Hydrochlorothiazide, phenylbutazone, aspirin and
    nitrofurantoin can cause oedema as an idiosyncratic response;
    interleukin-2 and tumour necrosis factor may cause increased
    permeability by an unknown process. Contrast media can induce
    arrhythmias, alter capillary wall permeability and produce a
    hyperosmolar load.
  9. Poisons
    (a) Inhaled—e.g. nitrogen dioxide (NO2), sulphur dioxide (SO2),
    carbon monoxide (CO), phosgene, hydrocarbons and smoke.
    (b) Circulating—paraquat and snake venom.
  10. Mediastinal tumours—producing pulmonary venous or
    lymphatic obstruction.
  11. Radiotherapy—several weeks following treatment. Ultimately it
    has a characteristic straight edge as fibrosis ensues.
  12. Altitude sickness—following rapid ascent to >3000 metres
18
Q

UNILATERAL PULMONARY OEDEMA
Pulmonary oedema ipsilateral to the
underlying abnormality

A
  1. Prolonged lateral decubitus position.
  2. Rapid lung reexpansion post thoracocentesis.
  3. Unilateral aspiration.
  4. Pulmonary contusion.
  5. Mitral regurgitation—rarely, the regurgitant jet flows into the
    right upper pulmonary vein, causing isolated right upper lobe oedema.
  6. Bronchial obstruction.
  7. Reperfusion injury postpulmonary vascular surgery or stenting.
  8. Large systemic artery to pulmonary artery shunts—e.g.
    Waterston (ascending aorta to RPA), Blalock–Taussig (right or
    left subclavian artery to RPA or LPA) and Pott (descending aorta
    to LPA)
19
Q

Pulmonary oedema contralateral to the underlying

abnormality (typically a perfusion defect).

A
  1. Congenital absence or hypoplasia of a pulmonary artery.
  2. Swyer-James syndrome.
  3. Thromboembolism.
  4. Unilateral emphysema.
  5. Lobectomy.
  6. Pleural disease
20
Q

SEPTAL (KERLEY B) LINES

Pulmonary venous hypertension/engorgement

A
  1. Left ventricular failure.
  2. Mitral stenosis.
  3. Pulmonary venoocclusive disease—smooth septal thickening,
    centrilobular ground-glass nodularity and signs of pulmonary
    arterial hypertension, but with a normal left heart.
  4. Pulmonary vein stenosis—e.g. post left atrial ablation (for
    atrial fibrillation), or associated with sarcoidosis or malignancy
21
Q

Lymphatic/interstitial infiltration of lungs 14

A
  1. Lymphangitis carcinomatosa/lymphomatosa—most often
    caused by lymphatic infiltration in patients with cancer of the
    lung, breast, stomach, pancreas, Kaposi sarcoma or lymphoma.
    Septal lines may be bilateral or unilateral (most other causes
    tend to be bilateral). Nodular interlobular septal thickening
    is the characteristic finding on CT. Leukaemia can also infiltrate
    interlobular septa, usually causing smooth thickening.
  2. Interstitial lung diseases—e.g. NSIP, LIP, UIP. Other features are
    also present.
  3. Sarcoidosis*—nodular septal thickening may be seen.
  4. Pneumoconioses—widespread nodularity may involve
    interlobular septa.
  5. Acute eosinophilic pneumonia—similar to pulmonary oedema
    on imaging.
  6. Alveolar proteinosis—smooth thickening of interlobular and
    intralobular septa in geographic areas of GGO (‘crazy-paving’
    pattern). Infiltration of air spaces and interstitium by surfactant
    proteins due to impaired alveolar macrophage function.
  7. Erdheim-Chester disease*—infiltration of pulmonary interstitium
    by histiocytes of non-Langerhans type. On CXR, reticulonodular
    infiltrate is seen in mid/upper zones. On CT, smooth interlobular
    septal thickening is characteristic, associated with GGO,
    centrilobular nodules and often chylous pleural effusions ±
    thickening.
  8. Idiopathic bronchiectasis—thickened interlobular septa are a
    feature in around one-third of patients.
  9. Recurrent diffuse pulmonary haemorrhage (haemosiderosis)—
    smooth septal thickening may be seen on CT.
  10. Diffuse pulmonary lymphangiomatosis—proliferation of
    lymphatic channels in pleura, interlobular septa and
    peribronchovascular connective tissue.
  11. Congenital lymphangiectasia—abnormal dilatation of lymphatic
    channels without an increase in their number (cf.
    lymphangiomatosis). May be associated with extrathoracic
    congenital anomalies (e.g. renal, cardiac); commonly seen in
    Noonan and Turner syndromes.
  12. Lysosomal storage diseases—Niemann-Pick, Gaucher disease.
    Smooth or nodular.
  13. Amyloidosis*—rare manifestation; usually nodular.
  14. Alveolar microlithiasis—calcified interlobular septal thickening
22
Q

Smooth interlobular septal

thickening 6

A
Any cause of interstitial oedema
Acute eosinophilic pneumonia
Alveolar proteinosis
Erdheim-Chester disease
Recurrent pulmonary haemorrhage
Lymphangiomatosis/lymphangiectasia
23
Q

Nodular interlobular septal

thickening 5

A
Lymphangitis carcinomatosa
Sarcoidosis
Pneumoconioses
Amyloidosis
Alveolar microlithiasis (calcified
24
Q

Multiple micronodules less than 2 mm

A

Soft-tissue or ground-glass attenuation
1. Miliary TB—widespread, secondary to haematogenous dissemination. Uniform size, random distribution. Indistinct margins, but discrete. No septal lines. Normal hila unless superimposed on primary TB.
2. Fungal infection—histoplasmosis, coccidioidomycosis, blastomycosis and cryptococcosis. Similar appearance to miliary TB.
3. Coal worker’s pneumoconiosis—predominantly midzones, sparing
the extreme bases and apices. Ill-defined, may be arranged in a circle or rosette. Septal lines.
4. Sarcoidosis
—predominantly upper/midzones and strikingly bronchocentric, causing ‘bronchovascular beading’ ± hilar lymphadenopathy.
5. Berylliosis—indistinguishable from sarcoidosis.

Greater than soft-tissue density
1. Post varicella infection—multiple tiny calcific nodules throughout
both lungs.
2. Haemosiderosis—secondary to chronic raised venous pressure
(seen in 10%–15% of patients with mitral stenosis), repeated pulmonary haemorrhage (e.g. Goodpasture’s syndrome) or idiopathic. Septal lines. Smaller than miliary TB.
3. Silicosis—relative sparing of bases and apices. Very well-defined
and dense when caused by inhalation of pure silica; ill-defined
and of lower density when due to mixed dusts. Septal lines.
4. Post lymphangiography—ethiodized oil (lipiodol) emboli.
Contrast medium may be visible in the terminal thoracic duct.
5. Siderosis—due to inhalation of iron particles. Lower density than
silica. Widely disseminated. Asymptomatic.
6. Stannosis—inhalation of tin oxide. Even distribution throughout
the lungs + septal lines.
7. Barytosis—inhalation of barium dust. Very dense, discrete
opacities. Generalized distribution but bases and apices usually spared.
8. Limestone and marble workers—inhalation of calcium.
9. Alveolar microlithiasis—rare familial disorder. Lung detail
obscured by widespread miliary calcifications. Few symptoms but
may progress to cor pulmonale. Pleura, heart and diaphragm may
be seen as ‘negative’ shadows on CXR

25
Q

Multiple nodules 2–5 mm
discrete 5
confluent 3

A

Soft-tissue or ground-glass attenuation and remaining discrete
1. Disseminated cancer—breast, thyroid, sarcoma, melanoma,
prostate, pancreas or lung (eroding a pulmonary artery). Variable
sizes, progressive increase in size, ± lymphatic obstruction.
2. Subacute hypersensitivity pneumonitis—centrilobular nodules,
GGO, lobular air trapping (on expiratory CT), ± scattered
thin-walled cysts. Smoking has a ‘protective’ effect (cf. respiratory
bronchiolitis).
3. Respiratory bronchiolitis—similar CT appearances to
hypersensitivity pneumonitis, but invariably linked to smoking.
May also see thickened interlobular septa and limited
emphysema.
4. Sarcoidosis.
5. Lymphoma
—usually with hilar or mediastinal lymphadenopathy.

