Chest Techniques and Applications


  • Silhouette sign – Loss of contour for localisation or detection of low density lesions. Falsly lost with underpenetration.
  • Air bronchograms – Seen in expiration/low volume lungs (esp paedric retrocardiac bronchi), air space shadowing, atelectasis, scarring, severe interstitial disease (airless lung next to dilated bronchi), sarcoidosis, AIS/BAC, lymphoma.
  • On lateral vertebral bodies should be progresively darker inferiorly, homogeneous opacity over heart, retrosternal the most transradiant region except immediately retrocardiac
  • Ground-glass pattern (grey lung) – Displaced air but vessels still seen. From thickened interstium, partial filling of airspace or reduced expansion.

Diffuse lung disease is classified into alveolar/airspace (lobar, segmental or ‘butterfly’ distribution, ill-defined margins) or interstitial (well defined linear/nodular/irregular patterns).

Line and Band Shadows

Band shadows are linear opacities >5mm thickness, line shadows <5mm. From skinfold, clothing/tubes, wall of ring shadow, discoid atelectasis, vessels, thickened fissures, pleural tail from nodule or:

  • Parenchymal/pleuro-parenchymal scar – Previous linear atelectassis, infarction or infection.
  • Bronchial/peribronchial thickening – Posterior wall bronchus intermedius >3mm. Oedema, inflammatory or neoplastic cells invade peribronchial interstitial space making wall appear thick and ill-defined.
  • Mucoid impaction (bronchocoele, mucocoele) – Branching from hilum, usually >10mm diameter, V/Y shaped. Gloved finger/tree-in-bud, jax. Implies bronchial obstruction. In ABPA or other obstructing lesion, collateral air drift maintains aeration. Invisible if there is adjacent atelectasis due to silhouette sign. Central perihilar from nonobstructive bronchiectasis (CF, ABPA), postobstructive bronchiectasis distal to endobronchial tumour, congenitally atretic bronchus. Peripheral in CF and post-tuberculous bronchiectasis.
  • Septal/Kerley lines – Rarely normally seen in thin patients with high quality film. Deep septal lines (Kerley A) <40mm radiating from hila, most obvious mid and upper zones. Interlobular (Kerley B) <10mm perpendicular along pleura but absent along fissures, usually bases. ‘Kerley C’ lines criss-crossing superimposed B lines. From oedema, lymphangitis carcinomatosa, viral and mycoplasmal pneumonia, pneumoconiosis, sarcoid, LIP, idiopathic pulmonary haemorrhage, interstitial fibrosis.

Airspace Filling/Shadowing

(Consolidation). Terminal airspaces replaced by blood, transudate, exudate or neoplastic cells. Intersegmental spread via pores of Kohn (interalveolar) and canals of Lambert (between preterminal bronchioles). Poorly marginated, airspace nodules/acinar shadows (6-8mm, sublobular usually peribronchiolar/centrilobular region) at the leading edge, lobar/segmental distribution, coalescence/confluent, air bronchograms/bronchiolograms/alveolograms (occasionally in severe interstitial disease eg ‘alveolar’ sarcoid), rapidly changing over time, sharp margin against pleura/fissures, vascular markings invisible/reduced. Usually peripheral. Low density due to mucin-filled airsapces (cf enhancing atelectatic lung).

Other features:

  • CT angiogram sign – Reverse of bronchogram when contrast seen in vessels, useful in atelectasis vs effusion.
  • Patchwork quilt appearance on CT – Multifocal consolidation which eventually coalesces.
  • Bat’s wing/butterfly/perihilar distribution – Central with abrupt margination before reaching peripheral lung for unkown reason. Represents oedema, haemorrhage, aspiration pneumonia or Pneumocystic carinii (esp immunocomprimised), inhalation of noxious gases or liquids, alveolar proteinosis, lymphangitis carcinomatosis, AIS/BAC, lymphoma.
  • Opacity >1/2 of lobe with no volume loss is diagnostic of consolidation; expansion of lobe suggests bacterial or central obstructive pneumonia ‘drowned lung’.
  • CT halo sign – Ground glass surrounding rounded consolidation suggesting infection with surrounding haemorrhage.
  • Multiple lobar/segmental airspaces shadows is pneumonia, infarction/haemorrhage from PE, oedema (rare) or neoplasm.
  • ‘Photographic negative of pulmonary oedema’ – Nonsegmental airspace peripheral, suggesting chronic eosinophilic pneumonia (esp UL), drug reactions, organising pneumonia.
  • Rapid clearing (hours) suggests oedema or haemorrhage.
  • Reappearing in same or different location suggests oedema, eosinophilic pneumonia or asthma/ABPA.
  • Fine punctate parenchymal calcificaiton (eg hyperparathyroidism) may simulate consolidation.
  • Tree-in-bud – Filling of distal bronchioles with branching.


