Adult respiratory distress syndrome

An overview of adult respiratory distress syndrome (adult respiratory distress synd rome, ARDS) is the original patients with normal heart and lung function, Because pulmonary or extrapulmonary process of serious illness permeability secondary acute pulmonary edema and hypoxic respiratory failure. Although its causes vary, but the damage lung tissue pathology and functional changes similar clinical manifestations are acute respiratory distress, refractory hypoxemia, because of similar clinical infant respiratory distress syndrome, but their etiology and pathogenesis of different it was called "adult" to show distinction. With the severe trauma, shock, infection and other diseases where the level of technology, many patients do not die directly from the original disease, so that the increasing incidence of ARDS, ARDS onset sharp, rapid development, if not treated early. their death rate was as high as 50% (25% -90%), and often died of multiple organ failure. Cause pathogenesis of ARDS many causes, such as severe shock, severe trauma, fracture of fat embolism. serious infections (particularly Gram-negative bacilli were sepsis-induced septic shock). inhalation of irritating gases and stomach contents, oxygen poisoning, drowning, massive blood transfusion, acute pancreatitis, drugs or drug intoxication. they can cause pulmonary alveolar-capillary acute injury, however this injury mechanism has not yet been completely clarified, with a variety of factors, the very existence of which, affect each other. Now, most scholars believe that many neurotransmitters involved in alveolar-capillary endothelial injury. with neutrophils (PMN) is the activation of capillary endothelial cells mainly due to the increase in permeability. Healthy pulmonary interstitial only a small number of PMN, and the trauma, acute pancreatitis, or the physical and chemical stimulation of the pump, As in many PMN chemotaxis factor role, to enable the pulmonary capillary PMN massive gathering adhesion and through various factors, such as complement activation system of C5a, lipopolysaccharide (LPS). PMN adhesion to endothelial cells in the surface, PMN activation of the release of a series of endothelial cells and damage lung tissues of harmful substances, mainly oxygen free radicals, multiple protease and arachidonic acid metabolites. If various protease plasmin, elastase, serine protease, collagenase, cathepsin, which collagenase and elastase digest basement membrane, and the pulmonary artery wall elastic organizational structure. Arachidonic acid metabolites by neutrophils, macrophages complement activation of phospholipase role from the plasma membrane phospholipid release of arachidonic acid, through its lipoxygenase and cyclooxygenase-2 metabolism grass, forming a series of highly reactive products (medium). Vascular and bronchial contraction caused pulmonary hypertension increased airway resistance, promote platelet aggregation, blood clots, and the release of fibrin degradation products, the proteolytic enzyme, increasing capillary liquidity. Because pulmonary capillary membrane injury, permeability, increasing permeability of pulmonary edema. ARDS lung pathology was dull purple or red dishes liver degeneration, we can see that edema, hemorrhage, weight increased significantly. See microscopic examination within 24 hours of congestive lung microvascular bleeding, thrombosis, pulmonary interstitial and alveolar protein within a water dispensing and inflammatory cell infiltration. Nearly 72 h, plasma protein condensation, cell sip films, fibers and residual pulmonary surfactant hyaline membrane formation, Focal or large alveolar collapse. Exudative acute lung damage type I cells necrosis, repair lung epithelial type II cell proliferation. Early fibroblast proliferation and collagen deposition, a week after alveolar separated from the transparent membrane fibrosis, pulmonary secondary infection. As the pathophysiology of pulmonary capillary endothelial cells and alveolar type II cell damage caused pulmonary interstitial and alveolar edema, hyperemia, Pulmonary surfactant reduced, causing the closure of small airway depression, alveolar collapse without sheets, lung compliance decreased functional residual capacity reduction. So that the ventilation / blood disorder, pulmonary arteriovenous shunt-like increase and diffusion barriers, ventilatory function caused serious damage to the hypoxemia, stimulate the carotid sinus aortic body chemoreceptor reflex can stimulate the respiratory center have hyperventilation and respiratory alkalosis. In late ARDS, a serious condition, respiratory muscle fatigue failure occurred ventilation, lack of oxygen is even more serious, retention with CO2 to form mixed acidosis. Figure 2 -6-6 hint of adult respiratory distress syndrome pathophysiological changes.