Summary
The acute respiratory distress syndrome (ARDS) is a severe lung injury in patients
with sepsis and other acute inflammatory insults, which is characterized by fibrin
deposition in the pulmonary parenchyma, vasculature, and airspaces. Recent evidence
suggests that progressive ARDS is closely linked to activation of inflammation and
coagulation. Coagulation becomes activated by circulating endotoxin or bacteria, and
a procoagulant state develops in the vascular and the alveolar compartments of the
lung. This state is Tissue Factor (TF)-dependent and associated with increased elaboration
of inflammatory cytokines. A similar procoagulant state is found in bronchoalveolar
lavage of patients with ARDS, suggesting that extravascular coagulation contributes
to lung inflammation. TF and other coagulation proteins, including Factor Xa, thrombin,
and fibrin, also contribute to the pathogenesis of acute lung injury through multi-level
interactions with inflammatory effectors, in which these proteins coordinately act
as regulators of tissue injury responses. Each coagulation protein has direct and
independent effects on inflammatory events that influences lung injury through changes
in cytokine elaboration, inflammatory cell migration and activation, surfactant function,
and repair mechanisms. New interventional strategies directed at procoagulant activity
highlight the importance of the coagulation system to acute lung injury and suggest
that blockade of initiation of coagulation may have therapeutic benefit in patients
with ARDS.
Keywords
Acute respiratory distress syndrome - sepsis - thromboplastin
