Morphological Changes in Adult Respiratory Distress Syndrome: Experimental and Clinical Data

Abstract

Adult respiratory distress syndrome (ARDS) (Fig. 1) is the pulmonary manifestation of a diffuse microcirculatory injury that causes exudation of a protein-rich fluid into the pulmonary interstitium and alveolar space. This statement by Meduri et al. (1991) is a very adequate characterization of the morphologic development of ARDS. During trauma, there are short intervals characterized by morphologic alterations that precede typical ARDS, e.g., the stage of “lung in shock” which constitutes the substrate for microcirculatory injury and may reoccur in ARDS itself with stronger intensity. During “early organ failure lung,” actual microcirculatory injury, reflected by the coinvolvement of the alveolar space, may also constitute the morphologic substrate for the subsequent development of ARDS, which is still associated with a mortality of 60%–70% (Bell et al. 1983; Montgomery et al. 1985). The characteristic inflammatory fibrotic process is seen at a later point of time and may be the cause of permanent lung damage.