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Crazy paving | Radiology Signs

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What causes the crazy paving pattern in the lungs on high-resolution computed tomography?

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The crazy paving pattern represents a nonspecific radiological finding characterized by the superimposition of patchy or diffuse ground-glass opacities with septal thickening on thin-section CT images. This pattern can result from multiple pathological processes affecting the lung parenchyma and interstitium. The differential diagnosis is broad and includes cardiogenic pulmonary edema, diffuse alveolar damage (often in the subacute phase), diffuse alveolar hemorrhage (particularly in the resolution phase after 7-10 days), various infections (including viral pneumonia, mycoplasma, CMV, influenza, and pneumocystis), eosinophilic pneumonia (acute eosinophilic pneumonia and eosinophilic granulomatosis with polyangiitis), pulmonary alveolar proteinosis, hypersensitivity pneumonitis, sarcoidosis, neoplastic disorders, and inhalational diseases. The appearance can originate from either interstitial pathology with thickened intralobular and interlobular septa or from airspace disease with linear deposition of material within the alveolar spaces.

Why is it called so?

The pattern is named for its visual resemblance to a crazy-paving or irregular street pavement, where the linear septal thickening creates an irregular network overlying the ground-glass opacities, mimicking the appearance of irregularly placed paving stones.

Pathophysiology

The crazy paving pattern develops through the combination of two radiological processes occurring simultaneously. Ground-glass opacities result from filling of alveolar spaces with fluid, blood, cells, or protein, or from interstitial thickening and inflammation that partially obscures the lung parenchyma. Septal thickening develops as the interlobular and intralobular septa undergo edema, fibrosis, or cellular infiltration. When these processes occur together, the superimposition creates the characteristic crazy paving appearance. The underlying mechanism varies by etiology: in cardiogenic pulmonary edema, hydrostatic forces cause fluid accumulation in both alveolar and interstitial spaces; in diffuse alveolar hemorrhage, blood fills alveoli and thickens septa; in infection, inflammatory exudates and cellular infiltrates create both components; and in pulmonary alveolar proteinosis, lipoproteinaceous material accumulates within alveolar spaces with associated septal involvement.

Alternative names: The sign is sometimes referred to as demonstrating a superimposition of ground-glass attenuation with interlobular septal thickening and intralobular lines.

 

 

 

 

 

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