Tending to confluence and/or varying in appearance over
hours to days
1. Multifocal pneumonia—including aspiration pneumonia and TB.
2. Pulmonary oedema—rapid fluid shifts can occur over a few hours,
in contrast to many other air-space diseases.
3. Diffuse pulmonary haemorrhage.

26
Q

Multiple nodules greater than 5 mm
Neoplastic 4
Infection 4

A
  1. Metastases—most commonly from breast, thyroid, kidney, GI
    tract and testes. In children: Wilms tumour, Ewing sarcoma, neuroblastoma and osteosarcoma. Predilection for lower lobes, more common peripherally. Range of sizes. Well-defined. Ill definition suggests prostate, breast or gastric metastases. Hilar lymphadenopathy and effusions are uncommon.
  2. Multiple synchronous lung cancers.
  3. Kaposi sarcoma—multiple bilateral perihilar and peribronchovascular ill-defined nodules (‘flame-shaped’) with thoracic lymphadenopathy, interlobular septal thickening ± pleural effusions.
  4. Benign metastasizing tumours—most commonly seen with
    uterine leiomyomas, but also reported with meningiomas,
    pleomorphic adenomas of the salivary glands, chondroblastomas
    and giant cell tumours of bone.

Infections
1. Abscesses—widespread distribution but asymmetrical. Commonly
Staphylococcus aureus. Cavitation common. No calcification.
2. Coccidioidomycosis—in endemic areas. Well-defined; predilection
for the upper lobes. Calcification and cavitation may be present.
3. Histoplasmosis—in endemic areas. Round, well-defined, few in
number. Sometimes calcify. Usually unchanged for many years.
4. Hydatid—more common on the right side and in the lower zones.
Well-defined unless there is surrounding pneumonia. Often ≥10 cm. May rupture and show the ‘water lily’ sign on CT.

27
Q

Multiple nodules greater than 5 mm

Infections 4

A
  1. Abscesses—widespread distribution but asymmetrical. Commonly
    Staphylococcus aureus. Cavitation common. No calcification.
  2. Coccidioidomycosis—in endemic areas. Well-defined; predilection
    for the upper lobes. Calcification and cavitation may be present.
  3. Histoplasmosis—in endemic areas. Round, well-defined, few in
    number. Sometimes calcify. Usually unchanged for many years.
  4. Hydatid—more common on the right side and in the lower zones.
    Well-defined unless there is surrounding pneumonia. Often
    ≥10 cm. May rupture and show the ‘water lily’ sign on CT
28
Q

Multiple nodules greater than 5 mm

Immunological

A
  1. Wegener’s granulomatosis*—bilateral nodules or masses ±
    cavitation, or uni/multifocal consolidation. Widespread distribution.
    Round, well-defined. No calcification.
  2. Rheumatoid nodules—peripheral, more common in the lower
    zones. Round, well-defined. No calcification. Cavitation common.
    May be associated with pneumoconiosis (Caplan syndrome).
  3. Progressive massive fibrosis—large conglomerate masses,
    typically in both mid-upper zones, usually symmetrical; starts
    peripherally and migrates centrally over years. Caused by chronic
    silicosis, coal worker’s pneumoconiosis, talcosis or sarcoidosis.
    Associated traction bronchiectasis and background widespread
    nodularity are also present.
  4. Organizing pneumonia.
  5. Amyloidosis*—multiple nodules of varying size, calcified in up
    to 50%.
  6. Hyalinizing granulomas—rare, unknown aetiology but can be
    associated with fibrosing mediastinitis, IgG4-related disease and
    other autoimmune disorders. Multiple (or occasionally solitary)
    lung nodules mimicking metastatic disease
29
Q

Multiple nodules greater than 5 mm

Vascular

A

Arteriovenous malformations—33% are multiple, especially in
hereditary haemorrhagic telangiectasia. Well-defined and lobulated;
may see feeding and draining vessels on CXR (best seen on CT).
Calcification is rare

30
Q
SOLITARY PULMONARY NODULE OR 
MASSLIKE LESION
granulomatous 3
Malignant 3
Benign 2
Infectious/inflammatory 6
Congenital 3
Vascular 2
A

Granulomatous
1. Tuberculoma—more common in upper lobes, R>L. Well-defined;
0.5–4 cm. Calcification frequent. 80% have satellite lesions.
Cavitation is uncommon, and if present, is small and eccentric.
Usually persists unchanged for years.
2. Histoplasmoma—in endemic areas (Mississippi and Atlantic coast
of USA). More frequent in lower lobes. Well-defined; seldom
>3 cm. Calcification is common and may be central (‘target’
appearance). Cavitation is rare. Satellite lesions are common.
3. Others—e.g. coccidioidomycosis, cryptococcosis.

Malignant tumours
1. Lung cancer—features suggesting malignancy include: recent
appearance or rapid growth (review previous imaging); size >4 cm;
lesion crossing a fissure (also seen in some fungal infections);
ill-defined, notched or spiculated margins; peripheral line shadows.
Calcification is rare. Most appear ‘solid’ on CT ± foci of fluid
attenuation (necrosis). Pure ground-glass/part-solid ground-glass
nodules >5 mm may represent premalignant lesions (atypical
adenomatous hyperplasia), adenocarcinoma in situ or invasive
adenocarcinoma.
2. Solitary metastasis—accounts for 3%–5% of asymptomatic
nodules. 25% of lung metastases may be solitary. Most likely
primary tumours are breast, sarcoma, seminoma and RCC.
Predilection for the lung periphery. Calcification is rare, but if
present suggests metastatic osteosarcoma or chondrosarcoma.
3. Rare malignant lung tumours—pleuropulmonary blastoma,
pleural and pulmonary sarcomas, plasmacytoma, atypical carcinoid

Benign tumours
1. Carcinoid tumour—‘typical’ carcinoids (90% of cases) are
generally central and tend to be more benign than atypical
tumours (10%), which tend to be peripheral. However, malignant
potential varies from benign to frank small cell carcinoma. May
calcify (often peripheral) and may be associated with ectopic ACTH
production (Cushing’s syndrome).
2. Hamartoma—96% occur >40 years of age. 90% are
intrapulmonary and usually <2 cm from the pleura. 10% cause
bronchial stenosis. Usually <4 cm. Well-defined, lobulated.
60% contain fat visible on CT. May calcify, especially if large.
Calcification may have a ‘popcorn’, craggy or punctate configuration.

Infectious/inflammatory
1. Pneumonia—especially pneumococcal.
2. Rounded atelectasis—typically the sequela of an exudative pleural
effusion. Peripheral mass + adjacent smooth pleural thickening and
parenchymal bands giving a ‘comet tail’ appearance.
3. Hydatid—in endemic areas. Most common in lower lobes, R>L.
Well-defined; 1–10 cm. Solitary in 70%. May have a bizarre shape.
Rupture results in the ‘water lily’ sign.
4. Wegener’s granulomatosis—solitary nodules in up to one-third
of patients, but more commonly multiple. May cavitate.
5. Sarcoidosis
—a solitary lung nodule is rare, but reported.
6. Organizing pneumonia—can mimic a (malignant) solitary
pulmonary nodule.

Congenital
1. Intrapulmonary lymph node—usually solitary, small (<2 cm),
peripheral (<2 cm from pleura) and well-defined. Common
incidental finding on CT in mid/lower zones. Typically triangular
in shape with a thin tether to the pleural surface. Usually benign,
even when detected in the context of a known malignancy.
2. Sequestration—intralobar (more common; no separate pleural
covering; venous drainage into pulmonary veins) or extralobar
(rare; separate pleural covering; venous drainage into systemic
veins). Nearly always in a lower lobe (L>R), contiguous with the
diaphragm. Well-defined, round or oval. Diagnosis confirmed by
identifying its systemic arterial supply on CT/MRI.
3. Bronchogenic cyst—usually mediastinal or hilar, but occasionally
intrapulmonary. Round or oval; smooth thin nonenhancing wall
(enhancement implies infection or alternative diagnosis).

