The main characteristic of ARDS is the damage to the alveolar-capillary membrane which results in the accumulation of protein-rich fluid inside the alveolar septa and inside the alveoli ( 6). Therefore, in current practice ARDS is usually differentiated from CPE by the clinical picture and by physical findings, and this distinction is often completed by the response to therapy. Nowadays, patients are presumed to have ARDS if they show respiratory distress which cannot be explained by findings of heart failure or fluid overload on a clinical basis and by using all the available data, because the pulmonary capillary wedge pressure measurement has been removed from this definition. The Berlin definition for ARDS ( 4) shows a better predictive power for mortality than the previous ARDS definition by the American-European Consensus Conference (AECC) ( 5), but it includes potential differential diagnostic inconsistencies, mainly related to the poor sensitivity and specificity of the chest radiographic criteria for distinguishing ARDS from CPE. Moreover, in septic patients with ARDS, the myocardium is dysfunctional due to systemic inflammatory activation and mitochondrial impairment, and sepsis related cardiomyopathy ( 3) is a recognized cause of left ventricular failure and of an increase in hydrostatic extravascular lung water and CPE. This diagnostic task becomes more difficult in older patients, where a higher number of morbidities often coexists. Differentiating between hydrostatic or cardiogenic pulmonary edema (CPE) and ARDS is challenging, especially in the early stages of illness ( 2). Watch closely for changes in your health, and be sure to contact your doctor or nurse advice line if you have any problems.Since its first description in 1967 ( 1), acute respiratory distress syndrome (ARDS) represents a well known major clinical problem in intensive care units (ICUs), carrying a high morbidity and mortality.
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