Among his many other prescient observations, in 1821, René Laennec described the appearance of edema in postmortem lung specimens.1 Using only his natural senses, he concluded that there were two pathophysiologically distinct forms of lung edema. One form was associated with pathology of the heart and, he concluded, was due to heart failure. The other form appeared in the absence of cardiac pathology, and Laennec called it “primary or idiopathic” pulmonary edema. Those observations were probably the first descriptions of the gross pathologic characteristics of hydrostatic pulmonary edema and permeability pulmonary edema—the latter being the clinical syndrome identified more than a century later as acute respiratory distress syndrome (ARDS). Laennec’s seminal contributions to the understanding of pulmonary edema were limited to gross pathologic observations, whereas greater understanding required technical advancements to study lung structure and function and keen interest from expert physiologists in the movement of fluid and solutes among anatomic compartments.
Noncardiogenic pulmonary edema refers to acute pulmonary edema that is caused by increased pulmonary capillary permeability due to direct or indirect injury to the lung. A decrease in the reflection coefficient of Starling’s law is the main mechanism that leads to the development of noncardiogenic pulmonary edema, manifest clinically as breakdown of the alveolocapillary barrier. This is in contrast to caiogenic pulmonary edema, where elevated hydrostatic pressure is responsible for fluid accumulation. There are many causes of noncardiogenic edema, with the most common cause being acute respiratory distress syndrome (ARDS). Common clinical characteristics that can aid in the diagnosis of noncardiogenic pulmonary edema are listed here.