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| Adult Respiratory Distress Syndrome |
| Etiology • Result of diffuse capillary damage in the lung with capillary leak |
| Pathogenesis • Endothelial cell damage (direct, secondary to inflammatory cells and mediators esp neutrophils, due to endotoxin) • Capillary leak into the alveolae with accumulation of edema and proteinaceous, necrotic material that forms hyaline membranes • Edema interferes with gas exchange, |
| Epidemiology • Direct toxicity due to smoke inhalation, drugs etc. • Secondary effect of profound hypoxia and circulatory failure |
| General Gross Description • Heavy lungs which are deep reddish purple and stiff |
| General Microscopic Description • Congestion of the vessels and proteinaceous acellular edema in the alveolae • Accumulation of vividly eosinophilic, acellular hyaline membranes against alveolar septae • Organize into circular fibrous swirls which over time replace alveoli • Occasionally resolve completely |
| Clinical Correlation • Sequel to severe trauma or other life threatening condition • Rapid development of profound respiratory failure • Fatality rate is approximately 60% |
| References • Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th edition. Philadelphia, W.B. Saunders, 1994, pp. 676-678. |
| Adult Respiratory Distress Syndrome |
| Synopsis by: Melinda Sanders M.D. (T28000D77050)[353] |
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