Acute respiratory distress syndrome ards is characterized by permeability pulmonary edema and refractory hypoxemia. Recently, the new definition of ards has been published, and this definition suggested severity oriented respiratory treatment by introducing three levels of severity according to pao₂ /fio₂ and positive end expiratory pressure. Through randomized trials, short term use of neuromuscular blockade at initial stage of mechanical ventilation, prone ventilation in severe ards, and extracorporeal membrane oxygenation in ards with influenza pneumonia showed beneficial efficacy. Therefore, early recognition of ards modified risk factors and the avoidance of aggravating factors during the patient's hospital stay can help decrease its development. In addition, efficient antifibrotic strategies in late stage ards should be developed to improve the outcome. Acute respiratory distress syndrome ards is a permeability pulmonary edema characterized by increased permeability of pulmonary capillary endothelial cells and alveolar epithelial cells, leading to hypoxemia that is refractory to usual oxygen therapy. In a national study in iceland, the incidence of ards almost doubled, but hospital mortality decreased during the 23 years of observation 1 .

In a prospective study in spain, despite use of lung protective ventilation, overall icu and hospital mortality of ards patients is still higher than 40% 2 . The first definition of ards dates to ashbaugh and colleagues in 1967 3 , followed by the american european consensus conference's definition in 1994. The american european consensus conference's definition in 1994, which has been challenged over the years in several studies since the assessment of oxygenation defect, does not require standardized ventilatory support 4 . Recently, a new consensus definition of ards, the berlin definition, has been published 5 . The new definition of ards maintains a link to the 1994 definition with diagnostic criteria of timing, chest imaging, origin of edema, and hypoxemia. According to the revised definition of ards, a minimum level of positive end expiratory pressure peep and mutually exclusive pao₂ /fio₂ thresholds was chosen to differentiate between three levels of severity mild, moderate, and severe of ards. The revised definition appears to have improved predictive validity for mortality of its spectrum of severity 5 .

The revised definition presents a severity oriented method for respiratory management of ards 6 . Histopathological findings have been correlated to severity and duration of ards 7 . Using clinical criteria, the revised definition for ards allowed for the identification of severe ards of more than 72 h as a homogeneous group of patients characterized by a high proportion of diffuse alveolar damage 7 .

In addition to the classical views of ards including the role of cellular and humoral mediators, the role of the renin angiotensin system ras has been highlighted. The ras is thought to contribute to the pathophysiology of ards by increasing vascular permeability. Angiotensin converting enzyme ace is a key enzyme of the ras that converts inactive angiotensin i to the vasoactive and aldosterone stimulating peptide angiotensin ii and also metabolizes kinins along with many other biologically active peptides. Ace is found in varying levels on the surface of lung epithelial and endothelial cells 8 . Angiotensin ii induces apoptosis of lung epithelial and endothelial cells and is a potent fibrogenic factor 9 .

Based on these biological properties of ace, there is considerable interest in its potential involvement in acute lung injury ali /ards 10. Since the first publication demonstrating the presence of pulmonary hypertension and elevated pulmonary vascular resistance in patients with severe acute respiratory failure 12 , the development of acute cor pulmonale in ards has been considered a poor prognostic factor. In two recent prospective observational studies, cor pulmonale occurrence was not negligible up to one fourth in ards patients ventilated with airway pressure limitations, was associated with sepsis, and was a risk factor for 28 day mortality 13. Considering these findings together with the association of high peep levels and elevated plateau pressure with pulmonary artery pressure 15 , careful monitoring of acute cor pulmonale is recommended in ards.

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Differential diagnosis between cardiogenic pulmonary edema cpe and ards is sometimes not easy. The accuracy of the portable chest radiograph to detect pulmonary abnormalities consistent with ards is significantly limited 16 . In a study using chest computed tomography, upper lobe predominant ground glass attenuation, central predominant ground glass attenuation, and central airspace consolidation were associated with high positive predictive values 95.2%, 92.3%, and 92.0%, respectively and moderate negative predictive values 47.5%, 51.4%, and 50.0%, respectively to diagnose cpe 17 . Measurement of the extravascular lung water index and the pulmonary vascular permeability index pvpi 18 using a transpulmonary thermodilution method seemed to be a useful quantitative diagnostic tool for ards in patients with hypoxemic respiratory failure and radiologic infiltrates.

In one study, a pvpi value of 2.6–2.85 provided a definitive diagnosis of ali/ards specificity, 0.90–0.95 , and a value lt 1.7 ruled out an ali/ards diagnosis specificity, 0.95 18 . Although ards is an acute lung inflammation in which diverse inflammatory cells and mediators are involved, multiple anti inflammatory interventions have not shown improved survival. Clinical trials using corticosteroids, prostaglandins, nitric oxide, prostacyclin, surfactant, lisofylline, ketoconazole, n acetylcysteine, and fish oil have been unable to show a statistically significant improvement in patient mortality. Moreover, the ardsnet study of steroid treatment 19 revealed that administration after 14 days of disease onset could be harmful. Up to now, the efficacy of low dose corticosteroids 20 for the alleviation of inflammation, to reduce organ dysfunction and to improve survival, especially in sepsis associated ards, has not been fully elucidated.

Numerous lines of evidence have demonstrated that inappropriate mechanical ventilatory settings can produce further lung damage to patients with ards. Ventilator induced lung injury seems to be attributed to end inspiratory overdistension and a low end expiratory lung volume, allowing repeated collapse and re expansion with each respiratory cycle tidal recruitment. Tidal recruitment results in high shear force on alveolar walls and small airways during inflation, especially at the interfaces between collapsed and aerated alveoli.

Ards Review Article Text

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