Acute lung injury carries a high burden of morbidity and mortality and is characterised by nonhydrostatic pulmonary oedema. The aim of this paper is to highlight the role of accurate quantification of extravascular lung water in diagnosis, management, and prognosis in “acute lung injury” and “acute respiratory distress syndrome”. Several studies have verified the accuracy of both the single and the double transpulmonary thermal indicator techniques. Both experimental and clinical studies were searched in PUBMED using the term “extravascular lung water” and “acute lung injury”. Extravascular lung water measurement offers information not otherwise available by other methods such as chest radiography, arterial blood gas, and chest auscultation at the bedside. Recent data have highlighted the role of extravascular lung water in response to treatment to guide fluid therapy and ventilator strategies. The quantification of extravascular lung water may predict mortality and multiorgan dysfunction. The limitations of the dilution method are also discussed. 1. Introduction In 1896, the physiologist Starling described the factors that influence fluid transport across semipermeable membranes like capillaries [1]. This description accounted for the net movement of fluids between compartments in relation to capillary and interstitial hydrostatic pressures, capillary and interstitial oncotic pressures, and coefficients of capillary permeability. Pulmonary oedema refers to the accumulation of fluid within the extravascular space of the lung and occurs when the Starling forces are unbalanced. This occurs most commonly from an increased pulmonary capillary hydrostatic pressure or an increased capillary permeability. The estimation of the severity of pulmonary oedema by chest auscultation, radiography, or arterial blood gas analysis is imprecise [2–4]. Chest auscultation may be altered by mechanical ventilation, and bedside chest radiographs in the critical care unit is subject to several technical limitations. There is poor correlation between the chest radiograph scores of pulmonary oedema and the actual amount of EVLW [5]. There is also high interobserver variability when applying the American-European Consensus Conference radiographic criteria for ARDS even amongst experts [6, 7]. Data from experimental studies suggest that EVLW on chest radiography may only be detectable when the lung water increases by more than 35% [8]. Experimental studies have also shown that arterial oxygenation decreased significantly only when the EVLW increases by more than 200% [4].
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