ABSTRACT
Since the recognition of ventilator-induced lung injury (VILI) as a clinically
relevant entity, the effects of deforming stress on lung structure and function have been examined in literally hundreds of experimental studies
(1-4). In many instances, diverse morphologic and biologic sequelae of
deforming stress have been referred to under the single term ‘‘lung injury,’’
and a number of scoring systems have been devised to grade its severity
(5-8). However, as the appreciation for specific injury mechanisms has
grown, so has the realization that the lungs’ responses to injurious stress
can be quite nuanced and nonuniform with respect to space and time. In
fact, in 1998, Tremblay and Slutsky coined the term ‘‘biotrauma’’ to precisely underscore this point (9). Because it would be naive to assume that
the many distinct manifestations of biotrauma contain identical prognostic
or mechanistic information, it would seem prudent to differentiate between
specific pulmonary stress responses. After all, the term ‘‘injury’’ has been
used to describe biologic responses ranging from altered gene expressions,
protein synthesis and release, abnormal respiratory mechanics, inefficient
gas exchange, and impaired vascular barrier properties to the remodeling of lung structures and scar formation.
