Even in my limited experience as a first year fellow, it seems that the decision to institute RRT seems to hinge on an idiosyncratic blend of patient and center-specific parameters. I was not surprised to learn that there have been a number of studies that have attempted to identify the optimal time of RRT initiation in AKI. While early case-control and retrospective studies suggested “early” RRT reduced mortality, two randomized clinical trials produced conflicting results. In 2002, a trial of 106 patients initiated “early” RRT if urine output was less than 30ml/hr after six hours but did not find a difference with regard to mortality or recovery of renal function in survivors. A 2004 trial found a large reduction in mortality with early dialysis, defined by postoperative urine output, (RR 0.17 95%CI 0.05-0.61) but weak methods and a small sample size (N =28) temper this conclusion. Observational data from PICARD have shown that the risk of death in critically ill AKI patients was significantly decreased by initiating RRT before levels of blood urea nitrogen were greater than 76mg/dl (adjusted hazard ratio 0.54, CI 0.34 to 0.86).
Such a confusing and contradictory set of conclusions suggests perhaps that neither BUN or creatinine nor urine output is the best guide to the decision to initiate RRT. A number of studies from the pediatric world have emerged over the past 10 years that suggest that the percent fluid overload (%FO) may be key. Specifically, retrospective work from the Prosepective Pediatric Continuous Renal Renal Replacement Therapy (ppCRRT) registry has repeatedly suggested that RRT initiation in AKI when at %FO of around 10% results in decreased mortality, independent of illness severity (see here, here, here and here). Similar findings have more recently been reproduced in adult studies (SOAP, PICARD) where positive fluid balance in AKI was found to correlate with increased mortality.
While some may argue that positive fluid balance merely correlates with illness severity, there seems to be an emerging notion that fluid accumulation in AKI is not an innocuous process but one with significant consequences.
Matt O'Rourke, MD
3 comments:
Great post. Any brief words on how one calculates the %FO in adults? Interested to hear if you think this number might have other clinical uses besides the context above.
Excellent post. Thank you.
While %FO may "merely" correlate with illness severity, that may be precisely why it could be a good tool for deciding when to start RRT. Correlation in epidemiology is not causality, but this is not an epidemiological problem and we are not looking for causality - we are looking for a biomarker that tell us when to act.
I agree that %FO is not fully evaluated and shouldn't be considered the last word in RRT triggers just yet. But, don't abandon it just because it may not be causal!
Nice work. Thanks
Benjamin Littenberg, MD
Henry and Carleen Tufo Professor of Medicine
University of Vermont
I think that fluid overload is an under appreciated problem in the ICU. Surgical and other patients are volume resuscitated and develop severe volume overload. Hypotension is frequently treated with IVF and pressers when I have found that cautious and close monitoring of cardiac hemodynamics is required to avoid volume overload so we do not have to initiate early CRRT. Cardiac output can actually decrease with LV dilatation and removing volume will actually improve cardiac output by decreasing LV size and improve stroke volume.
Great post.
Salil Gupta MD
Syracuse NY
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