Vascular
1. Haematoma—peripheral, smooth and well-defined. Slow
resolution over several weeks.
2. Arteriovenous malformation—66% are single. Well-defined,
lobulated. Feeding and draining vessels may be seen on CXR,
confirmed on CT. Calcification rare.

31
Q

APICAL MASS 8

A
  1. Pancoast tumour—look for adjacent rib destruction.
  2. Tortuous/aneurysmal subclavian artery—R>L, usually in older
    patients. Well-defined inferolateral margin, merges with
    mediastinum medially. Can be hard to differentiate from tumour
    on CXR—compare with previous imaging.
  3. Apical scarring/fibrosis—usually in older patients (bilateral) or
    post infection (e.g. TB) or radiotherapy (uni- or bilateral).
  4. Mycetoma in a preexisting apical cavity—look for air crescent
    sign.
  5. Metastasis—more common in lower zones.
  6. Pleural/chest wall tumours—mesothelioma, chondrosarcoma,
    Ewing sarcoma, metastasis, myeloma, lymphoma, neurogenic
    tumour.
  7. Plombage—historical treatment for cavitating TB. Apical density +
    multiple rounded lucencies.
  8. Meningocoele
32
Q
PULMONARY CAVITIES
Infective 7
Neoplastic 4
Vascular
Inflammatory 4
Traumatic 2
A

Infective
1. Staphylococcus aureus—thick-walled with a ragged inner lining.
Usually multiple; no lobar predilection. Associated with effusion or
empyema ± pneumothorax, especially in children.
2. Klebsiella pneumoniae—thick-walled with a ragged inner lining.
More common in the upper lobes. Usually single but may be
multilocular ± effusion.
3. TB*—thick-walled and smooth. Upper lobes and apical segment of
lower lobes mainly. Usually surrounded by consolidation ± fibrosis.
4. Septic emboli—e.g. in IV drug users, tricuspid/pulmonary valve
infective endocarditis, infected IV catheters/wires, septic
thrombophlebitis or following oropharyngeal infection (Lemierre
syndrome).
5. Aspiration—look for a foreign body, e.g. tooth.
6. Infection of a preexisting lung abnormality—e.g.
emphysematous bulla, sequestration, bronchogenic cyst. Internal
air–fluid level and surrounding consolidation may be present.
7. Others—gram-negative organisms, actinomycosis, nocardiosis,
histoplasmosis, coccidioidomycosis, aspergillosis, hydatid,
amoebiasis.

Neoplastic
1. Lung cancer—thick-walled with an eccentric cavity. Predilection
for upper lobes. Found in 2%–10% of carcinomas, especially if
peripheral. More common in SCC (may be thin-walled).
2. Metastases—especially in squamous cell, colonic and sarcoma
metastases. Thin- or thick-walled. May involve only a few of the
nodules.
3. Tracheobronchial papillomatosis—see Section 5.1. Parenchymal
involvement gives rise to multiple nodules that can cavitate.
Typically in children or young adults.
4. Lymphoma*—including lymphomatoid granulomatosis. Cavitation
is uncommon, may be thin- or thick-walled, typically in an area of
infiltration + hilar/mediastinal lymphadenopathy.

Vascular
Infarction—secondary infection of an initially sterile infarct can
occur. An aseptic cavitating infarct may also become infected.
Aseptic cavitation is usually solitary and arises in a large area of
consolidation after ~2 weeks; most common sites are apical or
posterior segments of an upper lobe or apical segment of a lower
lobe (cf. lower lobe predominance of noncavitating infarction).
Majority have scalloped inner margins and crosscavity band
shadows ± effusion.

Inflammatory
1. Wegener’s granulomatosis—cavitation in some of the nodules.
Thick-walled, becoming thinner with time. Can be transient.
2. Rheumatoid nodules—especially in lower lobes and peripherally.
Well-defined, thick-walled with a smooth inner lining; become
thin-walled with time.
3. Progressive massive fibrosis—mid and upper zones. Thick-walled
and irregular. Background nodularity.
4. Sarcoidosis
—thin-walled, usually in early disease. May later
develop mycetoma within cavity resulting in wall thickening.

Traumatic
1. Haematoma—peripheral. Air–fluid level if it communicates with a
bronchus.
2. Traumatic lung cyst—thin-walled and peripheral. Single or
multiple, unilocular or multilocular. Distinguished from cavitating
haematomas that present early, within hours of the injury

33
Q
CYSTIC LUNG DISEASE
post infect 3
post traumatic 1
congenital 2
neoplastic 2
diffuse lung diseases 9
A

Postinfective
1. Bacterial pneumonia—e.g. Staphylococcus aureus (a characteristic
feature in children, seen in 40%–60% of cases), Streptococcus
pneumoniae, Escherichia coli, Klebsiella pneumoniae, Haemophilus
influenzae, Legionella pneumophila. Cysts can appear during the
first 2 weeks of infection and may resolve over several months.
2. Pneumocystis jirovecii—usually multiple and in the upper zones;
cysts increase the risk of pneumothorax.
3. Hydatid cyst—initially fluid-filled, can contain air if they
communicate with the bronchial tree.

Posttraumatic
Lung laceration—cyst within an area of contusion; resolves over
time.

Congenital
1. Congenital pulmonary airway malformation (CPAM)—single
multiloculated cyst.
2. Bronchogenic cyst—if communicating with the bronchial tree
(generally following secondary infection).

Neoplastic
1. Following treatment of lung metastases—e.g. bladder cancer
and germ cell tumours. May only be visible on CT.
2. Cystic lung metastases—rare. Can occur with colonic
adenocarcinoma, epithelioid sarcoma and endometrial stromal
sarcoma.

Diffuse lung diseases
1. Langerhans cell histiocytosis (LCH)—cysts, sometimes bizarre
(noncircular) in shape, mid/upper zone predominance. In ‘early’
disease there are multiple nodules, which later cavitate. Relative
sparing of lower zones and medial tips of the middle lobe and
lingula. Usually presents in young adults, strongly linked to
cigarette smoking.
2. Lymphangioleiomyomatosis (LAM)
—exclusively in women of
childbearing age. Smooth muscle proliferation around vessels,
lymphatics and airways. Multiple cysts, relatively uniform in size
with no zonal predilection (cf. LCH).
3. Tuberous sclerosis—lung disease almost identical to LAM.
4. Lymphocytic interstitial pneumonia—usually occurs in the
context of dysproteinaemias, connective tissue disorders (especially
Sjögren’s syndrome and rheumatoid arthritis) or HIV infection.
Basal-predominant ill-defined centrilobular nodules, GGO and
lung cysts are characteristic ± septal thickening. May have
associated calcified nodules in the cyst walls due to amyloid
deposition.
5. Neurofibromatosis
—cystic lung disease and interstitial fibrosis are
reported.
6. Birt-Hogg-Dubé syndrome*—autosomal dominant multisystem
disorder characterized by lower zone predominant lung cysts
(typically ‘cigar-shaped’ ± recurrent pneumothoraces), cutaneous
fibrofolliculomas and increased risk of renal tumours.
7. Hypersensitivity pneumonitis—a few cysts may be seen in
the subacute or chronic fibrotic phase, but not a dominant
feature.
8. End-stage fibrotic diffuse interstitial lung diseases—e.g.
idiopathic pulmonary fibrosis, sarcoidosis. Peripheral
honeycombing.
9. Desquamative interstitial pneumonia—typically in heavy
smokers, at the severe end of the smoking related interstitial lung
disease spectrum. Also seen in connective tissue disease and
genetic disorders of surfactant protein dysfunction. Small cysts may
be seen but basal predominant GGO ± reticulation are the major
features

34
Q

PULMONARY CALCIFICATION
OR OSSIFICATION
Localized

A
  1. TB*—small nidus of calcification. Calcification ≠ healed.
  2. Histoplasmosis—in endemic areas. Calcification may be laminated,
    producing a target lesion ± multiple punctate splenic calcifications.
  3. Coccidioidomycosis.
  4. Blastomycosis—rare
35
Q