  • Pneumonia – Bacteria, Pneumocystis carinii, influenza, fungi (histoplasmosis, aspergillosis)
  • Pulmonary oedema – Cardiogenic, fluid overload/renal failure, noncardiogenic/ARDS (might only appear several hours after onset of Sx)
  • Atelectasis
  • Infarction
  • Contusion (may have associated air cyst)
  • Haemorrhage
  • Neoplasm – AIS, lymphoma
  • Alveolar proteinosis – Acute silica inhalation, lymphoma, leukaemia, AIDS
  • Organizing pneumonia

Chronic consolidation ‘BALLS’:

  • BAC (AIS)
  • Aspiration
  • Alveolar proteinosis
  • Lipoid pneumonia
  • Loeffler syndrome (eosinophilic)
  • Lymphoma
  • Sarcoid (alveolar)

Multiple cystic lesions/cavities

  • metastases – adenocarcinoma > SCC >  sarcoma
  • LCH – smokers, less predominant inferiorly
  • Wegeners
  • Septic emboli – esp IVDU
  • LIP – <30 cysts, Sjogren syndrome
  • LAM – females, TS

Nodules with ground glass halo

  • adenocarcinoma
  • infection/septic emboli
  • haemorrhagic metastasses

Interstitial Opacities

Central/axial/bronchovascular interstitium extends from mediastinum, enveloping bronchovascular bundles. Centrilobular interstitium surrounds small centrilobular arterioles and bronchioles within secondary pulmonary lobules. Subpleural/peripheral interstitium lines between visceral pleura and lung, ingavinating into lung forming interlobular septa. Intralobular/parenchymal/alveolar interstitium is the fine network within and supporting alveolar spaces. Secondary pulmonary lobule is 10-25mm polyhedral. Interlobular septa normally 0.1mm. Centrilobular ateries are 1mm, V- or Y-shaped centrally, branching into intralobular and acinar aa). Interstitial thickening from water, blood, tumour, cells or fibrosis. There may be subpleural thickening, perivascular haze, peribronchial thickening.

Patterns on CXR include:

  • Nodular – 1-9mm well defined round or irregular, may be calcified. >10mm nodules represent individual lesions.
  • Reticular/linear – Fine irregular lace/net-like, 1-2mm rings, includes septal lines. Clear-cut reticular more in upper zone suggests LCH, esp with airspaces >10mm.
  • Reticulonodular – Nodules usually irregular. Much more common than pure reticular or nodular patterns. At bases and peripheries with loss of volume, no pleural effusion or adenopathy is likely interstitial pulmonary fibrosis. Unilateral without zonal/lobar distribution, septal lines, pleural effusions is almost diagnostic of lymphangitis carcinomatosa. Coarse in upper zones esp with fibrotic contraction is chronic Tb or fungal disease (esp fibrocavitatory MAI). Coarse radiating from hila mid and upper zones sparing extreme apices, hilar lymphadenopathy suggests sarcoidosis.
  • Honeycombing – Coarse reticular/reticulonodular around small 3-10mm cystic spaces. Represents scarring around enlarged airspaces. Radiological honeycombing is different to pathological/histological honeycombing which is microscopic.

Patterns on HRCT include:

