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Nonventilatory Interventions in ALI/ARDS: Recent Work

injury, presence of chronic comorbidities, and nonpulmonary organ failures. The problem of severe hypoxemia has inspired methods to improve gas exchange by mechanical ventilation or nonventilatory interventions. Yet interventions that improve hypoxemia have not improved survival. The only intervention that improves survival for patients with ALI/ARDS is a protocol of low tidal volume ventilation, and low tidal volume ventilation initially worsens oxygenation but improves systemic inflammation (plasma interleukin-6). This suggests that reducing lung and systemic inflammation might be a greater priority than short-term improvement in gas exchange. Four decades of research in lung injury and repair have identified multiple cellular and molecular alterations that may be potential targets for interventions. What quantities of inflammation and fibroproliferation are necessary to regenerate functional lung remains unknown. Lung injuries that result from different causes, such as viruses, bacteria, aspiration, or trauma, share common pathological features but also have distinct cellular and biochemical changes and time courses of injury and repair. Changes in numerous mediators (cytokines, growth factors, chemokines, leukotrienes, heat shock proteins, oxidants, antioxidants, matrix proteins, adhesion molecules, and apoptotic factors) and cell types (neutrophils, T cells, macrophages, alveolar type I and II cells, endothelial cells, fibroblasts) are observed in injury and repair. Given the multiple etiologies of acute lung injury, diverse patient characteristics, and numerous interacting inflammatory mediators, it seems unlikely that a single intervention will be curative in all patients. Corticosteroid is a potent anti-inflammatory and antifibrotic agent with widespread and incompletely characterized effects in patients with acute lung injury (ALI)/ARDS. However, no trial has demonstrated a Managing patients with acute respiratory distress syndrome remains a challenge. We have learned much in only 40 years since Ashbaugh and co-workers coined the term acute respiratory distress syndrome (ARDS). In this issue of the Journal of Intensive Care Medicine, Schuster, Alouidor, and Barquist guide us through a collection of contemporary works of clinical research in ARDS. The authors describe and compare studies that influence current clinical practice and predict interventions that may appear in clinical use. The pattern of damage to lung tissue and cells in ARDS resembles pathological features of acute and chronic lung injury, whether injury is caused by trauma, inhalation, acid aspiration, endotoxin, or other provocations. Lung injury leads to inflammation, edema, and neutrophil influx. All components of the alveolus are affected: alveolar epithelial (type I) cells are lost and alveolar type II cells proliferate; the alveolar interstitium becomes filled with edema, neutrophils, and mesenchymal cells; capillaries surrounding alveoli become obliterated by thrombi and fibrosis. Within a week, fibroblast proliferation begins, followed by collagen deposition and healing that often restore the lung to normal structure and function. Lung injury is frequently associated with systemic inflammation and multiple-organ dysfunction associated with lung-derived inflammatory mediators. Survival is not dependent on the severity of hypoxemia but rather on the cause of the lung