PULMONARY CALCIFICATION
OR OSSIFICATION
Calcification in a solitary nodule

A

(a) Lung cancer ‘engulfing’ a preexisting calcified granuloma
(eccentric calcification).
(b) Solitary calcifying/ossifying metastasis—osteosarcoma,
chondrosarcoma, mucinous adenocarcinoma of the colon or
breast, papillary carcinoma of the thyroid, cystadenocarcinoma of
the ovary, carcinoid.
(c) Primary peripheral squamous cell or papillary adenocarcinoma

36
Q

PULMONARY CALCIFICATION OR OSSIFICATION
Diffuse or multiple calcifications
6

A
  1. Infections—healed miliary TB, histoplasmosis or varicella (chicken
    pox) pneumonia. The latter results in numerous 1–3mm calcifications.
  2. Chronic pulmonary venous hypertension—especially mitral
    stenosis. Up to 8 mm in size ± ossification; most prominent in mid
    and lower zones.
  3. Silicosis—in up to 20% of those showing nodular opacities.
  4. Metastases.
  5. Alveolar microlithiasis—often familial. Myriad minute calcifications
    in alveoli that obscure all lung detail. Due to the increased lung
    density, the heart, pleura and diaphragm may be seen as negative
    shadows on plain film.
  6. Metastatic due to hypercalcaemia—chronic renal failure,
    secondary hyperparathyroidism and multiple myeloma.
    Predominantly in upper zones
37
Q

PULMONARY CALCIFICATION
OR OSSIFICATION
Interstitial ossification 2

A
  1. Dendriform/disseminated pulmonary ossification—branching or
    nodular calcific densities extending along the bronchovascular
    distribution of the interstitial space. Seen in long-term busulphan
    therapy, chronic pulmonary venous hypertension (e.g. due to
    mitral stenosis), idiopathic pulmonary fibrosis, asbestosis, following
    ARDS, chronic bronchitis and chronic aspiration.
  2. Idiopathic.
38
Q

NONTHROMBOTIC PULMONARY EMBOLI

A
  1. Septic embolism—associated with indwelling venous catheters,
    pacemaker leads, tricuspid or pulmonary valve endocarditis and
    peripheral septic thrombophlebitis. Ill-defined nodules of varying
    sizes, predominantly in lower lobes ± cavitation.
  2. Iatrogenic embolism—common examples include cement post
    vertebroplasty and catheter tips or guidewires. Rarer causes include
    iodinated oil embolism post lymphangiography, cotton adherent
    to intravascular lines and air from pump injectors.
  3. Phlebolith embolism—most commonly from a pelvic vein ±
    additional thrombotic emboli.
  4. Fat embolism—1–2 days post trauma. Predominantly peripheral,
    associated with geographic areas of GGO ± septal thickening ±
    small nodules. Resolves in 1–4 weeks. Normal heart size. Pleural
    effusions uncommon.
  5. Amniotic fluid embolism—rare. The majority suffer
    cardiopulmonary arrest and the CXR shows pulmonary oedema.
  6. Tumour embolism—common sources are liver, breast, stomach,
    kidney, prostate and choriocarcinoma. CXR is usually normal.
  7. Talc embolism—in IV drug abusers. May result in pulmonary
    hypertension.
  8. Hydatid embolism
39
Q

FIBROSING LUNG DISEASES ON HRCT

A
  1. Usual interstitial pneumonia (UIP)—may be primary (idiopathic
    pulmonary fibrosis [IPF]) or secondary to connective tissue disease,
    asbestos exposure, medications. Typically affects men >50 years.
    Predominantly has a basal and subpleural reticular pattern +
    honeycombing. Often follows a ‘propeller blade’ distribution with
    disease more anterior toward the apices and more posterior at the
    bases. Atypical findings can occur, e.g. GGO (suggests an acute
    exacerbation). Increased risk of lung cancer.
  2. Nonspecific interstitial pneumonia (NSIP)—may be idiopathic,
    but more commonly is associated with other conditions, especially
    collagen vascular disease, drugs and immunological conditions.
    Typically affects middle-aged women. Predominantly basal, diffuse
    GGO ± evidence of fibrosis (fibrotic versus cellular NSIP).
  3. Fibrotic organizing pneumonia—many causes and associations,
    mirroring NSIP. Typical features include perilobular opacities,
    peripheral consolidation ± air bronchograms, and, in contrast to
    NSIP, more focal peribronchovascular GGO. Rarely the ‘reverse
    halo’ sign.
  4. Chronic (fibrotic) hypersensitivity pneumonitis—due to
    repeated or prolonged exposure to a wide variety of antigens
    originating from animals, plants, drugs, bacteria or fungi. Typical
    features include a reticular pattern ± honeycombing, GGO ±
    traction bronchiectasis, with lobular areas of ‘spared’ lung and air
    trapping. Upper/mid zone predominance (cf. UIP/NSIP).
  5. Sarcoidosis*—typically causes a symmetrical, bronchocentric
    reticular pattern in upper zones, seemingly ‘streaming’ from the
    hila. Calcified mediastinal and hilar nodes.
40
Q

Upper zone predominant fibrosis

A
Sarcoidosis
Old TB (usually unilateral)
Silicosis/pneumoconiosis/PMF
Chronic hypersensitivity pneumonitis
Radiation fibrosis
Ankylosing spondylitis
Pleuroparenchymal fibroelastosis
41
Q

Lower zone predominant

fibrosis

A
UIP
NSIP
DIP
Fibrotic organizing pneumonia
Asbestosis
Chronic aspiration pneumonitis
42
Q

NODULAR PATTERNS ON HRCT

Centrilobular

A
  1. Infective bronchiolitis
    (a) TB*—look for calcified granulomas and nodes, lung cavities
    (spillage of cavity contents into bronchial tree results in distant
    tree-in-bud). Nontuberculous mycobacterial (NTM) infection
    can look similar.
    (b) Aspiration—basal predominance.
    (c) Other infections—bacterial (e.g. mycoplasma), viral (e.g.
    influenza), fungal (e.g. invasive aspergillosis).
  2. Hypersensitivity pneumonitis—due to an allergic reaction to a
    variety of inhaled particles. Causes centrilobular nodularity in the
    subacute phase, typically without tree-in-bud. Lobular air trapping
    and GGO can also be seen.88 Aids to Radiological Differential Diagnosis
  3. Other causes of bronchiolitis
    (a) Respiratory bronchiolitis—almost exclusively in smokers.
    Upper zone predominance.
    (b) Follicular bronchiolitis—associated with autoimmune
    disorders, e.g. rheumatoid arthritis, Sjögren’s syndrome. Basal
    predominance.
    (c) Diffuse panbronchiolitis—typically seen in East Asia. Basal
    predominance.
  4. Diseases associated with bronchiectasis—e.g. cystic fibrosis,
    primary ciliary dyskinesia, NTM infection (Lady Windermere
    syndrome).
  5. Endobronchial spread of tumour—e.g. adenocarcinoma.
  6. Metastatic pulmonary calcification—fluffy ‘cotton-ball’
    centrilobular nodules, often dense/calcified, with an upper zone
    predominance. Most commonly due to chronic renal failure
43
Q

NODULAR PATTERNS ON HRCT

Perilymphatic

A
  1. Sarcoidosis*—characteristic feature.
  2. Lymphangitis carcinomatosa—nodular thickening of interlobular
    septa.
  3. Silicosis and coal worker’s pneumoconiosis.
  4. Lymphoma*.
  5. Amyloidosis
44
Q

NODULAR PATTERNS ON HRCT

Random

A
  1. Miliary TB*.
  2. Miliary metastases.
  3. Silicosis and coal worker’s pneumoconiosis.
  4. Other miliary infections—e.g. histoplasmosis, blastomycosis.
  5. Langerhans cell histiocytosis*—nodules often cavitate, forming
    irregular cysts. Upper zone predominance.
  6. Lymphocytic interstitial pneumonia—nodules may be
    centrilobular or subpleural. Lower zone predominance.
  7. Fungal infection—e.g. candidiasis, blastomycosis.
45
Q

