What Is the Acute Respiratory Distress Syndrome?

Abstract

It has been known for decades that shock and sepsis can cause a syndrome of acute respiratory failure with characteristics of non-cardiogenic pulmonary edema. Over the years, this syndrome has been given a number of names, including congestive atelectasis, traumatic wet lung, and shock lung. In 1967 the modern counterpart to this syndrome was described and subsequently called the "acute respiratory distress syndrome" (ARDS). This syndrome results from lung injury and inflammation. As with inflammation elsewhere, ARDS is accompanied by many cellular and molecular processes, some of them specific to the syndrome, others perpetuating the syndrome, and others inactivating the by-products of inflammation. Since no specific clinical sign or diagnostic test has yet been described that identifies ARDS, its diagnosis is based on a constellation of clinical, hemodynamic, and oxygenation criteria. Current ARDS treatment is mainly supportive, since these patients frequently have coexisting conditions. Although in 1994 a new standard ARDS definition was accepted, that definition failed to standardize the measurement of the oxygenation defect and does not recognize different severities of pulmonary dysfunction. Based on current evidence there is a need for a better definition and classification system that could help us to identify ARDS patients who would be most responsive to supportive therapies and those unlikely to benefit because of the severity of their disease process. This paper examines our current understanding of ARDS and discusses why the current definition may not be the most appropriate for research and clinical practice.

Biomarkers for the acute respiratory distress syndrome: how to make the diagnosis more precise

“…The acute respiratory distress syndrome (ARDS) is an acute inflammatory process of the lungs caused by direct or indirect insults to the alveolar-capillary membrane (1)(2)(3)(4)(5), and is associated with an overall mortality ranging from 35% to 50% (6). Pathologically, ARDS is characterized by diffuse alveolar damage (DAD) with injury to the epithelium and endothelium as well as interstitial and alveolar protein-rich edema, inflammatory cellular infiltration, atelectasis, capillary thrombosis, neovascularization, and pulmonary fibrosis (7).…”

“…Clinically, this syndrome is defined by acute hypoxemia and bilateral pulmonary infiltrates, in the absence of congestive heart failure. As with other inflammatory process in the body, lung injury in ARDS is accompanied by several biochemical and cellular processes; some might initiate the syndrome, others might perpetuate it, and others could inactivate the inflammatory mediators (4).…”

Should the ART trial change our practice?

“…Caused by pulmonary or systemic insults, is characterized clinically by hypoxemia that does not respond to the administration of high concentrations of oxygen (FiO 2 ) and by the presence of bilateral infiltrates on chest imaging due to high-permeability pulmonary edema (1). An integral part of the supportive therapy of ARDS is the application of mechanical ventilation (MV).…”

Inhibition of endotoxin-induced airway epithelial cell injury by a novel family of pyrrol derivates

“…1,2 Sepsis is the most common predisposing factor and sepsisassociated ARDS has a higher disease severity, poorer recovery from acute lung injury, and higher mortality compared with non-sepsis-related ARDS. 3 Bacterial lipopolysaccharide (LPS), also termed endotoxin, is the major component of the outer membrane of Gram-negative bacteria and one of the major pathogen-associated pattern recognition molecules that activate the innate immunity.…”