Effects of lactate-buffered and lactate-free dialysate in CAVHD patients with and without liver dysfunction.
BACKGROUND
Continuous modalities of renal replacement deplete patients of bicarbonate, which is traditionally replaced indirectly by lactate in dialysate or replacement fluids. We have compared a new lactate-free dialysate (unbuffered dialysate with separate bicarbonate replacement of dialytic bicarbonate loss) with standard lactate-buffered dialysate in terms of acid-base control, lactate accumulation, and hemodynamic stability in patients undergoing continuous renal replacement therapy in an intensive care unit.


METHODS
A nonrandomized crossover cohort study involving 54 patients with multi-organ failure (of whom 19 had significant hepatic dysfunction) was performed. All patients completed 24-hour continuous hemodiafiltration against both lactate-buffered and lactate-free dialysate. Arterial pH, blood gases, bicarbonate, and lactate, venous sodium, blood pressure, and inotrope requirements were measured before and at six hourly intervals during the first 24 hours of dialysis against each dialysate.


RESULTS
Lactate-free dialysate provided more rapid control of acidosis than lactate buffered with less total administration of buffer than that given during the lactate-buffered period (total mmol bicarbonate vs. total mmol lactate + bicarbonate). Lactate accumulation was slight in both periods, but was higher during lactate-buffered continuous venovenous hemodiafiltration (CVVHD). The mean arterial pressure rose during lactate-free dialysis with decreased inotrope doses and fell during lactate-buffered dialysis with increased inotrope requirement. Results in patients with liver dysfunction were not significantly different from those without it.


CONCLUSIONS
Over the time scale of 24 hours, lactate derived from continuous dialysis circuits is efficiently cleared from the blood of most patients with multi-organ failure, but with less effect on systemic acidosis than is produced by equivalent amounts of bicarbonate.
McLean
A G
AG
Centre for Nephrology, Royal Free Campus, Royal Free and University College Medical School, and Intensive Care Unit, Royal Free Hospital NHS Trust, London, England, United Kingdom. adamac@rfhsm.ac.uk
Davenport
A
A
Cox
D
D
Sweny
P
P
D018806:APACHE; D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000628:therapy; D058186:Acute Kidney Injury / Q000628:therapy*; D000328:Adult; D001639:Bicarbonates / Q000008:administration & dosage; D001794:Blood Pressure; D002021:Buffers; D015331:Cohort Studies; D018592:Cross-Over Studies; D015312:Hemodialysis Solutions / Q000008:administration & dosage*; D006440:Hemofiltration; D006801:Humans; D007773:Lactates / Q000008:administration & dosage* / Q000097:blood; D008107:Liver Diseases / Q000628:therapy*; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000401:mortality / Q000628:therapy*
D001639:Bicarbonates; D002021:Buffers; D015312:Hemodialysis Solutions; D007773:Lactates