Abstract
Objective
High volume hemofiltration (HVHF) has shown potential benefits in septic animals and a few reports suggested a hemodynamic improvement in humans. However, randomized studies are still lacking. Our goal was to evaluate the hemodynamic effects of HVHF in septic shock patients with acute renal failure (ARF).
Design and setting
Prospective randomized study in an intensive care unit (ICU).
Patients
Twenty patients with septic shock and ARF.
Interventions
Patients were randomized to either high volume hemofiltration [HVHF 65 ml/(kg h)] or low volume hemofiltration [LVHF 35 ml/(kg h). Vasopressor dose was adjusted to reach a mean arterial pressure (MAP) > 65 mmHg.
Measurements and results
We performed six hourly measurements of MAP, norepinephrine dose, PaO2/FiO2 and lactate, and four daily urine output and logistic organ dysfunction (LOD) score. Baseline characteristics of the two groups were comparable on randomization. Mean norepinephrine dose decreased more rapidly after 24 h of HVHF treatment compared to LVHF treatment (P = 0.004) whereas lactate and PaO2/FiO2 did not differ between the two treatment groups. During the 4-day follow-up, urine output was slightly increased in the HVHF group (P = 0.059) but the LOD score evolution was not different. Duration of mechanical ventilation, renal replacement therapy and ICU length of stay were also comparable. Survival on day 28 was not affected.
Conclusion
HVHF decreased vasopressor requirement and tended to increase urine output in septic shock patients with renal failure. However, a larger trial is required to confirm our results and perhaps to show a benefit in survival.
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Acknowledgments
Tourcoing hospital provided the financial support for this study.
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The authors have no financial involvement with any organization or entity with a financial interest in the subject discussed in the manuscript.
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Boussekey, N., Chiche, A., Faure, K. et al. A pilot randomized study comparing high and low volume hemofiltration on vasopressor use in septic shock. Intensive Care Med 34, 1646–1653 (2008). https://doi.org/10.1007/s00134-008-1127-3
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DOI: https://doi.org/10.1007/s00134-008-1127-3