Summary
Seventeen burned patients, 5 of whom developed the adult respiratory distress syndrome (ARDS), were investigated. Occurrence of ARDS was correlated with the severity of burn in ARDS patients (UBS: 82±27) and non ARDS patients (UBS: 36 ± 18) respectively (p < 0.005) and with inhalation injury.
Blood samples were collected immediately after admission, 6 – 12 h after injury, am/pm the first day and every day during a fortnight. This prospective study demonstrated abnormal C3 consumption as measured by the C3d/C3 ration in all burned patients, not related to the presence of ARDS. A significant protease-antiprotease imbalance was found in ARDS and non ARDS patients: leukocyte elastase was increased throughout the observation period, L 2 macroglobulin drastically decreased especially in ARDS patients, L 1 proteinase inhibitor early decreased below normal levels in ARDS patients. Finally, we found a time course delayed but persisting acute phase response: C-reactive protein, haptoglobin and L 1 acid glycoprotein reached a plateau on about day 5–7.
These biochemical investigations give no evidence for a specific mediator for acute respiratory failure.
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© 1987 Plenum Press, New York
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Faymonville, M.E. et al. (1987). Biochemical Mediators in Acute Respiratory Distress Syndrome (ARDS) after Burning Injury. In: Paubert-Braquet, M., Braquet, P., Demling, B., Fletcher, J.R., Foegh, M. (eds) Lipid Mediators in the Immunology of Shock. NATO ASI Series, vol 139. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0919-2_4
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DOI: https://doi.org/10.1007/978-1-4613-0919-2_4
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