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Effects of fluid administration on renal perfusion in critically ill patients

INTRODUCTION: Fluid administration is a first-line therapy for acute kidney injury associated with circulatory failure. Although aimed at increasing renal perfusion in these patients, this intervention may improve systemic hemodynamics without necessarily ameliorating intrarenal flow distribution or...

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Detalles Bibliográficos
Autores principales: Moussa, Mouhamed Djahoum, Scolletta, Sabino, Fagnoul, David, Pasquier, Pierre, Brasseur, Alexandre, Taccone, Fabio Silvio, Vincent, Jean-Louis, De Backer, Daniel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488122/
https://www.ncbi.nlm.nih.gov/pubmed/26070308
http://dx.doi.org/10.1186/s13054-015-0963-0
Descripción
Sumario:INTRODUCTION: Fluid administration is a first-line therapy for acute kidney injury associated with circulatory failure. Although aimed at increasing renal perfusion in these patients, this intervention may improve systemic hemodynamics without necessarily ameliorating intrarenal flow distribution or urine output. We used Doppler techniques to investigate the effects of fluid administration on intrarenal hemodynamics and the relationship between changes in renal hemodynamics and urine output. We hypothesized that, compared to systemic hemodynamic variables, changes in renal hemodynamics would better predict increase in urine output after fluid therapy. METHODS: We measured systemic hemodynamic variables and performed renal interlobar artery Doppler on both kidneys before and after volume expansion in 49 adult patients with acute circulatory failure. We measured systolic and diastolic velocities and computed the resistivity index (RI). We recorded urine output for 3 h before and after the fluid challenge. RESULTS: Fluid administration resulted in a small but consistent decrease in RI (from 0.73 ± 0.09 to 0.71 ± 0.09, p < 0.01). There was a concomitant increase in mean arterial pressure (from 75 ± 15 to 80 ± 14 mmHg, p < 0.01), pulse pressure (49 ± 19 to 55 ± 19 mmHg, p < 0.01) and urine output (55 ± 76 to 81 ± 87 ml/hour, p < 0.01). Changes in RI were negatively correlated with changes in urine output and mean arterial pressure but not in pulse pressure. The increase in urine output was predicted by changes in RI but not by changes in systemic hemodynamics. CONCLUSIONS: Changes in renal hemodynamics during a fluid challenge can be observed by Doppler ultrasonography before urine output increases. Moreover, these changes are better predictors of an increase in urine output than are mean arterial pressure and pulse pressure.