GROUND-GLASS OPACIFICATION
ON HRCT
Acute illnesses

A
  1. Pulmonary oedema—with smooth septal thickening and
    effusions.
  2. Infection—e.g. PCP, CMV. Both occur in immunocompromised
    patients. Cysts ± pneumothoraces may also be seen in PCP.
  3. Pulmonary haemorrhage—e.g. due to vasculitis (Wegener’s
    granulomatosis, Goodpasture’s syndrome), SLE, coagulopathy.
  4. ARDS and acute interstitial pneumonia (AIP)—both are
    characterized by widespread consolidation and GGO that may
    increase in density towards dependent areas, representing diffuse
    alveolar damage (DAD). ARDS has many causes (e.g. sepsis and
    other causes of systemic inflammatory response syndrome [SIRS]),
    AIP is idiopathic.
  5. Acute hypersensitivity pneumonitis—centrilobular ground-glass
    nodules, upper zone predominance. Many allergic triggers.
  6. Acute eosinophilic pneumonia—mimics pulmonary oedema on
    imaging. Usually in young adults.
46
Q

GROUND-GLASS OPACIFICATION
ON HRCT
Subacute/chronic illnesses
7

A
  1. Diffuse interstitial lung diseases
    (a) Nonspecific interstitial pneumonia—with reticulation and traction bronchiectasis. Basal predominance.
    (b) Organizing pneumonia—consolidation and GGO, occasionally with a ‘reverse halo’ morphology.
    (c) Respiratory bronchiolitis-interstitial lung disease (RB-ILD)—
    centrilobular ground-glass nodules and GGO, upper zone
    predominance. Almost exclusively in smokers (cf. hypersensitivity pneumonitis where smoking is protective).
    (d) Desquamative interstitial pneumonia—bilateral GGO ±reticulation ± cysts, lower zone predominance. Almost exclusively in smokers (more advanced stage of RB-ILD).
    (e) Lymphocytic interstitial pneumonia—with ill-defined nodules
    and lung cysts.
  2. Chronic hypersensitivity pneumonitis—bilateral GGO with an upper zone predominance + lobular ‘sparing’ due to air trapping +areas of fibrosis.
  3. Chronic eosinophilic pneumonia—peripheral migratory consolidation ± GGO.
  4. Drug-induced—amiodarone causes peripheral GGO and consolidation that is often hyperdense (due to iodine content); the liver ± myocardium may also be hyperdense, suggesting the diagnosis. Other causes of GGO include methotrexate, nitrofurantoin and chemotherapy agents.
  5. ‘Alveolar’ sarcoidosis*—uncommon form of the disease. Multifocal areas of GGO, mid/upper zone distribution. Small nodules may coexist, creating the ‘sarcoid galaxy’ sign.
  6. Alveolar proteinosis—with interlobular septal thickening, resulting
    in ‘crazy-paving’.
  7. Adenocarcinoma—can present as a solid/ground-glass nodule or
    a larger area of GGO/consolidation. Can be multifocal and
    bilateral
47
Q

MOSAIC ATTENUATION PATTERN
ON HRCT
Small airways diseases (obliterative bronchiolitis)
8

A
  1. Postinfective—i.e. Swyer-James syndrome.
  2. Posttransplantation—heart ± lung, bone marrow. Termed
    bronchiolitis obliterans syndrome (BOS) in chronic lung allograft
    dysfunction.
  3. Connective tissue diseases—especially rheumatoid arthritis,
    Sjögren’s syndrome.
  4. Drugs—penicillamine, Sauropus androgynus (Katuk leaves).
  5. Toxic fume inhalation.
  6. Diffuse idiopathic pulmonary neuroendocrine hyperplasia
    (DIPNECH)—mosaic attenuation + small well-defined lung nodules
    (representing neuroendocrine tumourlets).
  7. Bronchiectasis.
  8. Sarcoidosis*
48
Q

MOSAIC ATTENUATION PATTERN
ON HRCT
Pulmonary vascular diseases
he ‘black’ lung is abnormal, with smaller or fewer vessels
compared to the ‘grey’ areas, but without air trapping

A
  1. Chronic thromboembolic disease—usually with other features,
    e.g. laminar thrombus, webs, stenoses, pulmonary hypertension.
    NOT a feature of acute PE.
  2. Pulmonary arterial hypertension.
  3. Pulmonary artery tumours—e.g. sarcoma.
49
Q

MOSAIC ATTENUATION PATTERN
ON HRCT
Infiltrative lung diseases

A

The ‘grey’ lung is abnormal, with no disparity in vessel size
between ‘grey’ and ‘black’ areas. See Section 5.24, especially
chronic hypersensitivity pneumonitis (although note that this
does cause air trapping and can mimic small airways disease)

50
Q

UNILATERAL HILAR ENLARGEMENT

A

Lymph nodes
1. Lung cancer—hilar enlargement may be the tumour itself or
malignant lymph nodes.
2. Infection—e.g. primary TB, histoplasmosis, coccidioidomycosis,
Mycoplasma, pertussis.
3. Unicentric Castleman disease—benign lymph node hyperplasia,
presents as localized mediastinal or hilar lymphadenopathy that
classically enhances avidly on CT.
4. Lymphoma—unilateral involvement is unusual.
5. Sarcoidosis
—unilateral disease in only 1%–5%.
Pulmonary artery
1. Poststenotic dilatation—on the left side.
2. Aneurysm—in severe chronic pulmonary arterial hypertension,
Behçet’s and Hughes-Stovin syndromes, ± vessel wall calcification.
3. Pulmonary embolus—massive embolus to one lung; short dilated
ipsilateral proximal pulmonary artery. Peripheral oligaemia.
Others
1. Carcinoid tumour—most commonly arises from a central
bronchus ± distal collapse.92 Aids to Radiological Differential Diagnosis
2. Mediastinal mass—involving the hilum, e.g. bronchogenic cyst.
3. Perihilar pneumonia—ill-defined ± air bronchogram.

51
Q

BILATERAL HILAR ENLARGEMENT

A
  1. Sarcoidosis*—symmetrical and lobulated. Hilar ± unilateral or
    bilateral paratracheal lymphadenopathy ± calcification.
  2. Lymphoma*—typically asymmetrical.
  3. Lymph node metastases—often accompanied by lymphangitis
    carcinomatosa.
  4. Multicentric Castleman disease—usually related to HIV.
  5. Infective—e.g. viruses (most common in children), histoplasmosis,
    coccidioidomycosis. Primary TB is rarely bilateral and symmetrical.
  6. Silicosis—symmetrical ± egg-shell calcification. May also be seen in
    other inhalational diseases, e.g. berylliosis.
    Vascular
    Pulmonary arterial hypertension—tubular hilar enlargement (cf.
    lobulated enlargement seen in lymphadenopathy). Note that
    small-volume lymphadenopathy may also be seen on CT. See also
52
Q

‘EGG-SHELL’ CALCIFICATION OF
LYMPH NODES
Defined as shell-like peripheral calcifications <2 mm thick within
≥2 lymph nodes, in at least one of which the ring of calcification
must be complete and one of the affected lymph nodes must be
≥1 cm in maximum diameter. Calcifications may be solid or
broken ± central calcifications

4

A
  1. Silicosis—seen in ~5%. Predominantly affects hilar nodes.
    Calcification is more common in complicated pneumoconiosis.
    Lungs show multiple small nodular shadows or areas of massive
    fibrosis.
  2. Coal worker’s pneumoconiosis—seen in only 1%. Associated lung
    changes are identical to silicosis.
  3. Sarcoidosis*—nodal calcification in ~5%. Classically described as
    ‘icing-sugar-like’ but occasionally ‘egg-shell’ in appearance.
    Calcification appears ~6 years after disease onset and is nearly
    always associated with advanced lung disease and in some cases
    with steroid therapy.
  4. Lymphoma* following radiotherapy—1–9 years after therapy
53
Q

‘EGG-SHELL’ CALCIFICATION OF
LYMPH NODES
Differential diagnosis

A
  1. Aortic calcification—especially in the wall of a saccular aneurysm.
  2. Pulmonary artery calcification—a rare feature of severe
    pulmonary hypertension, common in Eisenmenger’s syndrome.
  3. Anterior mediastinal tumours—teratodermoids and thymomas
    may occasionally exhibit rim calcification.
  4. Fibrosing mediastinitis—often calcifies
54
Q

PLEURAL EFFUSION

Transudate (protein <30 g/l)

A

These usually cause bilateral effusions.

