Abstract
BackgroundCitrate, the currently preferred anticoagulant for continuous veno-venous hemofiltration (CVVH), may influence acid-base equilibrium.MethodsThe effect of 2 different citrate solutions on acid-base status was assessed according to the Stewart-Figge approach in two consecutive cohorts of critically ill adult patients. The first group received Prismocitrate 10/2 (PC10/2; 10 mmol citrate/L). The next group was treated with Prismocitrate 18/0 (PC18; 18 mmol citrate/L). Both groups received bicarbonate-buffered fluids in post-dilution.ResultsAt similar citrate flow, the metabolic acidosis present at baseline in both groups was significantly attenuated in PC18 patients but persisted in PC10/2 patients after 24 h of treatment (median pH 7,42 vs 7,28; p = 0.0001). Acidosis in the PC10/2 group was associated with a decreased strong ion difference and an increased strong ion gap (respectively 43 vs. 51 mmol/L and 17 vs. 12 mmol/L, PC10/2 vs. PC18; both p = 0.001). Chloride flow was higher in PC10/2 than in PC18 subjects (25.9 vs 14.3 mmol/L blood; p < 0.05).ConclusionCorrection of acidosis was blunted in patients who received 10 mmol citrate/L as regional anticoagulation during CVVH. This could be explained by differences in chloride flow between the applied citrate solutions inducing hyperchloremic acidosis.
Highlights
Citrate, the currently preferred anticoagulant for continuous veno-venous hemofiltration (CVVH), may influence acid-base equilibrium
Our findings suggest that a higher chloride-containing citrate solution (PC10/2) for RCACVVH may significantly reduce alkalosis-buffering capacity
In conclusion, the Stewart-Figge approach allowed to elaborate previous experience showing that metabolic acidosis is attenuated and buffer capacity increased when a citrate solution that contains less chloride is used for regional citrate anticoagulation (RCA)
Summary
The currently preferred anticoagulant for continuous veno-venous hemofiltration (CVVH), may influence acid-base equilibrium. Continuous veno-venous hemofiltration (CVVH) under regional citrate anticoagulation (RCA) is increasingly used for treatment of acute kidney injury (AKI) in critically ill patients [1]. In patients with decreased capacity to metabolize citrate (eg hepatic failure), accumulation can lead to high anion-gap metabolic acidosis [3,4,5]. Acid-base status is affected by the amount of administered chloride and bicarbonate buffer, and occasionally by respiratory (over)compensation [6, 7]. When administered as a trisodium salt, excess citrate may induce hypernatremia [8]
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