• G U Meduri.
• Division of Pulmonary and Critical Care Medicine, University of Tennessee-Memphis.
• New Horiz. 1993 Nov 1; 1 (4): 563-77.

AbstractLate adult respiratory distress syndrome (ARDS) refers to the clinical stage of ARDS when the lung attempts to repair the initial or persistent injury to the endothelial and epithelial lining of the respiratory units. Histologically, it is characterized by the replacement of damaged epithelial cells and the striking accumulation of mesenchymal cells (fibroproliferative phase) and their connective tissue products in the air spaces and walls of the intra-acinar microvessels. Unfortunately, this reparative process is frequently ineffective, leading directly or indirectly to the patient's death. Its evolution appears to be determined by the extent of initial insult to the lung and by the presence of a protracted inflammatory response. Continuous injury may result from persistent release of inflammatory cytokines in the lung. In late ARDS, injury to the endothelial surface appears to be the pathogenic mechanism behind persistent bronchoalveolar lavage neutrophilia and diffuse pulmonary uptake of gallium. Ineffective repair is characterized by progressive proliferation of myofibroblast and deposition of collagen in the alveoli, thereby producing worsening gas exchange and lung mechanics. Prolonged mechanical ventilation predisposes the patient to the development of pulmonary and extrapulmonary infections. Moreover, release of inflammatory cytokines from the lung with fibroproliferation causes fever and leukocytosis, making clinical distinction from pulmonary or extrapulmonary infections difficult, if not impossible. Anecdotal reports suggest that corticosteroid treatment may accelerate recovery in late ARDS.

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