ALTERATIONS IN PULMONARY SURFACTANT DURING THE COURSE OF SEPSIS-INDUCED ARDS PREDISPOSITION

To test the hypothesis that alterations of the endogenous surfactant s ystem persist and contribute to lung dysfunction in sepsis-induced ARD S predisposition, we analyzed sequentially obtained bronchoalveolar la vage fluid (BALF) from a homogeneous group of thirteen postoperative s epsis-induced ARDS at-risk patients. Beginning no later than 12 h afte r risk identification, we continued to analyze BALF for the biochemica l composition and surface properties of endogenous surfactant at 48 h intervals for seven days. Eleven non-smoking healthy patients prior to minor elective surgery served as control group. Five at-risk patients developed ARDS during the study period. In at-risk patients who did n ot develop ARDS the mean (+/-SE) percentage of PMN (p<0.001), SA/LA ra tio (p<0.05), and gamma min (p<0.001) was elevated, whereas SP-A conte nt (p<0.01) was decreased compared to the control group. The paO(2)/Fi O(2) was 271.3 +/- 12.0 and P(A-a)O-2 was 154.1 +/- 19.5 mmHg. Static compliance of the respiratory system was inversely related to gamma mi n. During the time course SP-A remained significantly decreased and ga mma min significantly elevated at every point of measurement compared to the control group. Our data show that profound alterations in endog enous surfactant not only occure initially but also persist in septic patients during the early clinical course of their ARDS predisposition , and correspond with lung dysfunction even prior to the possible deve lopment of the syndrome.