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CT patterns of lung disease 

CT patterns of lung disease
Author(s):

Stephen Chapman

, Grace Robinson

, John Stradling

, Sophie West

, and John Wrightson

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date: 26 October 2021

Airspace consolidation

Process

Causes

Fluid/secretion accumulation in alveoli

Pneumonia, pulmonary oedema or haemorrhage, ARDS, COP, lymphoma, drugs, bronchoalveolar cell carcinoma, eosinophilic pneumonia

Fig. A4.1 Chronic organizing pneumonia (COP). Air bronchograms clearly present.

Fig. A4.1 Chronic organizing pneumonia (COP). Air bronchograms clearly present.

Fig. A4.2 Extensive airspace consolidation due to eosinophilic pneumonia.

Fig. A4.2 Extensive airspace consolidation due to eosinophilic pneumonia.

Air trapping

Process

Causes

Partial small airway obstruction

Asthma, obliterative bronchiolitis, COPD

Fig. A4.3 Subject prone. On expiration, the denser area becomes more dense, indicating the lung has deflated; other parts of the lung remain lucent, indicating that air is trapped behind narrowed airways.

Fig. A4.3 Subject prone. On expiration, the denser area becomes more dense, indicating the lung has deflated; other parts of the lung remain lucent, indicating that air is trapped behind narrowed airways.

Fig. A4.4 Structure of two 2° pulmonary lobules abutting the pleural surface. The 2° pulmonary lobule is the smallest anatomical area visible on CT. Tree-in-bud appearance will be in the acinus around the central bronchovascular core. Reticular patterns will be centred on the interlobular septae and/or draining lymphatics. Mosaic patterns and air trapping will tend to follow outlines of the lobule or sets of lobules.

Fig. A4.4 Structure of two 2° pulmonary lobules abutting the pleural surface. The 2° pulmonary lobule is the smallest anatomical area visible on CT. Tree-in-bud appearance will be in the acinus around the central bronchovascular core. Reticular patterns will be centred on the interlobular septae and/or draining lymphatics. Mosaic patterns and air trapping will tend to follow outlines of the lobule or sets of lobules.

Cystic airspaces

Process

Causes

Clearly defined air-containing space with definable wall

LAM, LCH, end-stage UIP, PCP, LIP, septic emboli

Fig. A4.5 Langerhans cell histiocytosis (LCH). Walls are thin, but more pronounced, irregular, and widely spread than emphysematous holes.

Fig. A4.5 Langerhans cell histiocytosis (LCH). Walls are thin, but more pronounced, irregular, and widely spread than emphysematous holes.

Fig. A4.6 Peripheral cysts (honeycombing) of usual interstitial pneumonitis (UIP). Characteristic subpleural distribution.

Fig. A4.6 Peripheral cysts (honeycombing) of usual interstitial pneumonitis (UIP). Characteristic subpleural distribution.

Fig. A4.7 Holes in the lungs due to emphysema. No real ‘walls’.

Fig. A4.7 Holes in the lungs due to emphysema. No real ‘walls’.

Fissural, bronchovascular, and subpleural nodularity

Process

Causes

Nodules seen along the pulmonary fissures, along the bronchovascular bundles, and subpleurally

Sarcoidosis. Also described in Kaposi’s sarcoma

Fig. A4.8 Sarcoidosis, perihilar, and bronchovascular distribution of nodularity.

Fig. A4.8 Sarcoidosis, perihilar, and bronchovascular distribution of nodularity.

Fig. A4.9 Sarcoidosis, subpleural nodules.

Fig. A4.9 Sarcoidosis, subpleural nodules.

Fig. A4.10 Irregular/nodular thickening of fissures and bronchovascular bundles.

Fig. A4.10 Irregular/nodular thickening of fissures and bronchovascular bundles.

Ground-glass shadowing

Process

Causes

Grey appearance to lung interstitium; air in bronchus looks blacker

Parenchymal inflammatory conditions such as sarcoidosis, alveolitis, early UIP and other IIPs, HP, pulmonary oedema or haemorrhage, PCP, alveolar proteinosis, drug/radiation injury

Fig. A4.11 Subtle ground-glass shadowing in early UIP. Airways appear blacker, but lung is diffusely more dense. Early reticular pattern at right base also.

Fig. A4.11 Subtle ground-glass shadowing in early UIP. Airways appear blacker, but lung is diffusely more dense. Early reticular pattern at right base also.

Fig. A4.12 More marked ground-glass shadowing in UIP. Very early honeycombing and traction bronchial dilatation (bronchiectasis) as well.

Fig. A4.12 More marked ground-glass shadowing in UIP. Very early honeycombing and traction bronchial dilatation (bronchiectasis) as well.

Honeycomb lung

Process

Causes

End-stage fibrotic lung

UIP, asbestosis

Fig. A4.13 Honeycombing in UIP. Usually mainly peripheral.

