By A. F. Junod (auth.), Dr. J. L. Vincent (eds.)
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Extra info for 6th International Symposium on Intensive Care and Emergency Medicine: Brussels, Belgium, April 15–18, 1986
Am Rev Respir Dis 132:479-484 17. Weibel ER (1984) The pathway for oxygen. Harvard University Press, Cambridge, Mass and London p 231-271 18. Weinberg PF, Matthay MA, Webster RO, Roskos KV, Goldstein 1M, and Murray JF. (1984) Biologically active products of complement and acute lung injury in patients with the sepsis syndrome. Am Rev Respir Dis 130:791-796 19. Whitcomb ME, Dixon GF (1984) Gallium scanning, bronchoalveolar lavage, and the national debt. Chest 85: 719-721 20. White DA, Gellene RA, Gupta S, Cunningham-Rundles C, Stover DE (1985) Pulmonary cell populations in the immunosuppressed patient.
This may be particularly true for direct chest trauma or exposure to toxic products since these experimental triggers have no physiological equivalent in the most common clinical situations predisposing to ARDS. With this minor but interesting restriction in mind, we feel that the key role of PMN remains strongly documented. 24 1. Duchateau, M. Braun, and M. Lamy Complement Activation and ARDS Activation of the complement system has been clearly documented in several conditions associated with a risk of ARDS [1, 2].
The patient in this situation usually succumbs to a nosocomial infection and sepsis with an organism that is particularly resistant to antibiotic therapy. Also in the postoperative surgical patient there may be subsequent sepsis due to abcess formation that has not been clinically diagnosed and treated. If death occurs during the acute episode without an apparent recovery period usually this indicates that there has been severe and irreversible cerebral hypoxia or the physiologic consequences of the initial insult have been so great as to cause irreversible pulmonary destruction of a major portion of the lung.