“…4,44 Finally, in hyaline membrane disease of the neonate, it is possible that an immature lung, anatomically structured with small, wet, and homogeneous distal airways (pseudoglandular and saccular phases of development, hyaline membranes, and atelectasis), could induce massive internal reverberations with mechanisms like the ones observed in our experiment in the 3-dimensional layer of smaller bubbles. 45 Evidence found in the past and recent literature and the finding of different densities and arrangements of B-lines confirm the genetic hypothesis of Lichtenstein et al 8 to be reductive because it only includes a minority of cases of interstitial syndrome in a spectrum of acoustic representations ranging from septal syndrome to echographic white lung. 3,4,16,38 Although convincing in some cases of cardiogenic pulmonary edema, ULCs are rarely distributed so purely and regularly and are rarely able to signal an effective anatomic distance between interlobular septa, which, as we found, are actually separated by 10 to 30 mm.…”