Vs Air in airspaces Interstitial lung and small airways tissues Wall of the alveoli Small airways Capillaries, blood in these
Reduction in the volume (expansion) of the airspaces Partial or total replacement of the air in the airspaces by fluid or cells
Increase in blood flow and blood volume in vessels Thickening of the interstitial tissues and of the alveolar wall
Degree of Opacification
Ground-glass opacity - hazy increase in lung opacity that does not obscure the underlying vessels and bronchi Lung consolidation or consolidation - vessels and bronchial walls are obscured
Increased lung attenuation that have a density that is greater than soft tissue density
Development of calcifications within existing lesions Deposition of calcium within the lung parenchyma Diffuse or multifocal pulmonary ossification
GGO located near centre of the secondary pulmonary lobules and then look like ill-defined nodules
Prone scans Dependent density is no longer visible against the posterior chest wall and may appear against the anterior chest wall
Partial filling of the alveolar spaces + Thickening of the interstitium, alveolar walls = Crazy paving
Alveolar proteinosis Areas of ground-glass opacity with intralobular reticular pattern superimposed creating the crazy-paving pattern
Mosaic perfusion
Decreased attenuation Increased lung attenuation
Narrowing or obstruction of the blood vessels Small airways narrowing Reflex vasoconstriction
GGO Vs Mosaic perfusion Calibre of the blood vessels Delineation of the ground-glass opacity Density changes after deep expiration
Thickening of Parenchymal Interstitium / Alveolar Wall Minimal thickening of the alveolar wall, parenchymal interstitium = groundglass opacity Inflammation or infiltration Intraalveolar cellular infiltrate, filling the airspaces Acute inflammation i.e indicating active disease or reactivation of disease
GGO
Fibrosis and result from fibrotic thickening of the alveolar wall and interstitium
Usual interstitial pneumonia in Systemic sclerosis GGO in the dorsal and basal subpleural region of both lungs, i.e active lung disease
When a lung biopsy is performed, areas of ground-glass opacity are the best locations to be targeted, especially when no signs of fibrosis are present
Diffuse ground-glass opacity in chronic hypersensitivity pneumonitis Bronchial deformation indicates pulmonary fibrosis
Crazy-Paving Pattern
Superposition of a linear pattern on groundglass opacity = Crazy paving Pulmonary alveolar proteinosis
Acute radiation pneumonitis in a patient treated for leftsided breast cancer Ground-glass opacity and consolidation Faint intralobular reticular pattern Crazy-paving pattern
Lung Consolidation
Increase in lung density with obscuration of the underlying vessels & bronchial walls Bronchi can be recognised as an air bronchogram, i.e. low-density branching tubular structures Lung consolidation are similar to the lung changes that are responsible for ground-glass opacity
Most frequent cause is a decrease in the amount of air in the airspaces Replacement of this air by fluid, cells, tissue or other substances Interstitial pneumonia (UIP) Sarcoidosis
Consolidation margins
Consolidation has one or more sharply defined borders because the pathology reaches an anatomic structure such as a fissure Borders of consolidation that are not adjacent to the fissure may be,
Sharply defined Irregular and blurred Possibly surrounded with ground-glass opacity
Airspace filling is the most frequent cause of consolidation, this pattern is often associated with,
presence of centrilobular airspace nodules - early airspace filling, i.e bronchial distribution
Metastatic calcification
Deposition of calcium typically within the parenchymal, peribronchovascular interstitium
Hypercalcaemia abnormal calcium and phosphate metabolism Chronic renal failure Secondary hyperparathyroidism
Areas of GGO with calcification that may be inconspicuous or very dense or present as patchy areas of consolidation Consolidated lung parenchyma appears abnormally dense
Metastatic calcification in consolidated lung in chronic renal failure and secondary hyperparathyroidism