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Enhancing Edema Clearance

Modulation of Oncotic Pressure

Endogenous albumin is an important regulator of endothelial integrity [70, 71]. From a hemodynamic point of view, hypoalbuminemia results in a decrease in plasma oncotic pressure; therefore, pulmonary edema forms at a lower hydrostatic pressure because the oncotic pressure gradient between plasma and the interstitium decreases [72]. Administration of albumin to raise oncotic pressure and promote the water movement from the interstitial to the intravascular space has been suggested as a method to reduce pulmonary edema. This approach can be combined with the use of furosemide to facilitate the removal of the excess fluid from the plasma. The efficacy of this approach was initially evaluated by Martin et al. in a trial of 37 hypoproteinemic patients with acute lung injury randomized to receive protocolized albumin replacement and continuous infusion of furosemide versus double placebo

[73]. The patients treated with albumin and furosemide showed improvement of oxygenation with better hemodynamics and fluid balance compared with controls. Based on the results of this study, it was estimated that the albumin/furosemide protocol accelerated the edema clearance, by 3-4 days compared with its natural evolution [74]. The beneficial effect of albumin administration was subsequently evaluated in a small trial which compared the efficacy of furosemide and albumin compared to furosemide alone [75]. This trial suggested that albumin is a critical component of this regimen, for both maintenance of hemodynamic stability and improved oxygenation. While these studies suggest promise, it is important to stress, however, that both studies excluded patients with hemodynamic instability and/or receiving vasopressor support suggesting that the full-blown phase of ARDS was already overcome in the enrolled patients. Larger trials are needed to confirm the findings and define the optimal timing of colloid/diuretic administration.

 
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