Lung surfactant alterations in pulmonary thromboembolism

Abstract

Beside neonatal respiratory distress syndrome, secondary surfactant deficiency may occur in patients with mature lungs. Recent studies revealed quantitative and qualitative changes of lung surfactant in pulmonary thromboembolism (PTE) concerning the total phospholipids content in BAL fluid, alterations in surfactant phospholipids classes and a large-to-small aggregates ratio. Reduced expression of surfactant protein A (SP-A) mRNA and SP-A in lung tissue after pulmonary embolism was found. Serum levels of SP-A were significantly higher in patients with PTE than in other lung diseases, except COPD. Surfactant changes in PTE may result from damage of type II cells by hypoxia, leakage of plasma proteins into the airspaces and/or by reactive oxygen species. They can contribute to lung atelectasis and edema, and a further reduction in oxygen saturation as seen in clinical picture of PTE. Surfactant changes are reliable marker of lung injury that might become a prognostic indicator in patients with pulmonary thromboembolism.

Figure 1

Mechanisms and pathophysiological consequences of surfactant inactivation in pulmonary thromboembolism.