Fig. A4.13 Honeycombing in UIP. Usually mainly peripheral.

Fig. A4.14 More subtle honeycombing at the lung periphery with other features of UIP. Traction bronchial dilatation due to surrounding lung fibrosis and a reticular pattern beginning to outline the 2° pulmonary lobule.

Fig. A4.14 More subtle honeycombing at the lung periphery with other features of UIP. Traction bronchial dilatation due to surrounding lung fibrosis and a reticular pattern beginning to outline the 2° pulmonary lobule.

Mosaic attenuation pattern

Process

Causes

Well-defined areas of normal lung abutting abnormal lung, giving a mosaic pattern. Seen particularly in expiration

Indicates small airways disease, such as asthma, vascular disease, such as PE, or infiltrative disease such as obliterative bronchiolitis, HP

Fig. A4.15 Bronchiectasis with small airways disease that is causing the mosaic pattern. In addition, there are markedly bronchiectatic airways in the left lower lobe, with considerable airway crowding due to distal lung collapse.

Fig. A4.15 Bronchiectasis with small airways disease that is causing the mosaic pattern. In addition, there are markedly bronchiectatic airways in the left lower lobe, with considerable airway crowding due to distal lung collapse.

Fig. A4.16 Non-specific interstitial pneumonitis (NSIP), showing patchy and mosaic-like pattern of increased attenuation.

Fig. A4.16 Non-specific interstitial pneumonitis (NSIP), showing patchy and mosaic-like pattern of increased attenuation.

Nodularity

Process

Causes

Small discrete dots 1–10mm, may be in airspaces or interstitium

Metastases, sarcoidosis, pneumoconiosis, HP, miliary TB, fungal infection, idiopathic pulmonary haemorrhage, alveolar microlithiasis, varicella pneumonitis

Fig. A4.17 Multiple dense nodules of varying size due to metastases.

Fig. A4.17 Multiple dense nodules of varying size due to metastases.

Fig. A4.18 Sarcoid. Multiple small nodules throughout lung but usually associated with other features of sarcoid such as fissural nodularity and bilateral hilar node enlargement.

Fig. A4.18 Sarcoid. Multiple small nodules throughout lung but usually associated with other features of sarcoid such as fissural nodularity and bilateral hilar node enlargement.

Poorly defined centrilobular nodules

Process

Causes

Peribronchiolar inflammation in the absence of intraluminal secretion

HP, RB-ILD

Fig. A4.19 Soft centrilobular nodularity due to HP (also called extrinsic allergic alveolitis, EAA).

Fig. A4.19 Soft centrilobular nodularity due to HP (also called extrinsic allergic alveolitis, EAA).

Fig. A4.20 Another example of HP, enlarged to show position of soft nodules in the centre of the 2° pulmonary lobules.

Fig. A4.20 Another example of HP, enlarged to show position of soft nodules in the centre of the 2° pulmonary lobules.

Reticular (or linear) pattern

Process

Causes

Linear fine lines, indicating thickened interlobular septa. Subpleural reticulation

ILD (e.g. UIP, asbestosis), pulmonary oedema, drug-induced fibrosis, pulmonary haemorrhage, lymphangitis

Fig. A4.21 Lymphangitis carcinomatosis. Infiltrated lymphatics widen and thicken the interlobular septa.

Fig. A4.21 Lymphangitis carcinomatosis. Infiltrated lymphatics widen and thicken the interlobular septa.

Fig. A4.22 Pulmonary oedema due to left heart failure. Fluid-distended lymphatics outlining the 2° pulmonary lobules. Worse in dependent areas. Fluid in the fissures, bilateral pleural effusions, and some airspace filling with pulmonary oedema.

Fig. A4.22 Pulmonary oedema due to left heart failure. Fluid-distended lymphatics outlining the 2° pulmonary lobules. Worse in dependent areas. Fluid in the fissures, bilateral pleural effusions, and some airspace filling with pulmonary oedema.

Tree in bud

Process

Causes

Mucus/pus/secretions filling bronchioles and causing dilatation

Small airways disease, particularly infection, including mycobacteria, Haemophilus influenzae, diffuse pan-bronchiolitis, CF, yellow nail syndrome, 1° pulmonary lymphoma

Fig. A4.23 Extensive tree-in-bud appearance in the left lower lobe from opportunistic mycobacterial disease.

Fig. A4.23 Extensive tree-in-bud appearance in the left lower lobe from opportunistic mycobacterial disease.

Fig. A4.24 Tree-in-bud appearance, enhanced by a post-processing technique called ‘maximum intensity projection’. Effectively, this squashes denser structures from several thin cuts into one, allowing branching structures to be viewed in their entirety.

Fig. A4.24 Tree-in-bud appearance, enhanced by a post-processing technique called ‘maximum intensity projection’. Effectively, this squashes denser structures from several thin cuts into one, allowing branching structures to be viewed in their entirety.