Abstract

Acute respiratory distress syndrome (ARDS) is a clinically and biologically heterogeneous disorder associated with many disease processes that injure the lung, culminating in increased non-hydrostatic extravascular lung water, reduced compliance, and severe hypoxemia. Despite enhanced understanding of molecular mechanisms, advances in ventilatory strategies, and general care of the critically ill patient, mortality remains unacceptably high. The Berlin definition of ARDS has now replaced the American-European Consensus Conference definition. The recently concluded Large Observational Study to Understand the Global Impact of Severe Acute Respiratory Failure (LUNG-SAFE) provided worldwide epidemiological data of ARDS including prevalence, geographic variability, mortality, and patterns of mechanical ventilation use. Failure of clinical therapeutic trials prompted the investigation and subsequent discovery of two distinct phenotypes of ARDS (hyper-inflammatory and hypo-inflammatory) that have different biomarker profiles and clinical courses and respond differently to the random application of positive end expiratory pressure (PEEP) and fluid management strategies. Low tidal volume ventilation remains the predominant mainstay of the ventilatory strategy in ARDS. High-frequency oscillatory ventilation, application of recruitment maneuvers, higher PEEP, extracorporeal membrane oxygenation, and alternate modes of mechanical ventilation have failed to show benefit. Similarly, most pharmacological therapies including keratinocyte growth factor, beta-2 agonists, and aspirin did not improve outcomes. Prone positioning and early neuromuscular blockade have demonstrated mortality benefit, and clinical guidelines now recommend their use. Current ongoing trials include the use of mesenchymal stem cells, vitamin C, re-evaluation of neuromuscular blockade, and extracorporeal carbon dioxide removal. In this article, we describe advances in the diagnosis, epidemiology, and treatment of ARDS over the past decade.

Highlights

  • Described over 50 years ago[1], acute respiratory distress syndrome (ARDS) remains a devastating manifestation of heterogeneous disease processes that injure the lung and cause non-hydrostatic pulmonary edema[2,3]

  • Diagnosis The first concerted effort to define ARDS as a clinical syndrome appeared in 1988, when Murray et al assigned points to the chest radiograph, partial pressure of oxygen/fraction of inspired oxygen (P/F) ratio, applied positive end expiratory pressure (PEEP), and lung compliance to create a lung injury score that ranged from 0 to 410

  • The American European Consensus Conference (AECC) defined ARDS as the acute onset of hypoxemia with bilateral infiltrates on a frontal chest radiograph, with no clinical evidence of left atrial hypertension and a P/F ratio of less than or equal to 200 mmHg

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Summary

Invited Reviewers

F1000 Faculty Reviews are written by members of the prestigious F1000 Faculty. They are commissioned and are peer reviewed before publication to ensure that the final, published version is comprehensive and accessible. The reviewers who approved the final version are listed with their names and affiliations. Any comments on the article can be found at the end of the article

Introduction
Syndrome Subphenotypes Respond Differently to Randomized Fluid
Writing Group for the Alveolar Recruitment for Acute Respiratory Distress
Extracorporeal Circulation the Future of Acute Respiratory Distress Syndrome
Findings
Open Peer Review
Full Text
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