Acute respiratory distress syndrome historical perspective

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Historical Perspective

Although the first pathologic descriptions of what was likely ARDS date back to the 19th century, our understanding of the distinct pathophysiologic features of ARDS evolved alongside the development of medical technologies that facilitated a more in-depth study of the syndrome. The advent of radiography permitted visualization of the bilateral pulmonary infiltrates (originally termed double pneumonia), while the development of arterial blood gas measurement and positive-pressure mechanical ventilation allowed for identification of the impaired oxygenation and reduced lung compliance that are now recognized as central features of ARDS.[1]

Ashbaugh and colleagues published he first description of what is now widely recognized as ARDS in a case series of 12 patients with rapidly progressive respiratory failure with bilateral pulmonary infiltrates and profound hypoxemia following trauma or infection in The Lancet in 1967.[2] The clinical syndrome was called the "adult respiratory distress syndrome" (ARDS) to distinguish it from the respiratory distress syndrome of infancy due to hyaline membrane disease, although the A in ARDS was later changed from acute to adult once it was recognized that the syndrome could also present in infants as a distinct entity from hyaline membrane disease.

Historical Perspective

  • Acute respiratory distress syndrome was first described in 1967 by Ashbaugh et al.[3] Initially there was no definition, resulting in controversy over incidence and mortality. In 1988 an expanded definition was proposed which quantified physiologic respiratory impairment.
  • In 1994 a new definition was recommended by the American-European Consensus Conference Committee.[4] It had two advantages: 1 it recognizes that severity of pulmonary injury varies, 2 it is simple to use.[5]
  • ARDS was defined as the ratio of arterial partial oxygen tension (PaO2) as fraction of inspired oxygen (FiO2) below 200 mmHg in the presence of bilateral alveolar infiltrates on the chest x-ray.
  • These infiltrates may appear similar to those of left ventricular failure, but the cardiac silhouette appears normal in ARDS.
  • Also, the pulmonary capillary wedge pressure is normal (less than 18 mmHg) in ARDS, but raised in left ventricular failure.
  • A PaO2/FiO2 ratio less than 300 mmHg with bilateral infiltrates indicates acute lung injury (ALI). Although formally considered different from ARDS, ALI is usually just a precursor to ARDS.

Consensus after 1967 and 1994

  • ARDS is characterized by:[4]
  • Acute onset
  • Bilateral infiltrates on chest radiograph
  • Pulmonary artery wedge pressure < 18 mmHg (obtained by pulmonary artery catheterization), if this information is available; if unavailable, then lack of clinical evidence of left ventricular failure suffices
  • if PaO2:FiO2 < 300 mmHg acute lung injury (ALI) is considered to be present
  • if PaO2:FiO2 < 200 mmHg acute respiratory distress syndrome (ARDS) is considered to be present

References

  1. Bernard GR (2005). "Acute respiratory distress syndrome: a historical perspective". Am J Respir Crit Care Med. 172 (7): 798–806. doi:10.1164/rccm.200504-663OE. PMC 2718401. PMID 16020801.
  2. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE (1967). "Acute respiratory distress in adults". Lancet. 2 (7511): 319–23. PMID 4143721.
  3. Ashbaugh D, Bigelow D, Petty T, Levine B (1967). "Acute respiratory distress in adults". Lancet. 2 (7511): 319–23. PMID 4143721.
  4. 4.0 4.1 Bernard G, Artigas A, Brigham K, Carlet J, Falke K, Hudson L, Lamy M, Legall J, Morris A, Spragg R (1994). "The American-European Consensus Conference on ARDS. Definitions, mechanisms, relevant outcomes, and clinical trial coordination". Am J Respir Crit Care Med. 149 (3 Pt 1): 818–24. PMID 7509706.
  5. Ware L, Matthay M (2000). "The acute respiratory distress syndrome". N Engl J Med. 342 (18): 1334–49. PMID 10793167.


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