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(Chest. 1999;116:1S-2S.)
© 1999 American College of Chest Physicians

41st Aspen Lung Conference: Overview*

Thomas L. Petty, MD, Master FCCP

* From Presbyterian/St. Luke's Hospital, Denver, CO.

Correspondence to: Thomas L. Petty, MD, Master FCCP, University of Colorado Health Science Center, 1850 High St, Denver, CO 80218

A variety of catastrophic events have been known to lead to acute lung injury since World War I. Early terms for acute lung injury were "shock lung," "postperfusion lung," "traumatic wet lung," and "congestive atelectasis." These massive lung injury states were described only following autopsies. In the mid 1960s, the Denver group recognized a common denominator in patients who had suffered shock, trauma, overwhelming infections, and miscellaneous other conditions that resulted in the dramatic onset of acute respiratory distress, refractory hypoxemia, bilateral symmetric pulmonary infiltrates, and reduced lung compliance. Five of 12 patients survived with the application of mechanical ventilation and the use of positive end-expiratory pressure. This clinical state was first described as "acute respiratory distress in adults" and later as ARDS.1 2 The "adult designation," however, was inappropriate, since the youngest patient in our original series was 11 years old, and the next oldest was 15 years old. The mean age was 29.4 years.

In our original description of ARDS, we recognized surfactant defects in the two autopsy specimens studied and the presence of destructive proteolytic enzymes. In observing ARDS for > 30 years, a huge amount of basic science has identified a myriad of cellular and humoral mediators in acute lung injury, with a panoply of inflammatory cytokines and chemokines, while enhancing and inhibiting mediators of inflammation. Supportive care of patients during the past third of a century has improved to the point that > 50% can survive.3 Thus far, clinical trials investigating the efficacy and safety of new pharmaceuticals aimed at blocking the inflammatory mediators of disease have not proved successful.4 The development of an ARDS clinical trials consortium offers the machinery to test additional new therapeutic agents.5 Although it is doubtful that a single "silver bullet" will stop the cascade of events resulting in ARDS, it is possible that the replacement of surfactant in early stages or a combination of mediator blockers might alter the outcome of the basic biological processes resulting in ARDS.

The first Aspen Lung Conference on ARDS was the 16th, in 1973.6 7 The second was in 1993.8 Now, 25 years later, the 41st Aspen Lung Conference has enlightened us further about the basic nature of ARDS. Future progress depends on the clinical application of new therapeutic agents aimed at the basic biological processes associated with ARDS. An imaginative approach to therapy is needed in the future.

References

  1. Ashbaugh, DG, Bigelow, DB, Petty, TL, et al (1967) Acute respiratory distress in adults. Lancet 2,319-323
  2. Petty, TL, Ashbaugh, DG (1971) The adult respiratory distress syndrome: clinical features, factors influencing prognosis and principles of management. Chest 60,233-239
  3. Milberg, JA, Davis, DR, Steinberg, KP, et al (1995) Improved survival of patients with acute respiratory distress syndrome (ARDS): 1983–1993. JAMA 273,306-309
  4. Levy, PC, Utell, MJ, Sickel, JZ, et al (1995) The acute respiratory distress syndrome: current trends in pathogenesis and management. Compr Ther 21,438-444
  5. Bernard, GR, Artigas, A, Brigham, KL, et al (1994) The American-European Consensus Conference on ARDS: definitions, mechanisms, relevant outcomes, and clinical trial coordination. Am J Respir Crit Care Med 149,818-824
  6. Petty, TL, Hudson, LD, Ashbaugh, DG (1974) The 16th Aspen Lung Conference. Chest 65(Suppl;part 1),1S-67S
  7. Petty, TL, Hudson, LD, Ashbaugh, DG (1974) The 16th Aspen Lung Conference. Chest 65(Suppl;part 2),1S-46S
  8. Petty, TL (1994) The acute respiratory distress syndrome: historical perspective. Chest 105(Suppl),44S-47S




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