CT-Definable Subtypes of Chronic Obstructive Pulmonary Disease: A Statement of the Fleischner Society

Abstract

The purpose of this statement is to describe and define the phenotypic abnormalities that can be identified on visual and quantitative evaluation of computed tomographic (CT) images in subjects with chronic obstructive pulmonary disease (COPD), with the goal of contributing to a personalized approach to the treatment of patients with COPD. Quantitative CT is useful for identifying and sequentially evaluating the extent of emphysematous lung destruction, changes in airway walls, and expiratory air trapping. However, visual assessment of CT scans remains important to describe patterns of altered lung structure in COPD. The classification system proposed and illustrated in this article provides a structured approach to visual and quantitative assessment of COPD. Emphysema is classified as centrilobular (subclassified as trace, mild, moderate, confluent, and advanced destructive emphysema), panlobular, and paraseptal (subclassified as mild or substantial). Additional important visual features include airway wall thickening, inflammatory small airways disease, tracheal abnormalities, interstitial lung abnormalities, pulmonary arterial enlargement, and bronchiectasis.

(©) RSNA, 2015.

Figures

Figure 1:

Visually defined patterns of COPD at CT. * = If there are fewer than four to five small (≤1 cm) juxtapleural circumscribed areas of lucency in the apex of a lung, ignore. A1AT = α1-antitrypsin.

Figure 2:

Comparison of frozen lung slices and micro-CT images from, A, donor (control) lung to lungs affected by, B, centrilobular, C, panlobular, or, D, paraseptal phenotypes of emphysematous destruction. A, Micro-CT image of control lung shows a terminal bronchiole (white arrow) connecting to respiratory bronchiole (green arrow) supplying alveoli of normal size. B, Extensive centrilobular destruction (arrowheads) is seen in lung slice, and micro-CT scan of primary lesion shows dilatation and destruction of proximal respiratory bronchioles (green arrow), with sparing of alveoli near lobular septa (blue arrow). Moreover, terminal bronchiole leading into centrilobular lesion is narrowed (yellow arrow) and then opens up again (white arrow), a feature that can be better appreciated in video associated with the article by McDonough et al (7). C, In contrast, the panlobular phenotype of emphysema in this case of α1-antitrypsin deficiency shows relatively mild destruction of gross specimen (arrowheads), and micro-CT scan shows uniform destruction of alveoli extending right up to lobular septa (blue arrow). Terminal bronchiole (white arrow) and respiratory bronchiole (green arrow) are normal. D, Paraseptal phenotype of emphysema shows typical lesions (arrowheads) beneath pleural surface on gross specimen, and micro-CT scan shows that alveoli adjacent to lobular septa are dilated and destroyed, with sparing of center of lobule. Terminal bronchiole (white arrow) and respiratory bronchiole (green arrow) are normal. Images from control lung and lung affected by PSE came from organ donors and were released for research when judged to be unsuitable for transplantation, whereas lungs affected by CLE and panacinar emphysema were donated by patients treated by means of lung transplantation. The protocol for the preparation of the specimens is fully described in reference 7. x on A, C, and D indicates interlobar fissure(s).

Figure 3:

Mild CLE. CT scan in patient with GOLD stage I COPD shows scattered centrilobular lucencies, separated by large regions of normal lung, involving an estimated 0.5% of upper lung zone.

Figure 4:

Moderate CLE. CT scan in patient with GOLD stage I COPD shows many well-defined centrilobular lucencies that occupy more than 5% of upper lung zone. PSE is seen in anteromedial right and left lungs.

Figure 5:

Confluent CLE. CT scan in patient with GOLD stage I COPD shows multiple lucencies that span several secondary pulmonary lobules (circled in left lung) but are not associated with extensive hyperexpansion of secondary pulmonary lobules or distortion of pulmonary architecture.

Figure 6:

Advanced destructive emphysema. CT scan in patient with GOLD stage I COPD shows hyperexpansion of secondary pulmonary lobules with distortion of pulmonary architecture.

Figure 7:

PLE related to α1-antitrypsin deficiency. CT scan through lower lungs shows widespread confluent areas of hyperlucency spanning one or several lobules. Some lobules, outlined by intact interlobular septa, appear hyperexpanded (arrowheads).

Figure 8:

Mild PSE. CT scan in smoker without COPD shows subpleural foci of low attenuation separated by intact interlobular septa along the mediastinum (arrows), measuring less than 1 cm.

Figure 9:

Substantial PSE. CT scan in patient with GOLD stage I COPD shows numerous well-demarcated areas of subpleural emphysema along chest wall and mediastinal pleural margins.

Figure 10:

Normal bronchial walls. CT scan in asymptomatic nonsmoker with normal spirometric findings demonstrates normal airways.

Figure 11:

Bronchial wall thickening. CT scan in cigarette smoker demonstrates marked thickening of segmental and subsegmental airways but no emphysema.

Figure 12:

Widespread small centrilobular nodules. Centrilobular nodules (circled) in cigarette smoker are suggestive of respiratory bronchiolitis. Mild CLE and PSE are also present.

Figure 13a:

Gas trapping at expiratory CT. (a) Inspiratory and (b) expiratory CT scans in patient with severe airway obstruction (GOLD stage III) but only minimal emphysema. Lung attenuation fails to increase on expiratory scan, which is indicative of diffuse gas trapping owing to small airway obstruction.

Figure 13b:

Gas trapping at expiratory CT. (a) Inspiratory and (b) expiratory CT scans in patient with severe airway obstruction (GOLD stage III) but only minimal emphysema. Lung attenuation fails to increase on expiratory scan, which is indicative of diffuse gas trapping owing to small airway obstruction.

Figure 14:

CT-defined subtypes of COPD. Most subjects with emphysema have significant airway disease. Airway-predominant disease represents subjects with minimal or no emphysema as defined at quantitative CT (QCT ). * =There is a group of subjects without visually defined emphysema who have more than 6% of pixels less than −950 HU at quantitative CT. Further work is needed to understand the importance of this finding, and these individuals cannot currently be classified. A1AT = α1-antitrypsin.