© 2005 American Thoracic Society
Should We Start Considering Surfactant for Atelectasis?To the Editor:We read with great interest the article by Dr. van Kaam and colleagues (1) on the potential role of exogenous surfactant and reduction of atelectasis in prevention of pneumonia. Their findings share the same direction with our clinical data (2), and although the extrapolation of these results to humans is quite complex, they offer a stimulating background for the pathways connecting atelectasis, pneumonia, and surfactant. We recently monitored bronchoalveolar lavage (BAL) fluid alterations prior to, during, and after atelectasis in eight mechanically ventilated patients with previously normal lungs (2). BAL of the involved atelectatic area revealed quantitative and qualitative alterations of the surfactant system (decreased total phospholipids, reduced large aggregates fraction, reduced fraction of phosphatidylcholine) and permeability defects (increased total protein and albumin), as well as findings compatible with local inflammatory reaction (increased neutrophils, reduced alveolar macrophages, and increased platelet-activating factor (PAF) and PAF-acetylhydrolase levels). We also found a significant reduction of proteins in the 30,000 x g BAL subfraction suggesting a decrease in SPA, a finding potentially related to impairment of pulmonary immune function. Within 48 to 72 hours after resolution of atelectasis, capillary–alveolar membrane permeability and inflammation markers returned to pre-atelectasis values, but surfactant alterations persisted, indicating prolonged alveolar II cell injury. The degree of the above BAL fluid alterations correlated with the duration of atelectasis, and in some long-standing cases of atelectasis, there was significant overlap with ventilator-associated pneumonia (VAP) (2). Besides optimal ventilatory management, physiotherapy, and position changes, nothing can be done to prevent or treat atelectasis in the clinical setting. Atelectasis can provoke lung injury and the atelectatic alveolar microenvironment favors the development of pneumonia. Since surfactant dysfunction represents one of the most profound characteristics of atelectasis, administration of exogenous surfactant could be a biologically plausible therapy. Moreover, recent clinical data imply that exogenous surfactant might be effective in direct lung injury (3). Unfortunately, the situation may not be that simple. Mechanical ventilation per se seems to affect many aspects of the surfactant system, even when the lung is intact and modest ventilator settings are employed (4). Consequently, exogenous surfactant replacement requires the recognition of some kind of threshold that could guide its use, and the identification of specific situations (e.g., persisting atelectasis) that could justify such a costly approach in specific cases of atelectasis. Although the theoretical rationale is attractive, and experimental and early clinical data are encouraging, the road to successful clinical trials and effective clinical practice seems long.
University of Ioannina, Ioannina, Greece FOOTNOTES Conflict of Interest Statement: H.T. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript; M.L. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript; G.N. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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