Articles: respiratory-distress-syndrome.
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J. Physiol. Pharmacol. · Dec 1997
ReviewMechanisms of acute respiratory distress syndrome: role of surfactant changes and mechanical ventilation.
Acute respiratory distress syndrome (ARDS) is a condition characterized by a high permeability oedema due to loss of the integrity of the alveolo-capillary barrier with impairment of normal surfactant function, resulting in an increased collapse tendency of the alveoli. Mechanical ventilation on such alveoli with repeated alveolar collapse and subsequent reexpansion results in severe lung parenchymal injury and may induce further surfactant impairment. ⋯ Recent evidence from experimental studies has shown that ventilator modes which allow end-expiratory collapse can induce bacterial translocation from the lung into the bloodstream and trigger the release of inflammatory mediators, which can also be presented by maintaining end-expiratory alveolar volume. These data suggest that the interaction between surfactant changes and mechanical ventilation may play a role in the transition of ARDS into the systematic inflammatory disease process of multiple system organ failure (MSOF).
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J. Physiol. Pharmacol. · Dec 1997
ReviewPhysiologic, metabolic and mediator responses in posttrauma ARDS and sepsis: is oxygen debt a critical initiating factor?
Posttrauma adult respiratory distress syndrome (ARDS) and sepsis initiate complex humoral and cellular inflammatory responses that initially effect the microvascular system, but rapidly extend to involve and modulate the solid organ metabolic response. It is discussed whether the interaction between these cellular processes and the organs which they involve appear to be initiated by the trauma induced oxygen debt.
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Intensive care medicine · Dec 1997
Practice Guideline GuidelineUK guidelines for the use of inhaled nitric oxide therapy in adult ICUs. American-European Consensus Conference on ALI/ARDS.
Although unlicensed, inhaled nitric oxide (NO) therapy is now widely used in the United Kingdom. Our aim was to produce guidelines for the clinical application of inhaled NO in adult intensive care practice, based upon the current level of published information. ⋯ The need for additional quality research to establish evidence of efficacy and safety was emphasized. The guidelines are designed to act within the context of current practice and knowledge and should be revised as further data emerge.
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The authors sought to evaluate the pathogenetic and prognostic role of a procoagulant and hypofibrinolytic state in the adult respiratory distress syndrome (ARDS). Twenty-two consecutive patients admitted to the intensive care unit (ICU) for respiratory monitoring (n = 2) or mechanical ventilation (n = 20) were studied, of whom 13 had ARDS and 9 were at risk for the syndrome. Plasma levels of thrombin-antithrombin III complexes (TAT), the plasmin-alpha2-antiplasmin complexes (PAP), tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1) were measured within 48 h after admission, together with respiratory variables allowing computation of the lung injury score (LIS), and pulmonary microvascular permeability [67Gallium-transferrin pulmonary leak index (PLI)], as measures of pulmonary dysfunction. ⋯ Neither circulating coagulation nor fibrinolysis variables correlated to either LIS or PLI. Furthermore, the course of haemostatic variables did not relate to outcome. These data indicate that systemic activation of coagulation and impaired fibrinolysis do not play a major role in ARDS development and outcome in patients with acute lung injury.