  1. Cardiac failure.
  2. Hepatic failure.
  3. Renal failure—especially nephrotic syndrome
55
Q

PLEURAL EFFUSION

Exudate (protein >30 g/l)

A
  1. Infection.
  2. Malignancy—primary or metastatic.
  3. Collagen vascular diseases—e.g. SLE, rheumatoid arthritis.
  4. Pulmonary infarction—may also be haemorrhagic.
56
Q

PLEURAL EFFUSION

Haemorrhagic

A
  1. Lung cancer.
  2. Trauma—look for rib fractures.
  3. Coagulopathy.
  4. Pleural endometriosis—R»L side.
57
Q

PLEURAL EFFUSION

Chylous

A

Obstructed or leaking thoracic duct—due to surgery, trauma,

malignant invasion, lymphangiomatosis or filariasis.

58
Q

PLEURAL EFFUSION DUE TO

EXTRATHORACIC DISEASE

A
  1. Pancreatitis—acute, chronic or relapsing. Effusions are
    predominantly left-sided. Elevated amylase content.
  2. Subphrenic abscess—with elevation and restricted motion of the
    ipsilateral diaphragm and basal atelectasis or consolidation.
  3. Post abdominal surgery—especially after upper abdominal
    surgery, most often on the side of the surgery. Resolves after
    2 weeks.
  4. Meigs syndrome—usually right-sided, with ascites and a benign
    ovarian tumour (usually fibroma).
  5. Nephrotic syndrome.
  6. Fluid overload—e.g. due to renal disease.
  7. Cirrhosis.
59
Q

PLEURAL EFFUSION DUE TO

INTRATHORACIC DISEASE

A

Infective
1. Parapneumonic effusion or empyema—can occur as an isolated
pleural infection without pneumonia. Presence of scoliosis concave
to the side of the fluid suggests empyema.
2. Primary TB—in adults > children. Rarely bilateral.
3. Viruses and mycoplasma—effusions are usually small.
Neoplastic
1. Lung cancer—effusion may hide a peripheral carcinoma.
2. Metastases—most commonly from breast; less commonly
pancreas, stomach, ovary and kidney. Look for evidence of surgery.
3. Mesothelioma—effusion in 90%; often massive and obscures the
underlying pleural disease.
4. Lymphoma
—effusion is usually associated with lymphadenopathy
or pulmonary infiltrates.
5. Primary adenocarcinoma of the pleura.
Immunological
1. Systemic lupus erythematosus—effusion is usually small, but
may be massive or bilateral. Cardiomegaly may also be present.Chest 95
5
2. Rheumatoid arthritis
—almost exclusively in males. Usually
unilateral and may predate joint disease. Tends to remain
unchanged for a long time.
Others
1. Pulmonary embolus—effusion is common and may obscure an
underlying area of infarction.
2. Trauma—effusion may contain blood, lymph or food (due to
oesophageal rupture, e.g. Boerhaave syndrome). The latter is
almost always left-sided.
3. Asbestosis—mesothelioma and lung cancer should be excluded,
but an effusion may be present in their absence. Frequently
bilateral and recurrent

60
Q

PLEURAL CALCIFICATION

A
  1. Asbestos exposure—pleural plaques most commonly form
    adjacent to the anterior rib ends and over the diaphragm. Usually
    bilateral.
  2. Prior infection—especially previous tuberculous pleuritis/
    empyema. Usually a unilateral large calcified plaque.
  3. Talc pleurodesis—NB: the resulting calcified pleural thickening can
    remain PET avid for years and should not be mistaken for
    malignancy.
  4. Prior haemothorax—may leave a residual calcified haematoma
61
Q

FOCAL PLEURAL MASS

A
  1. Loculated pleural effusion—or empyema.
  2. Metastases—e.g. from lung or breast. Often multiple ± effusion.
  3. Malignant mesothelioma—usually causes diffuse thickening, but
    can be focal. Nearly always related to asbestos exposure. May be
    obscured by an effusion.
  4. Solitary fibrous tumour of the pleura (SFT)—benign in most
    cases. Usually a smooth lobular mass, up to 15 cm in diameter
    (may opacify entire hemithorax). May change position due to
    pedunculation. Patients are usually >40 years of age and
    asymptomatic. High rate of hypertrophic osteoarthropathy.96 Aids to Radiological Differential Diagnosis
  5. Extrapleural haematoma—in the setting of trauma.
  6. Chest wall masses—e.g. lipoma, nerve sheath tumour, rib lesions,
    sarcoma. Look for scalloping or destruction of ribs
62
Q

DIFFUSE PLEURAL THICKENING

8

A
  1. Exudative pleural effusion—including empyema. Mild smooth
    pleural thickening + associated effusion. The thickening is best
    seen on postcontrast CT (in the portal phase). Pleural thickening
    often persists after resolution of an empyema.
  2. Benign asbestos-related pleural thickening—often bilateral,
    usually smooth, does not extend over the mediastinal pleural
    surface. Associated pleural plaques are typically present.
  3. Malignant mesothelioma—typically unilateral, lobulated contour,
    extends over mediastinal pleural surface. Often associated with a
    small hemithorax.
  4. Extrapleural fat proliferation—bilateral and symmetrical, smooth,
    usually seen in midzones. Associated with increased mediastinal
    and pericardial fat.
  5. Pleural metastases—can be diffuse, usually lobulated + effusion.
  6. Post haemothorax.
  7. Post thoracotomy or pleurodesis.
  8. Related to peripheral lung fibrosis—e.g. pleuroparenchymal
    fibroelastosis (apical and bilateral).
63
Q

PNEUMOTHORAX

A
  1. Spontaneous—M&raquo_space; F, especially in tall, thin patients, usually due
    to ruptured blebs or bullae. ± Small pleural effusion. Association
    with Marfan and Loeys-Dietz syndromes.
  2. Iatrogenic—following chest aspiration, positive pressure
    ventilation, lung biopsy or central line/pacemaker insertion.
  3. Trauma—± rib fractures, haemothorax, surgical emphysema or
    pneumomediastinum.
  4. Secondary to lung disease—e.g. emphysema, cystic fibrosis,
    cystic lung diseases (LAM, LCH, PCP, etc.), bronchopleural fistula
    (e.g. due to lung abscess or carcinoma), lung metastases (e.g.
    from osteosarcoma and other sarcomas).
  5. Extension of pneumomediastinum—see Section 5.36.
  6. Extension of pneumoperitoneum—air passage through a
    pleuroperitoneal foramen
64
Q

PNEUMOMEDIASTINUM

A
  1. Extension of pulmonary interstitial emphysema (PIE)—a sudden
    rise in intraalveolar pressure, often with airway narrowing, causes
    air to dissect through the interstitium to the hilum and then to the
    mediastinum.
    (a) Spontaneous—most common cause, may follow coughing or
    strenuous exercise.
    (b) Positive pressure ventilation.
    (c) Chest trauma.
    (d) Vaginal delivery—due to repeated Valsalva manoeuvres.
    (e) Asthma—but usually not <2 years of age.
    (f) Foreign body aspiration—especially if <2 years.
  2. Perforation of oesophagus, trachea or bronchus—a ruptured
    oesophagus is often associated with a hydrothorax or
    hydropneumothorax, usually on the left side.
  3. Perforation of a hollow abdominal viscus—with extension of gas
    via the retroperitoneal space and diaphragmatic hiatus
65
Q

