Th e Berlin consensus group met recently after 18 years of defi ning acute respiratory distress syndrome (ARDS) using the American European Consensus Committee (AECC) criteria because, in their words, ‘a number of issues regarding various criteria of the AECC defi nition have emerged, including a lack of explicit criteria for defi ning acute, sensitivity of PaO 2 /FiO 2 to diff erent ventilator settings, poor reliability of the chest radiograph (CXR) criterion, and diffi culties distinguishing hydrostatic edema’ [1]. Save for defi ning acute, they arrived at a new defi nition using nearly these exact same criteria and thus did not answer their original concerns. When defi ning ARDS, as the late Daniel Schuster championed for years, the defi nition should include some direct measure of lung injury, at once eliminating much of what confounds the AECC and now the Berlin criteria – atelectasis, aspiration, eff usion, pneumonia, left ventricular dysfunction, and the eff ects of ventilator settings on the PaO 2 /FiO 2 ratio and CXR. Th is idea has been dismissed for years on grounds of feasibility – and dismissed yet again in Berlin – but given the very poor predictive value of the Berlin criteria for outcome and poor correlation with postmortem fi ndings as regards severity classifi cation and proper identifi cation [2], I would argue it is indeed time to take another look. If we are to progress in our research eff orts, it becomes imperative to identify homogeneous treatment groups – specifi c to a treatment strategy. Berlin criteria do not have the reliability, sensitivity or specifi city to do so or even to properly prognosticate. An area under the receiver operating charac teristic curve of 0.577 (95% confi dence interval, 0.561 to 0.593) regarding the predictive validity for mortality found for the Berlin defi nition is abysmal, and should not be pointed to as progress. Quite the contrary, it is a rallying call for change. Th e idea that hydrostatic and permeability causes of edema and hypoxemia are mutually exclusive, as implied by the AECC and now by the Berlin group, should be abandoned. Cardiomyopathy of sepsis and acute heart failure are common in ARDS – occurring in upwards of 60% of patients with severe sepsis – the number one cause of ARDS [3]. Considering that left ventricular dysfunction and cardiomyopathy of severe systemic infl am matory response syndrome/sepsis have better prognoses than diff use alveolar injury, some measure of the relative contribution to CXR and PaO 2 /FiO 2 ratio changes of hydrostatic versus pulmonary injury causes in ARDS then becomes important for identifi cation, severity classifi cation, prognostication and treatment. Increased extravascular lung water is at the center of the pathophysiologic changes in ARDS. Indexing extravascular lung water to pulmonary blood volume – the
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Jun 1, 2013
F Bandinelli + 7
Open Access