Background: Echographic vertical artifacts (B-lines) in chest ultrasonography have often been associated with pathological patterns. A scientifically sound explanation of these artifacts has not yet been proposed. Objectives: The ‘spongy' nature of the lung in its liquid and solid components and the changes that take place in peripheral airspace (PAS) geometry might be the key point to understanding these phenomena. Methods: Six excised right rabbit lungs were obtained. Each lung underwent direct ultrasound evaluation in two different conditions: at complete tissue elastic recoil volume and at pulmonary expansion volume achieved by applying a constant positive pressure of 12 cm H₂O. Lung volumes and densities were reported in both conditions. Histological examination was performed on three naturally collapsed lungs and on three lungs under positive pressure inflation after having been fixed in formalin solution. Results: Mean volumes of naturally collapsed lungs and fixed expanded lungs were 11.2 ± 0.36 and 44.83 ± 3.03 ml, respectively. Mean densities were 0.622 ± 0.016 and 0.155 ± 0.007 g/ml, respectively. Ultrasound evaluation of collapsed lungs showed dense vertical artifacts and a ‘white lung' pattern, while the evaluation of expanded lungs showed hyperechoic line and horizontal artifacts of reflection. Histological evaluation showed a different PAS geometry in collapsed lungs caused by alveolar size reduction and shape changes with unfolded and closed units modifying the peripheral porosity of the frothy nature of the lung. Conclusions: Airspace geometry, frothy nature and porosity are the determinants of the different behavior of ultrasound interacting with the subpleural lung parenchyma. Chest ultrasound may thus be interpreted as an indirect ‘estimator' of lung porosity.

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TNF-α expression in DD seems to be related to the severity of the disease. In particular, it appears to be overexpressed in DD with inflammation (AUD and SUDD) compared with DD without (AD).

Five type A patients taking therapy (83.33%), two type A not taking therapy (50%), all type C patients (100%), five type B patients (62.5%) and none of type D (0%) were under continuous remission at the end of the follow-up. All type D patients required further steroid course to obtain remission, and two patients required azathioprine to maintain remission. INTERPRETATIONS/CONCLUSIONS: SCAD B and D patients fail to maintain long-term remission, often requiring immunosuppressive treatment. SCAD A and C patients show a more benign course; however, long-term treatment guarantees longer remission also in those patients.

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