DIAPHRAGMATIC HUMPS

A

At any site
1. Collapse/consolidation of adjacent lung.
2. Localized eventration.
3. Subpulmonary effusion—often moves apex of ‘diaphragm’
shadow laterally on erect CXR. If on the left side, the distance
between lung and stomach bubble is increased.
4. Pulmonary infarct—Hampton’s hump.
5. Subphrenic abscess.
6. Hepatic abscess, metastasis or hydatid cyst—may extend
through the diaphragm.
Medially
1. Pericardial fat pad.
2. Hiatus hernia.
3. Aortic aneurysm.
4. Pleuropericardial cyst.
5. Pulmonary sequestration.98 Aids to Radiological Differential Diagnosis
Anteriorly
Morgagni hernia.
Posteriorly
1. Bochdalek hernia.
2. Neurogenic tumour—e.g. schwannoma, paraganglioma,
plexiform neurofibroma, etc

66
Q

UNILATERAL ELEVATED HEMIDIAPHRAGM

Causes above the diaphragm

A
  1. Phrenic nerve palsy—smooth hemidiaphragm. No movement on
    respiration. Paradoxical movement on sniffing. The mediastinum is
    usually central. The cause may be evident on the X-ray.
  2. Lung collapse.
  3. Pleural disease—e.g. old haemothorax, empyema, thoracotomy.
  4. Splinting of the diaphragm—due to pain associated with rib
    fractures, pleurisy or subphrenic abscess.
  5. Hemiplegia—upper motor neuron lesion, e.g. stroke.
67
Q

UNILATERAL ELEVATED HEMIDIAPHRAGM

Diaphragmatic causes

A
  1. Eventration—left > right. The heart is often displaced to the
    contralateral side. Limited movement on normal respiration.
  2. Herniation—right-sided may result in liver herniation with no
    gas above the diaphragmatic defect. Left-sided is generally more
    obvious with aerated bowel in the thoracic cavity. May be
    congenital or traumatic (rupture); both are more common on
    the left.
68
Q

UNILATERAL ELEVATED HEMIDIAPHRAGM

Causes below the diaphragm

A
  1. Subphrenic inflammation—e.g. subphrenic abscess, hepatic or
    splenic abscess, pancreatitis.
  2. Marked hepatomegaly or splenomegaly—e.g. extensive liver
    metastases.
  3. Gaseous distension of the stomach or splenic flexure—left side
    only. May be transient.
69
Q

BILATERAL ELEVATED HEMIDIAPHRAGMS

A

General causes
1. Poor inspiratory effort.
2. Obesity.
3. Muscular weakness and myopathy—myotonia, SLE.
4. Lordotic projection—causes apparent elevation of the diaphragm.
The clavicles will also appear abnormally high.
Causes above the diaphragm
1. Bilateral basal lung collapse—e.g. due to infarction, obstructive
atelectasis or poor inspiratory excursion.
2. Small lungs—congenital (e.g. hypoplastic lung) or acquired (e.g.
fibrotic lung disease).
Causes below the diaphragm
1. Ascites.
2. Pneumoperitoneum.
3. Pregnancy.
4. Hepatosplenomegaly.
5. Large intraabdominal tumour.
6. Bilateral subphrenic abscesses.

70
Q

ANTERIOR MEDIASTINAL MASSES
IN ADULTS
REGION 1

A
  1. Retrosternal goitre—on a PA CXR it appears as an inverted
    truncated cone with its base uppermost. It is well-defined,
    smooth or lobulated, without a visible upper margin. The trachea
    may be displaced posteriorly and laterally and may be narrowed.
    Calcification is common. CT shows the connection with the
    thyroid. Relatively high attenuation compared with other
    mediastinal structures and tumours. Uptake by iodine-123
    is diagnostic when positive, but the thyroid may be
    nonfunctioning.
  2. Lymphadenopathy—due to lymphoma, metastases, Castleman
    disease or granulomatous disorders.
  3. Thymic tumours/enlargement
    (a) Thymoma—usually in middle-aged patients; occurs in 15% of
    those with myasthenia gravis and 40% of these will be
    malignant. If malignant it is usually locally invasive and can
    spread along pleura to involve the diaphragm and even into
    the abdomen. Can contain calcification.
    (b) Thymic hyperplasia—lymphoid hyperplasia most commonly
    occurs in myasthenia gravis but can be seen in other
    autoimmune disorders. True hyperplasia can occur post
    chemotherapy (‘rebound’ hyperplasia), steroid therapy,
    radiotherapy, burns and other systemic stressors. Thymus is
    diffusely enlarged but normal in shape.
    (c) Thymic germ cell tumour—teratodermoid, benign and
    malignant teratomas.
    (d) Thymic lymphoma—thymus can be infiltrated in Hodgkin
    disease but there is always associated lymphadenopathy.
    (e) Thymolipoma—usually children or young adults.
    Asymptomatic. Contains fat on CT.
    (f) Thymic cyst—can develop after radiotherapy for lymphoma.
  4. Ectopic parathyroid adenoma—typically small (only visible on
    CT), often avidly enhancing, may mimic a lymph node.
71
Q

ANTERIOR MEDIASTINAL MASSES IN ADULTS
REGION 2
3

A
  1. Germ cell neoplasms—including dermoids, teratomas,
    seminomas, choriocarcinomas, embryonal carcinomas and
    endodermal sinus tumours. Most are benign. Usually larger than
    thymomas (but not thymolipomas) and peak in a younger age
    group. Round/oval, smooth, ± calcification especially rim
    calcification or fragments of bone/teeth, the latter being
    diagnostic. Fat may be seen within teratodermoids.
  2. Thymic tumours (thymoma,hyperplasia,cyst,thymolipoma,carcinoma)
  3. Sternal tumours—metastases (breast, lung, kidney and thyroid)
    are the most common. Of the primary tumours, malignant
    (chondrosarcoma, myeloma, lymphoma) are more common than
    benign (chondroma, aneurysmal bone cyst, giant cell tumour).
72
Q

Region III (anterior cardiophrenic angle masses)

A
  1. Pericardial fat pad—especially in the obese. A triangular opacity
    in the cardiophrenic angle on the PA view, less dense than
    expected due to the fat content. CT is diagnostic. Excessive
    mediastinal fat can be the result of steroid therapy.
  2. Diaphragmatic eventration—commonest in the anteromedial
    portion of the right hemidiaphragm.
  3. Morgagni hernia—through a defect between the septum
    transversum and costal portion of the diaphragm. Almost
    invariably on the right side, but occasionally extends across the
    midline. Often contains a knuckle of colon ± stomach. Appears
    solid if it contains omentum and/or liver.
  4. Pericardial cysts—either a true pericardial cyst or a pericardial
    diverticulum. Oval or spherical, usually situated in the right
    cardiophrenic angle. Fluid attenuation on CT
73
Q

MIDDLE MEDIASTINAL MASSES
IN ADULTS
6

A
  1. Lymphadenopathy—paratracheal, tracheobronchial,
    bronchopulmonary and/or subcarinal nodes may be enlarged. This
    may be due to metastases (most frequently from lung cancer),
    lymphoma (most frequently Hodgkin disease), infection (e.g. TB,
    histoplasmosis or coccidioidomycosis), sarcoidosis or Castleman
    disease.
  2. Bronchogenic carcinoma—arising from a major bronchus.
  3. Tortuous subclavian artery—common finding in the elderly; R>L.
    Can mimic a Pancoast tumour.
  4. Aortic aneurysm—peripheral rim calcification is a useful sign if
    present.
  5. Bronchogenic cyst—usually subcarinal or right paratracheal site.
    50% homogeneous water density, 50% hyperattenuating due to
    protein or milk of calcium content. May contain air if
    communicating with the airway (generally due to prior infection).
  6. Fibrosing mediastinitis—infiltrative mass that can encase and
    narrow mediastinal vessels and airways. Causes include
    histoplasmosis (most common, usually focal and calcified),
    IgG4-related disease (usually diffuse and noncalcified), TB, fungal
    infection and radiotherapy
74
Q

