Acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is acute respiratory failure syndrome characterized by serious lung diseases lead to diffuse pulmonary capillary injury and permeability increasing, the main Pathological changes with pulmonary edema, hyaline membrane, atelectasis, the clinical features with progressive respiratory distress and refractory hypoxemia. ARDS is a typical example of the advanced stage Acute lung injury. This disease rapid attack and development, poor prognosis, the mortality rate as high as 50%. Clinical characteristics of Acute respiratory distress syndrome is respiratory distress, progressive hypoxemia, X-ray showed diffuse alveolar infiltration. ARDS is similar with infant respiratory distress syndrome, but its etiology and pathogenesis is different.

Mechanism for respiratory failure that caused by ARDS: As the alveolar - capillary membrane injury and the role of inflammatory mediators in alveolar epithelium and capillary endothelial permeability increased permeability cause pulmonary edema, diffuse pulmonary dysfunction. Type Ⅱ alveolar epithelial cell injury induced by generation so that to reduce the surfactant, together with the dilution of tissue fluid and alveolar hyperventilation surfactant consumption, so that increased alveolar surface tension, lung compliance decreased, the formation of atelectasis. Atelectasis, pulmonary edema give rise to airway obstruction, as well as the inflammatory mediators induced bronchospasm can lead to intrapulmonary shunt; DIC and inflammatory mediators in the lungs caused by pulmonary vasoconstriction can lead to kind of dead space ventilation. Pulmonary diffusion dysfunction, intrapulmonary shunt and dead space ventilation were so kind PaO2 decreased, leading to respiratory failure type Ⅰ. Condition serious lung disease as a result of a wide range of reduced total lung ventilation, can occur with type Ⅱ respiratory failure.

According to the pathological changes, ARDS can be divided into three interrelated stages include exudation, hyperplasia and fibrosis.

1. the exudation period: in the first week after onset. Lung showed a dark purple or red degeneration of the liver, showing edema and hemorrhage. A marked increase in weight. Examination within 24 hours see pulmonary microvascular hyperemia, hemorrhage, micro-thrombosis, pulmonary interstitial and alveolar edema fluid protein and inflammatory cell infiltration. If the cause for the emotional etiology, the alveolar space and the infiltration of PMNs aggregation becomes more apparent. 72 hours after the plasma protein coagulation, cell fragmentation, formation of transparent cellulose film, a large focal alveolar collapse or atelectasis. Exudation in the acute phase of type Ⅰ necrosis cell damage.

2. the proliferative phase: injury after 1 ~ 3 weeks, lung epithelial cells type Ⅱ cover off of the basement membrane, alveolar sac and alveolar fibrosis tube can be seen, small muscle cells of arteries occur intimal hyperplasia, resulting in cut-lumen reduction in the area.

3. the fibrosis phase: the survival of more than 3 ~ 4 weeks of ARDS in patients with extensive alveolar septal wall thickening and gas, loose connective tissue collagen in the separation of diffuse irregular hyperplasia induced fibrosis. Pulmonary vascular bed extensive fibrous thickening of the wall, twisted deformation artery, pulmonary vasodilator line. Even if the cause of non-infectious cause of ARDS, is not inevitable in the post-pulmonary infection, often organized necrosis and micro-abscess.