  • Interlobular/septal lines – Thickened (>1mm) interlobular septa. Peripherally (Kerley B) they are thin, short, 10-20mm perpendicular to pleura; centrally (Kerley A) they are longer (20-60mm), more oblique and may envelope complete lobules.
  • Intralobular lines (reticulation) – Lattice of fine lines within lobule in a ‘spoke-wheel’/’spiderweb’ pattern. Thickened intralobular/parenchymal interstitium, usually from fibrosis.
  • ‘Thickened’ fissures – Thickened interlobular septa extending to subpleural interstitium. Smooth thickening indistinguishable from fluid in the fissure. Nodular thickening seen in sarcoidosis and lymphangitic carcinomatosis (nodules in subpleural lymphatics).
  • Thickened bronchovascular structures – Thickened peribronchovascular interstitium with peribronchial cuffing, tram tracking. Smooth thickening in pulmonary oedema. Nodular/irregular in sarcoidosis, UIP. Lymphangitic carcinomatosis may cause smooth or irregular thickening.
  • Centrilobular (lobular core) abnormalities – ‘Tree-in-bud’ opacities from filling of centrilobular bronchioles, distention, wall thickening or peribronchiolar inflammation; seen within 3-5mm of pleural surface. Centrilobular ground glass nodules reflect disease of the bronchiole and adjacent parenchyma. May be impacted with mucus, pus, blood, fluid or cells. From infectious bronchiolitis (esp endobronchial spread ot TB), subacute hypersensitivity pneumonitis, COP, bronchiectasis (CF, Kartageners), panbronchiolitis, obliterative bronchiolitis, follicular bronchiolitis, ABPA, mucoid impaction, aspiration, endobronhial cells (AIS, mets). DDx intravascular tumour emboli from filling of centrilobular arteries.
  • Subpleural lines – 50-100mm curvilinear parallel to and within 10mm of pleura esp posterior lower lobes, unchanged on prone scans. Probably early fibrosis in asbestosis, IPF.
  • Parenchymal bands – Nontapering, nonbranching, linear 20-50mm extending to pleural surface, with associated regional parenchymal distortion. Fibrotic bands from asbestosis, IPF, sarcoidosis.
  • Honecombing – 6-10mm cystic spaces with thickened 1-3mm walls mostly posterior subpleural lower lobes from end-stage fibrosis. Cysts lined by bronchiolar epithelium, from bronchiolectasis.
  • Thin-walled cysts – 10mm, uniform with thin walls, do not have shared walls, evenly distributed in upper lobes ± lower lobes, normal intervening lung. From late stage LCH, LAM.
  • Micronodules – 1-3mm, round, sharply marginated conglomerates of granulomas or tumour within interstitium. Along central bronchovascular structures (sarcoidosis, LCH), interlobular septa or subpleural interstitium (sarcoidosis, lymphangitic carcinomatosis, silicosis), or within the substance of the lobule (miliary TB, metastatic adenocarcinoma).
  • Ground-glass opacity (GGO) – Hazy increased density, respecting lobular borders. Thickened alveolar septa ± partial filling of alveolar spaces with exudate or fluid. From DIP, PCP, acute hypersensitivity pneumonitis, NSIP, oedema. Implies reversible active inflammatory process or oedema.
  • Architectural distortion – Irregular lung-mediastinal, lung-pleural and lung-vascular interfaces. Common in sarcoidosis, UIP.
  • Traction bronchiectasis – Fibrosis causing irregular dilatation or bronchi (segmental and subsegmental), with traction bronchiolectasis contributing to honeycombing. Common in IPF and other UIP, long-standing sarcoidosis.
  • Conglomerate masses – Masses of fibrotic tissue in parahilar regions upper lobes, crowded vessels and dilated bronchi, occasionally associated with peripheral bullae. In end-stage sarcoidosis, silicosis with progressive massive fibrosis (PMF), radiation fibrosis, IVDU with granulomatous fibrosis due to IV talc or starch in narcotics.

Pulmonary Lucency

Focal lucencies:

  • Cavitation implies necrosis and liquefaction. If communication with airway then air enters with air-fluid level. Walls are irregular/lobulated, >1mm thick. Lung abscess or necrotic neoplasm.
  • Ring shadow – Discrete round/oval with thin <2mm wall, may contain fluid. Widespread ring shadows/cystic pattern >10mm suggests cystic bronchiectasis.
    • Bleb – <10mm within layers of visceral pleura, usually apex, indistinguishable from paraseptal emphysema. Rupture -> spontaneous pneumothorax.
    • Bulla – >10mm with <1mm wall. Focal parenchymal destruction (emphysema), may contain fibrous strands, residual blood vessels or alveolar septa.
    • Air cyst – Well circumscribed, >10mm, smooth <4mm wall. Some have true epithelial lining (bronchogenic cyst communicating with bronchus), most don’t (postinflammatory of posttraumatic). Bronchiectatic cysts are multiple, thin-walled in clusters in lower lobes in varicose/cystic bronchiectasis.
      • Pneumatocoele – Air cysts after infection (PCP, staph pneumonia), trauma or hydrocarbon ingestion. Traumatic from laceration following blunt trauma, usually resolves in 4-6/12.

Diffuse lung lucencies:

  • Unilateral lung hyperlucency:
    • Overlying soft tissue, grid cutoff, rotation, congenital absence of pectoralis (Poland syndrome), mastectomy.
    • Contralateral pleural effusion/thickening or ipsilateral pneumothorax.
    • Reduced blood flow – Hypoplastic pulmonary artery (causes lucent small lung), extrinsic compression (tumour, fibrosing mediastinitis), PE, shunting from airtrapping.
      • Swyer-James syndrome – Adenoviral infection during infancy with asymmetric obliterative bronchiolitis with severe air trapping, unilateral PA hypoplasia.
    • Check-valve effect (air-trapping) – Endobronchial tumour/foreign body.
    • Lobectomy/atelectasis – Hyperexpanded remaining lobes.
    • Assymetric emphsema with severe bullous disease.
  • Bilateral hyperlucent lungs:
    • Overpenetrated film, thin patient.
    • Reduced PA flow from congenital pulmonary stenosis (tetralogy of Fallot), extrinsic compression, PA HTN, chronic thromboembolic disease, fibrosing mediastinitis.
    • Emphsema with air trapping, pulmonary microvasculature destruction.
    • Asthma with transient air trapping.

