[Role of coagulation in acute pulmonary lesion physiopathology. Parallelism with sepsis].
Acute respiratory distress syndrome and acute lung injury for a part of a devastating syndrome characterized by acute onset, hypoxemia and bilateral infiltrates in the chest x-ray with absence of heart failure signs. Acute lung injury is the response of the lung to a local or systemic aggression, resulting in local inflammation and coagulation disorders, this leading to increased inflammatory pulmonary edema. Acute lung injury/acute respiratory distress syndrome are associated with increased procoagulant and reduced fibrinolytic activities mainly in alveoli and interstitial spaces in the lung. Fibrin deposits, which are the hallmark of early phase acute lung injury, stimulate fibroblast aggregation and collagen secretion, participating to the constitution of pulmonary fibrosis. The only clinical intervention found to have a significant impact on mortality in acute respiratory distress syndrome, despite the significant pro - gress in the understanding of the disease made over the past 10 years, is the use of low tidal volume ventilation. In severe sepsis, only recombinant human activated protein C administration has demonstrated a mortality reduction, together with faster improvement in respiratory dysfunction and shorter duration of mechanical ventilation. Future clinical trials should consider the potential benefit of anticoagulants administrated systemically or locally in the lungs to determine the role of anticoagulants in the treatment of acute pulmonary injury/acute respiratory distress syndrome.
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Centro de Críticos, Hospital de Sabadell, Corporación Sanitaria Parc Taulí, CIBER Enfermedades Respiratorias, Instituto Universitario Parc Taulí, Universidad Autónoma, Barcelona, España. rferrer@tauli.cat
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D055371:Acute Lung Injury / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology*; D000925:Anticoagulants / Q000627:therapeutic use; D001777:Blood Coagulation; D005337:Fibrin / Q000378:metabolism; D006801:Humans; D011486:Protein C / Q000627:therapeutic use; D011654:Pulmonary Edema / Q000209:etiology; D011658:Pulmonary Fibrosis / Q000209:etiology; D012121:Respiration, Artificial; D012128:Respiratory Distress Syndrome / Q000097:blood / Q000188:drug therapy / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D018805:Sepsis / Q000188:drug therapy / Q000503:physiopathology* / Q000628:therapy; D013997:Time Factors
D000925:Anticoagulants; D011486:Protein C; D005337:Fibrin