Acute respiratory distress syndrome (ARDS)

Essential Evidence

Last Updated on 2019-12-03 © 2019 John Wiley & Sons, Inc.

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Authors:
Jennifer L. Good, MD, Associate Director Altoona Family Physicians, Altoona Regional Health System

Editors:
Kenny Lin, MD, MPH, Professor of Family Medicine, Georgetown University
Linda French, MD, Professor and Chair, Department of Family Medicine, University of Toledo
Gary Ferenchick, MS, MD, Professor of Medicine, Michigan State University

Overall Bottom Line

  • Brain natriuretic peptide (BNP) is helpful in differentiating acute respiratory distress syndrome (ARDS) from cardiogenic pulmonary edema. C
  • In patients with indeterminate levels of BNP, echocardiogram or pulmonary artery catheterization may be required to make the diagnosis of ARDS. C
  • Ventilatory strategies using lower tidal volumes (6 mL/kg) and lower airway pressures (end-expiratory plateau pressure of <30 cm H2O) have been associated with lower mortality from ARDS and have decreased the length of time required for mechanical ventilation. A
  • There is some evidence that corticosteroids can reduce mortality and time on the ventilator. B

Background

ARDS is a severe manifestation of acute lung injury (ALI). ALI is defined as a syndrome of acute and persistent lung inflammation with increased vascular permeability. 16

Incidence

  • A prospective multicenter cohort study indicated that ALI was more common than previously thought, with an age-adjusted incidence of 86.2 per 100,000 patient years and a mortality of 38%.
  • Extrapolation of these data suggests 190,600 cases of ALI per year, associated with 74,000 deaths. 15

Other Impact

  • Among ICU patients, 10% to 15% of all patients meet criteria for ARDS, and up to 20% of intubated patients meet criteria for ARDS.

Causes of the Condition

  • Sepsis (the most common cause of ARDS)
  • Aspiration of gastric contents
  • Infectious pneumonia
  • Severe trauma and surface burns
  • Massive blood transfusion
  • Transfusion-related lung injury (TRALI)
  • Relief of upper airway obstruction
  • Lung or bone marrow (and stem cell) transplantation
  • Drug overdose (aspirin, cocaine, opioids, phenothiazines, tricyclic antidepressants)
  • Idiosyncratic drug reactions (protamine, nitrofurantoin, many chemotherapeutic agents)

Pathophysiology

  • The exudative phase is the initial pathologic state, which is characterized by diffuse alveolar damage due to inflammatory injury. This is manifest by proteinaceous fluid in the alveoli and functional loss of surfactant leading to alveolar collapse. The consequences of this lung injury are impaired gas exchange, decreased pulmonary compliance, and pulmonary hypertension.
  • The proliferative phase occurs over the first week as there is resolution of alveolar edema and the hyperplasia of type II pneumocytes, interstitial myofibroblasts, and deposition of interstitial collagen.
  • The fibrotic phase is a third phase not seen in all patients and is characterized by disruption of lung architecture, diffuse lung fibrosis, and cyst formation.