Acute respiratory distress syndrome historical perspective

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Brian Shaller, M.D. [2]

Overview

Although the pathologic features of acute respiratory distress syndrome (ARDS) were first documented in the 19th century, characterization of its clinical features did not arise until the 1960s. The most recently updated definition is the Berlin definition devised by the European Society of Intensive Care Medicine in 2012.

Historical Perspective

Although the first pathologic description of ARDS dates back to 1821,[1] our understanding of the distinct pathophysiologic features of ARDS has volved 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.[2]

In 1967, Ashbaugh and colleagues first described the clinical entity "acute respiratory distress in adults" characterized by a clinical and pathological course of events remarkably similar to the infantile respiratory distress syndrome.[3] In the case series, 12 patients developed severe dyspnea, tachypnea, cyanosis refractory to oxygen therapy, decreased pulmonary compliance, and diffuse alveolar infiltration following trauma, viral infection, or acute pancreatitis. Autopsy findings of the lungs include atelectasis, vascular congestion, hemorrhage, pulmonary edema, and hyaline membrane formation.

In 1988, Murray et al. proposed an expanded definition of ARDS that utilized a four-point lung injury scoring system to assess the physiologic respiratory impairment based on oxygenation status, level of positive end-expiratory pressure, static pulmonary compliance, and chest radiograph involvement.[4] Although the scoring system may be used to quantify the extent of lung injury in the research setting, the lack of survival predictability has limited its clinical usefulness.[5][6]

In 1994, a standardized definition of ARDS was devised by the American European Consensus Conference (AECC).[7] The AECC committee defined acute lung injury (ALI) as "a syndrome of inflammation and increased permeability that is associated with a constellation of clinical, radiologic, and physiologic abnormalities that cannot be explained by, but may coexist with, left atrial or pulmonary capillary hypertension" that "is associated most often with sepsis syndrome, aspiration, primary pneumonia, or multiple trauma". The term ARDS was reserved for the end of this spectrum with the most severe oxygenation deficit. ALI and ARDS are acute in onset and persistent, are associated with one or more known risk factors, and are characterized by arterial hypoxemia resistant to oxygen therapy alone and diffuse radiologic infiltrates. Despite the wide acceptance of the AECC definition, there are limitations across all four diagnostic criteria such as unspecified timing of acute onset, no minimum requirement of PEEP which can influence oxygenation status, and poor inter-observer agreement on interpretation of chest radiographs or pulmonary artery catheter tracings.[8]

In 2012, the AECC definition was superseded by the Berlin definition from the European Society of Intensive Care Medicine.[9] The major changes to the Berlin definition of ARDS include: the term ALI was removed, pulmonary artery wedge pressure requirement was removed, subgroups by severity of oxygenation deficit were added, minimal PEEP or CPAP levels across subgroups were added, and chest CT was incorporated as an alternative imaging modality for determination of lung infiltrates. Data from the pooled cohorts suggested that each stage is associated with a progressive increase in the mortality as well as the duration of mechanical ventilation among survivors. Compared with the AECC definition, the Berlin definition was deemed to be a better predictor of mortality among patients with ARDS.[10]

References

  1. Laennec, René Théophile Hyacinthe, and Sir John Forbes. A Treatise on the Diseases of the Chest, and on Mediate Auscultation. Samuel S. and William Wood, 1838.
  2. 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.
  3. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE (1967). "Acute respiratory distress in adults". Lancet. 2 (7511): 319–23. PMID 4143721.
  4. Murray, J. F., M. A. Matthay, J. M. Luce, and M. R. Flick. “An Expanded Definition of the Adult Respiratory Distress Syndrome.” The American Review of Respiratory Disease 138, no. 3 (September 1988): 720–23. doi:10.1164/ajrccm/138.3.720.
  5. Doyle, R. L., N. Szaflarski, G. W. Modin, J. P. Wiener-Kronish, and M. A. Matthay. “Identification of Patients with Acute Lung Injury. Predictors of Mortality.” American Journal of Respiratory and Critical Care Medicine 152, no. 6 Pt 1 (December 1995): 1818–24. doi:10.1164/ajrccm.152.6.8520742.
  6. Zilberberg, Marya D., and Scott K. Epstein. “Acute Lung Injury in the Medical ICU.” American Journal of Respiratory and Critical Care Medicine 157, no. 4 (April 1, 1998): 1159–64. doi:10.1164/ajrccm.157.4.9704088.
  7. “The American-European Consensus Conference on ARDS. Definitions, Mechanisms, Relevant Outcomes, and Clinical Trial Coordination. (ATS Journals).” http://www.atsjournals.org/doi/abs/10.1164/ajrccm.149.3.7509706.
  8. Sweeney, Rob Mac, and Daniel F. McAuley. “Acute Respiratory Distress Syndrome.” Lancet (London, England), April 28, 2016. doi:10.1016/S0140-6736(16)00578-X.
  9. The ARDS Definition Task Force*. “Acute Respiratory Distress Syndrome: The Berlin Definition.” JAMA 307, no. 23 (June 20, 2012): 2526–33. doi:10.1001/jama.2012.5669.
  10. The ARDS Definition Task Force*. “Acute Respiratory Distress Syndrome: The Berlin Definition.” JAMA 307, no. 23 (June 20, 2012): 2526–33. doi:10.1001/jama.2012.5669.