Articles: respiratory-distress-syndrome.
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Med. Clin. North Am. · Jul 1986
ReviewClinical indicators in sepsis and septic adult respiratory distress syndrome.
Sepsis and septic ARDS remain clinical problems of great significance because of the numbers of patients affected each year and the high mortality associated with development of the syndrome. The standard therapies for these conditions, judicious antibiotic administration and supportive care, continue to be the mainstays of treatment for these patients, but mortality even with optimal conventional therapy is between 50% and 90% for septic ARDS. ⋯ Two therapies that are used extensively in the intensive care unit today--corticosteroid administration and PEEP--have not been shown to reduce the overall mortality of sepsis or septic ARDS. Newer therapeutic modalities, designed to protect against or reverse cardiovascular consequences of sepsis, reduce the incidence of multiorgan system failure, and diminish the high incidence of uncontrolled infections in these patients, are needed; investigations of these interventions are in progress.
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The predominant mechanism of abnormal gas exchange in patients with the adult respiratory distress syndrome is intrapulmonary shunting. However, other abnormalities of cardiopulmonary function may modify the degree of hypoxemia that is seen, and must be considered when interpreting the effect of therapy.
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ARDS is well recognized as a major medical emergency resulting in respiratory failure and refractory hypoxemia. The risk factors and attack rate of ARDS have been identified and principles of management established. ⋯ Certain roentgenographic features can be identified in both acute and late phases of ARDS. The prognosis of survivors is favorable in the long term.
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Despite the wide range of insults that can lead to the development of ARDS, a common sequence of pathologic changes can be identified in the lung. These changes can be divided into three phases: the acute, or exudative, phase (up to 6 days), in which hyaline membranes are a characteristic feature; the subacute, or proliferative, phase (4 to 10 days), in which metaplasia of the alveolar lining cells and early evidence of fibrosis are seen; and the chronic phase (8 days and on), when organizing fibrosis is a major finding. Structural changes of chronic pulmonary hypertension are also found in the patients with ARDS of longer duration. ⋯ For example, a single infusion of E. coli endotoxin into sheep mimics the pathophysiologic changes of ARDS, offering a model for study of the initial insult on the lung. In addition, animals exposed to high concentrations of oxygen also show morphologic changes similar to those seen in patients with ARDS. Whether the hyperoxia is responsible for such changes, or whether it potentiates the injury induced by some other insult, is not certain.