ALI/acute respiratory distress syndrome (ARDS) is characterized by diffuse alveolar damage, alveolar capillary leakage, lung edema, neutrophil-derived inflammation, and surfactant dysfunction.

These changes lead to clinical manifestations of decreased lung compliance, severe hypoxemia, and bilateral pulmonary infiltrates.

In the first chapter the authors describe how two different models of multi-causality (intuitively appealing threshold model and abstract sufficient cause model), both of which are commonly used in the description of the etiology of diseases, can be applied to transfusion related acute lung injury (TRALI) and can both be used to describe the same observed relations between multiple risk factors and TRALI.

In the second chapter, a dysfunction of the normal endothelial–epithelial barriers and its role in the development of acute lung injury is described.

Two leading pathogenic mechanisms of ALI are increased endothelial permeability and reduced alveolar liquid clearance capacity.

Understanding of the fundamental mechanisms involved in the regulation of endothelial permeability is essential for the development of barrier protective therapeutic strategies.

The authors review the use of various pharmacological agents (including corticosteroids, neutrophil elastase inhibitors, anticoagulants, pulmonary vasodilators, antioxidants, methylxanthines, exogenous surfactant, gene-therapy, cell therapy, nitric oxide, myorelaxants, beta-agonists) and critically evaluate their effects in animal models and in patients with ALI/ARDS.

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