Abstract

Ultrasound lung comets (ULCs) now have an acknowledged correlation with extravascular lung water, but they present in different orders and numbers in different pathologic pulmonary entities. How these artifacts are created is not yet known, and the literature gives discordant hypotheses. Understanding their formation is the first step in understanding lung disease. The purpose of this study was to show the morphologic and genetic variability of interstitial lung disease studied with echography and thus to propose a unitary mechanism for the formation of ULCs. This study included 3 parts: (1) a retrospective analysis of echographic lung images of patients with interstitial syndrome; (2) an analysis of the literature for definitions of the size of the pulmonary lobule; and (3) an experimental model of different air-water interfaces scanned with varying ultrasonic frequencies. The retrospective analysis of echographic lung images included 176 patients with diffuse ULCs: 118 patients had acute pulmonary edema; 18 had acute lung injury/acute respiratory distress syndrome; and 40 were premature neonates with respiratory distress syndrome. Experimental models permitted us to discover that ring-down artifacts are produced only by single and double layers of bubbles in specific structural settings. Reverberation between bubbles with a critical radius seems to be at the origin of ring-down artifacts. Echographic manifestations of interstitial lung disease, whose genesis lies in the partial air loss of lobes and segments, are acoustic phenomena originating from variations in the tissue-fluid relationship of the lung. A correlation between anatomopathologic characteristics and structures of sonographic artifacts could allow more rapid and noninvasive diagnoses.

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