Imaging Techniques


  • Posteroanterior (PA) – 140kVp, FFD 1.8m, grid and phototimer.
  • Portable anteroposterior (AP) – Limited kVp (hence longer exposure, motion artifact). Short FID and AP magnifies anterior structures. Supine elevates diaphragm, decreased volumes, increased upper lobe vascular markings, widened upper mediastinum/vascular pedicle (increased venous return), layering hides effusions and pneumathoraces
  • Lateral decubitus – For small effusions/pneumothorax (5mL fluid or 15mL air can be seen), to characterise free-flowing effusions. Downside diaphgram is higher than upside. Air trapping in dependent lung.
  • Expiratory radiograph – For focal/diffuse air trapping, detection of small pneumothorax.
  • Apical lordotic view (caudocephalad tube angulation) – For lung apices. Enhances middle lobe atelectasis by having minor fissure on tangent and increasing AP thickness of atelectatic middle lobe.
  • Chest fluoroscopy – For diaphragmatic paralysis and to determine location of opacities.

Assess adequacy – Penetration (faint visualisation of disc spaces, vessels behind heart and diaphragms), rotation (midpoint medial clavicles and spinous processes), inspiration (apex of right diaphragm below 10th posterior rib) and motion (sharp heart borders, diaphragm, pulmonary vessels).

Lateral CXR:

  • RUL bronchus more superior to LUL bronchus
  • Adenopathy forms doghnut sign around the LUL bronchus (usually seen end-on).
  • RPA (oval) at antero-superior hilum; LPA (arch-like or wedge-shaped) is postero-superior.
  • Posterior wall of bronchus intermedius is linear within air column above LUL bronchus.
  • Superior pulmonary vein seen end on below the hilum.


Indications for thoracic CT – Evaluation of abnormality on CXR, cancer staging, metastases/nodes, empyema vs lung abscess, PE, aortic disease.

Indications for HRCT (1.25mm) – Solitary pulmonary nodule, Sx or abnormal spirometry with normal/equivocal XR, diffusely abnormal CXR, baseline for chronic diffuse lung disease, determine approach of biopsy. Noncontrast for parenchymal disease. Contrast for mediastinal mass, cancer staging, arterial evaluation or cardiac study. Expiratory study for air trapping in small airways disease. Nodules seen as small as 2mm.

Ultrasound of the Chest

Indications include pleural, peripheral parenchyma, mediastinal lesions, phrenic nerve paralysis, subpulmonic and subphrenic collection. Guided pleural, or pleural based masses/abscesses. Gliding sign – echogenic visceral pleura/lung interface moving with respiration, absent with pneumothorax. Consolidation may have air alveolograms (bright globular echoes with comet-tail artifacts), air bronchograms or fluid bronchograms. Atelectasis causes volume reduction and crowding of vessels, associated pleural effusion.

MRI of Mediastinum

Superior to CT in chest wall or mediastinal invasion due to high tumour/fat/muscle/fibrosis contrast. Indications – aortic disease in stable patients, superior sulcus tumours, mediastinal/vascular/chest wall invasion, lung cancer staging in iodine allergic, posterior mediastinal mass.

Medical Devices in the Thorax

  • Thoracostomy tubes (chest drains) – Should not enter the interlobar fissure.
  • Pigtail catheter – For empyema draiange.
  • Plombage – ‘Ping-pong’ ball or was plombage, previous treatment for TB.
  • Endotracheal tube (ETT) – tip should be 50 ±20 mm above the carina with head and neck in neutral position. Too high may cause vocal cord trauma, too low bronchus intubation.
  • Central venous catheter – Ideally in the SVC.
  • Intra-aortic balloon pump (IABP) – In descending thoracic aorta, with tip in distal aortic arch (below L SCA origin). Inflated at onset of diastole, deflated just prior to systole. Goal to increase myocardial oxygen supply, improve cardiac output.
  • Swan-Ganz (pulmonary artery) catheter
  • Permanent cardiac pacemeaker (PPM) – consists of a pulse generator (baterry pack and control unit in infraclavicular region) and lead wires with electrodes for contact with the endocardium/myocardium.
    • Single chamber – lead in RV.
    • Dual chamber – leads in RA appendage and RV apex
    • Biventricular – LV epicardial, usually associated with RA appendage and RV apex leads. LV electrode may be introduced through the coronary sinus, and wedged into a LV cardiac vein.
  • Automatic implantable cardioverter defibrillator (AICD/ICD) – Various sensing and shocking electrodes, frequently combined with a pacemaker.