Mosaic Attenuation: Pulmonary Detection and Clinical Value

Mosaic attenuation is a radiologic pattern seen on high-resolution CT scans of the lungs, characterized by patchy areas of differing lung density. It is not a diagnosis but a clue suggesting underlying airway, vascular, or interstitial lung disease. Recognizing this pattern is essential for guiding further evaluation and management.

Determining the cause requires careful interpretation of imaging findings alongside clinical history and additional diagnostic tests.

Identifying Characteristics in Imaging

Mosaic attenuation appears on high-resolution computed tomography (HRCT) as a patchwork of lung regions with varying densities, reflecting differences in ventilation, perfusion, or parenchymal integrity. This pattern results from heterogeneous involvement of the pulmonary architecture, where alternating areas of normal and abnormal lung tissue create a striking contrast. The key to interpretation lies in distinguishing whether density variations stem from small airway obstruction, vascular pathology, or interstitial processes.

A defining feature of mosaic attenuation is its behavior on expiratory imaging. On inspiratory scans, affected regions may appear subtly different in density, but during expiration, areas of air trapping become more pronounced, remaining lucent while normally ventilated lung parenchyma increases in attenuation. This change is particularly useful in identifying small airway diseases such as obliterative bronchiolitis, where impaired airflow leads to persistent hypodense regions. In contrast, vascular causes, such as chronic thromboembolic pulmonary hypertension (CTEPH), exhibit relatively unchanged attenuation differences between inspiratory and expiratory phases, as the issue lies in perfusion rather than ventilation.

The distribution of mosaic attenuation also provides diagnostic clues. Airway diseases often present a diffuse or patchy pattern without a clear lobar predilection, whereas vascular causes follow a more segmental or lobar distribution, corresponding to areas of altered perfusion. Associated findings, such as bronchial wall thickening, centrilobular nodules, or dilated pulmonary arteries, further refine the differential diagnosis. In hypersensitivity pneumonitis, for example, mosaic attenuation frequently appears alongside ground-glass opacities and air trapping, reflecting a combination of interstitial inflammation and small airway involvement.

Variations in Airway vs Vascular Disorders

Distinguishing between airway and vascular causes of mosaic attenuation requires an understanding of how each condition alters pulmonary structure and function. Airway diseases involve obstruction, inflammation, or remodeling of the bronchioles, leading to impaired ventilation and air trapping. Vascular disorders primarily affect perfusion, resulting in regions of reduced or absent blood flow that manifest as areas of altered lung density.

Small airway diseases, such as obliterative bronchiolitis, exemplify the ventilatory causes of mosaic attenuation. Inflammation and fibrosis narrow the bronchioles, preventing adequate gas exchange in affected regions. The hallmark of this pathology is air trapping, which becomes evident on expiratory HRCT when diseased areas fail to increase in attenuation due to retained air. Additional indicators, such as centrilobular nodules or bronchial wall thickening, support an airway-centered pathology. Conditions like hypersensitivity pneumonitis and respiratory bronchiolitis-associated interstitial lung disease (RB-ILD) contribute to a similar pattern through inflammatory processes affecting both the bronchioles and adjacent parenchyma.

Vascular etiologies present a distinct mechanism of mosaic attenuation driven by perfusion abnormalities. In chronic thromboembolic pulmonary hypertension (CTEPH), persistent emboli obstruct pulmonary arteries, leading to regional hypoperfusion. Unlike airway-related mosaic attenuation, these density variations remain unchanged between inspiratory and expiratory phases. Other vascular conditions, such as pulmonary veno-occlusive disease (PVOD) and pulmonary arterial hypertension (PAH), also contribute by altering vascular resistance and capillary recruitment. Findings like enlarged pulmonary arteries, right ventricular hypertrophy, or interlobular septal thickening help differentiate vascular pathology from airway disease.

Diagnostic Criteria and Techniques

Evaluating mosaic attenuation requires integrating imaging findings with clinical context and adjunct diagnostic tools. High-resolution computed tomography (HRCT) remains the cornerstone for detection, offering detailed visualization of regional density variations. However, a definitive diagnosis relies on differentiating mosaic attenuation from other patterns, such as ground-glass opacities or reticular changes. Expiratory CT scans are particularly valuable, highlighting air trapping in small airway diseases while leaving vascular abnormalities unchanged.

Beyond HRCT, pulmonary function testing (PFT) provides complementary insights by quantifying airflow limitation and gas exchange abnormalities. In suspected small airway disease, a reduced forced expiratory flow at 25–75% of vital capacity (FEF25-75) can indicate early obstruction. For vascular disorders, diffusion capacity for carbon monoxide (DLCO) may be diminished, reflecting impaired pulmonary perfusion. When imaging and functional tests suggest a vascular etiology, ventilation-perfusion (V/Q) scintigraphy can further delineate perfusion deficits, particularly in chronic thromboembolic pulmonary hypertension (CTEPH), where unmatched perfusion defects are characteristic.

Bronchoscopy with transbronchial biopsy or bronchoalveolar lavage (BAL) may be necessary when histopathologic confirmation is required. BAL fluid analysis can reveal inflammatory profiles suggestive of hypersensitivity pneumonitis or respiratory bronchiolitis, while biopsy samples help distinguish interstitial lung diseases from airway-centered processes. In vascular disorders, right heart catheterization assesses pulmonary arterial pressures and confirms conditions such as pulmonary arterial hypertension (PAH) or pulmonary veno-occlusive disease (PVOD). This invasive procedure provides hemodynamic data essential for accurate classification of pulmonary hypertension subtypes.

Significance in Clinical Assessment

Recognizing mosaic attenuation on high-resolution CT scans helps refine differential diagnoses and guide further evaluation. Its presence often signals a need for targeted testing, particularly when symptoms such as unexplained dyspnea, chronic cough, or exercise intolerance are present. Careful correlation of imaging findings with patient history and laboratory results helps narrow diagnostic possibilities and avoid unnecessary investigations.

The prognostic implications of mosaic attenuation depend on the underlying disease. In chronic airway disorders, persistent air trapping may indicate progressive small airway remodeling, leading to irreversible airflow limitation. In vascular diseases, the extent of perfusion abnormalities can reflect disease severity and guide treatment decisions. In CTEPH, for instance, the degree of perfusion mismatch on imaging correlates with pulmonary hemodynamics, influencing eligibility for therapies such as pulmonary endarterectomy or balloon pulmonary angioplasty. These therapeutic decisions rely not only on radiologic findings but also on functional assessments, reinforcing the importance of a comprehensive clinical approach.