Regional citrate anticoagulation in CVVH: a new protocol combining citrate solution with a phosphate-containing replacement fluid

Introduction

Regional citrate anticoagulation (RCA) is a highly effective anticoagulation (AC) method in CRRT and different combinations of citrate (Citr) and CRRT solutions can affect the acid-base (A-B) balance. Regardless of the AC protocol, hypophosphatemia occurs frequently in CRRT (80%). The aim was to evaluate safety and effects on A-B balance of a new RCA-CVVH protocol using 18 mmol/l Citr solution combined with a phosphate-containing hemofiltration (HF) solution.

Methods

In our center, RCA-CVVH is routinely performed with a 12 mmol/l predilution Citr solution (Prismocitrate 10/2) and a postdilution HF solution (HCO₃^- 32, Ca²⁺ 1.75, Mg²⁺ 0.5, K⁺ 2 mmol/l) (protocol A). In the case of persistent acidosis, not related to Citr accumulation, NaHCO₃ infusion is started. In order to optimize the buffer balance, a new protocol has been designed throughout a mathematical model developed to estimate Citr and HCO₃^- mass transfer. Recently introduced solutions have been adopted: 18 mmol/l predilution Citr solution (Prismocitrate 18), postdilution HF solution (Phoxilium, HCO₃^- 30, phosphate 1.2, Ca²⁺ 1.25, Mg²⁺ 0.6, K⁺ 4 mmol/l) (protocol B). In relation to Qb, the Citr solution rate was set to meet the target circuit Citr concentration (3 mmol/l). To maintain systemic Ca²⁺ (1.1 to 1.25 mmol/l), CaCl₂ 10% was started according to estimated Ca²⁺ loss.

Results

In a cardiac surgery patient with AKI, A-B status and electrolytes have been evaluated comparing protocol A (five circuits, 301 hours) versus protocol B (two circuits, 97 hours): pH 7.39 ± 0.03 versus 7.44 ± 0.03 (P < 0.0001), blood HCO₃^- 22.3 ± 1.8 versus 22.6 ± 1.4 mmol/l (P = NS), BE -2.8 ± 2.1 versus -1.6 ± 1.2 (P < 0.01), serum phosphate 0.85 ± 0.2 versus 1.3 ± 0.5 mmol/l (P = 0.027), serum K⁺ 4 ± 0.2 versus 4.2 ± 0.3 mmol/l (P = NS) with KCl infusion 4 ± 0.2 versus 1.4 ± 1.5 mmol/hour (P < 0.0001). Protocol A required NaHCO₃ and Na-phosphate infusion (8.9 ± 2.8 mmol/hour and 5 g/day, respectively) while protocol B allowed one to stop both supplementations. Systemic and circuit Ca²⁺ were easily maintained in the target range with both protocols.

Conclusion

Although needing confirmation in an adequate number of patients, protocol B was able to provide a buffer balance more positive than protocol A and allowed one to adequately control the A-B status without additional NaHCO₃ infusion and in the absence of alkalosis, despite the use of a standard HCO₃^- concentration HF solution. Furthermore, the combination of a phosphate-containing replacement fluid appeared effective to prevent hypophosphatemia. Finally, the use of a mathematical model allowed predicting the effects of different replacement solutions and/or RCA-CVVH settings on the mass balance of the main solutes.