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The acute respiratory distress syndrome
Michael A. Matthay, … , Lorraine B. Ware, Guy A. Zimmerman
Michael A. Matthay, … , Lorraine B. Ware, Guy A. Zimmerman
Published August 1, 2012
Citation Information: J Clin Invest. 2012;122(8):2731-2740. https://doi.org/10.1172/JCI60331.
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Review Series

The acute respiratory distress syndrome

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Abstract

The acute respiratory distress syndrome (ARDS) is an important cause of acute respiratory failure that is often associated with multiple organ failure. Several clinical disorders can precipitate ARDS, including pneumonia, sepsis, aspiration of gastric contents, and major trauma. Physiologically, ARDS is characterized by increased permeability pulmonary edema, severe arterial hypoxemia, and impaired carbon dioxide excretion. Based on both experimental and clinical studies, progress has been made in understanding the mechanisms responsible for the pathogenesis and the resolution of lung injury, including the contribution of environmental and genetic factors. Improved survival has been achieved with the use of lung-protective ventilation. Future progress will depend on developing novel therapeutics that can facilitate and enhance lung repair.

Authors

Michael A. Matthay, Lorraine B. Ware, Guy A. Zimmerman

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Figure 1

Chest radiograph of a patient with influenza-related pneumonia that illustrates early ALI, which progressed over 48 hours to more classic ALI that required positive-pressure ventilation.

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Chest radiograph of a patient with influenza-related pneumonia that illu...
(A) Anterior-posterior portable chest radiograph of a previously healthy 41-year-old man who presented to the emergency department with a 2-day history of myalgias and fever, a productive cough, and shortness of breath. Chest auscultation revealed rales and rhonchi posteriorly in both lung fields. The chest radiograph demonstrates patchy infiltrates in the right lower lung field and also in the left lower lung field. (B) Anterior-posterior chest radiograph 48 hours after the chest radiograph in A, 1 hour after endotracheal intubation (arrow) and initiation of positive-pressure ventilation using the ARDS Network lung-protective ventilation protocol (97). There was marked progression of the bilateral radiographic infiltrates, with dense consolidation in the right upper, right lower, and left lower lung zones. The patient’s hypoxemia steadily worsened during the 48 hours following his initial presentation, accompanied by an increase in respiratory rate to 40 breaths/minute. Diagnostic evaluation confirmed H1N1 influenza infection. All cultures for bacteria were negative. Recent clinical investigation indicates that it is possible in some patients to diagnose ALI in an early phase (9), as shown in A, well before the progression of acute respiratory failure to the need for mechanical ventilation, as illustrated in B. Earlier diagnosis of ALI could facilitate testing of therapeutic strategies that may have time-dependent efficacy prior to the development of established ALI that requires intubation and mechanical ventilation.
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