POSTERIOR MEDIASTINAL MASSES
IN ADULTS
Region I (paravertebral)

A
  1. Lymphoma*, myeloma and metastases—bone destruction with
    preserved discs.
  2. Abscess—with disc space and/or vertebral body destruction.
  3. Extramedullary haematopoiesis—with splenomegaly ± bone
    changes of the underlying haematological disorder.
  4. Neurogenic tumours—e.g. neurofibroma, ganglioneuroma
    (young adults). Often extends through neural foramina into the
    spinal canal ± vertebral remodelling.
  5. Meningocoele—with associated vertebral remodelling.
  6. Pancreatic pseudocyst—fluid can extend into the mediastinum
    through a diaphragmatic hiatus and form a pseudocyst.
  7. Neurenteric cyst—with an associated congenital spinal anomaly
75
Q

POSTERIOR MEDIASTINAL MASSES

IN ADULTS

A

Region II
1. Dilated oesophagus—especially in achalasia. Contains mottled gas
shadows ± an air–fluid level. Confirmed on barium swallow.
2. Descending aorta—unfolded, dilated or ruptured.
3. Oesophageal duplication cyst.
Region III
Hiatus hernia—often contains an air–fluid level that is projected
through the cardiac shadow on a penetrated PA view

76
Q

MEDIASTINAL MASS CONTAINING FAT

A
  1. Hernia containing fat—e.g. hiatal (adjacent to oesophagus),
    Morgagni (anterior), Bochdalek (posterior).
  2. Teratodermoid—usually also contains cystic and/or calcified
    components.
  3. Thymolipoma—in anterior mediastinum, contains fat and
    soft-tissue strands, and can be very large. No cystic or calcified
    elements (cf. teratodermoid).
  4. Mediastinal lipomatosis—generalized increase in mediastinal fat;
    related to obesity and steroids (endogenous or exogenous).
  5. Lipoma/liposarcoma—discrete fatty mass; the latter contains
    soft-tissue elements that are typically more irregular than
    thymolipoma.
  6. Extramedullary haematopoiesis—paravertebral mass or masses
    that may contain fat + signs of an underlying haematological
    disorder.
  7. Myelolipoma—rare in the mediastinum, usually paravertebral in
    location.
  8. Epipericardial fat necrosis—focal area of fat necrosis in
    pericardial fat pad resulting in focal fat stranding. Resolves
    spontaneously.
  9. Haemangioma—often contains phleboliths, may show
    heterogeneous enhancement.
  10. Hibernoma—very rare in the mediastinum.
77
Q

AVIDLY ENHANCING MEDIASTINAL MASS

A
  1. Saccular aneurysm.
  2. Retrosternal thyroid goitre.104 Aids to Radiological Differential Diagnosis
  3. Varices—may be ‘uphill’ (found around distal oesophagus, due
    to portal hypertension) or ‘downhill’ (found around upper
    oesophagus, due to SVC obstruction).
  4. Hypervascular nodal metastases—e.g. from RCC, melanoma,
    thyroid cancer.
  5. Castleman disease—avidly enhancing hyperplastic lymph nodes.
  6. Ectopic parathyroid adenoma—usually small and in the upper
    mediastinum.
  7. Paraganglioma—usually in posterior mediastinum or pericardial.
  8. Haemangioma—may contain phleboliths.
  9. Bacillary angiomatosis—in AIDS patients; avidly enhancing
    nodes due to Bartonella infection.
  10. Kaposi sarcoma—also in AIDS patients; nodes may enhance
    avidly and are usually accompanied by ill-defined lung
    nodules
78
Q

FOCAL RIB LESION (SOLITARY OR MULTIPLE

A
  1. Healed rib fracture.
  2. Rib metastases—e.g. from lung, kidney, prostate or breast.
  3. Fibrous dysplasia—most common benign rib lesion. Expansile,
    ground-glass density.
  4. Paget’s disease*—rib expansion + cortical thickening.
  5. Rib destruction by an adjacent invasive mass.
    (a) Neoplastic—e.g. lung cancer, mesothelioma, lymphoma.
    (b) Infective—e.g. TB (tuberculous empyema), actinomycosis
    (lung mass), blastomycosis, nocardiosis.
  6. Primary malignant tumours.
    (a) Multiple myeloma/plasmacytoma*—plasmacytoma is solitary
    and expansile, myeloma is multiple and punched-out.
    (b) Chondrosarcoma—most common primary malignant rib
    neoplasm.
    (c) Ewing sarcoma of chest wall—in children or young adults.
    Large soft-tissue mass, may fill hemithorax.
  7. Benign tumours.
    (a) Osteochondroma—usually in multiple hereditary exostosis, at
    costochondral junction.
    (b) Enchondroma—lucent ± endosteal scalloping ± chondroid
    matrix.
    (c) Langerhans cell histiocytosis*—lytic, variable appearance.
    Young patients.
    (d) Aneurysmal bone cyst—lytic and expansile, usually in
    posterolateral rib.
    (e) Osteoblastoma—lytic + sharp sclerotic margins, usually in
    posterolateral rib.Chest 105
    5
    (f) Osteoid osteoma—rare. Lucent nidus + surrounding sclerosis
    that may involve adjacent ribs. Usually posterior ± painful
    scoliosis if close to the spine.
    (g) Giant cell tumour—rare. Lytic and expansile.
  8. Nonneoplastic.
    (a) Brown tumour—well-defined and lytic ± other features of
    hyperparathyroidism.
    (b) Infection—tuberculous (most common, well-defined margins),
    bacterial (usually at costochondral or costovertebral junction),
    fungal (e.g. aspergillosis) or parasitic (e.g. hydatid—welldefined expansile multiloculated cystic lesion).
    (c) Radiation osteitis.
    (d) Lymphangiomatosis—rare, involves multiple bones
79
Q

RIB NOTCHING—INFERIOR SURFACE

A

Enlarged collateral vessels
1. Coarctation of the aorta—third to eighth ribs, usually bilateral,
but may be right-sided if coarctation is proximal to the left
subclavian artery, or left-sided if there is an anomalous right
subclavian artery distal to the coarctation. Prominent ascending
aorta, small descending aorta with an intervening notch.
2. Proximal subclavian artery occlusion—e.g. in Takayasu arteritis or
after a Blalock shunt for tetralogy of Fallot (upper two ribs).
3. Interrupted aortic arch.
4. Abdominal aortic occlusion—notching of lower ribs bilaterally.
5. Lung/chest wall arteriovenous malformation.
6. SVC obstruction—venous collaterals less likely to cause notching.
Neurogenic
1. Neurofibromatosis*—intercostal neurofibromas may scallop the
inferior rib margin. Dysplastic ‘ribbon ribs’ may also be seen.
2. Schwannoma—single notch

80
Q

RIB NOTCHING—SUPERIOR SURFACE

7

A
  1. Connective tissue disorders—e.g. rheumatoid arthritis, SLE,
    scleroderma, Sjögren’s syndrome, Marfan syndrome.
  2. Hyperparathyroidism*—subperiosteal bone resorption. Can also
    involve inferior surface.
  3. Iatrogenic—chest drains, thoracotomy retractors, radiotherapy.
  4. Osteogenesis imperfecta.
  5. Neurofibroma/vascular collaterals—if large enough, can cause
    superior + inferior notching.
  6. Intercostal muscle atrophy—e.g. due to paralysis, poliomyelitis or restrictive lung disease. Reduced mechanical stress leads to bone loss.
  7. Progeria—thin slender osteoporotic ribs
81
Q

WIDE OR THICK RIBS

7

A
  1. Fibrous dysplasia.
  2. Healed fractures with callus.
  3. Chronic anaemias—e.g. thalassaemia. Due to marrow hyperplasia.
  4. Paget’s disease*.
  5. Tuberous sclerosis*.
  6. Achondroplasia*—short, wide ribs.
  7. Mucopolysaccharidoses*—ribs are widened distally
82
Q

Aortic rupture

A

Haematoma widens mediastinum, causes apical capping, displaces the
trachea to the right, depresses the left main bronchus and causes a pleural effusion.