Literature DB >> 12018805

Acute respiratory distress syndrome.

Michael P Mortelliti1, Harold L Manning.   

Abstract

Acute respiratory distress syndrome is the clinical manifestation of severe, acute lung injury. It is characterized by the acute onset of diffuse, bilateral pulmonary infiltrates secondary to noncardiogenic pulmonary edema, refractory hypoxia, and decreased lung compliance. Acute respiratory distress syndrome occurs most frequently in the setting of sepsis, aspiration of gastric contents, trauma, or multiple transfusions. Its complex pathophysiology involves an inciting local or systemic event that initiates pulmonary endothelial and epithelial damage and subsequent increased permeability. Tachypnea, hypoxia, and respiratory alkalosis are typical early clinical manifestations, and they are usually followed by the appearance of diffuse pulmonary infiltrates and respiratory failure within 48 hours. Early identification and treatment of the underlying disorder, along with aggressive supportive care, are essential. Experimental therapies, including those using nitric oxide and surfactant, have not been shown to improve mortality in patients with ARDS, but new therapeutic approaches such as low-volume ventilation have been shown to decrease mortality. Many patients who survive ARDS have permanent, mild to moderate impairment of lung function. Quality of life after hospitalization with ARDS may be poorer than that in similar patients without ARDS.

Entities:  

Mesh:

Year:  2002        PMID: 12018805

Source DB:  PubMed          Journal:  Am Fam Physician        ISSN: 0002-838X            Impact factor:   3.292


  14 in total

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8.  Plasma neutrophil elastase and elafin imbalance is associated with acute respiratory distress syndrome (ARDS) development.

Authors:  Zhaoxi Wang; Feng Chen; Rihong Zhai; Lingsong Zhang; Li Su; Xihong Lin; Taylor Thompson; David C Christiani
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9.  Krüppel-like factor 5 mediates proinflammatory cytokine expression in lipopolysaccharide-induced acute lung injury through upregulation of nuclear factor-κB phosphorylation in vitro and in vivo.

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