Hyperlactatemia Predicts Citrate Intolerance With Regional Citrate Anticoagulation During Continuous Renal Replacement Therapy

Purpose: We aim to determine whether hyperlactatemia, which suggests multi-organ dysfunction and impaired organic substrate metabolism, may predict intolerance to regional citrate anticoagulation (RCA) during continuous venovenous hemofiltration (CVVH). Methods: We performed a single-center, retrospective observational study in critically ill patients with acute kidney injury or end-stage renal disease and evaluated the association of peak serum lactate levels with citrate intolerance (CI) during the initial 72 hours of RCA-CVVH, defined by serum total-to-ionized calcium >2.5 plus systemic hypocalcemia. Results: Eighty-eight patients were studied (aged 59 ± 14 years, 66% males, Acute Physiology and Chronic Health Evaluation II: 31 ± 8). Citrate was dosed at median 2.1 mmol/L of blood flow, with citrate load of 30 mmol/h, and CVVH effluent of 43 mL/kg/h. Twenty patients developed CI. Comparing patients with CI versus none, peak lactate levels were 8 (5-11) versus 3 (2-6) mmol/L, calcium replacement was 13 (10-17) versus 11 (8-12) mmol/h, and standard base excess was −4 (−12 to 1) versus 2(−4 to 7) mmol/L, respectively ( P < .05). Citrate intolerance developed in 38%, 44%, and 55%, in patients with peak lactate >4, >6, >7 mmol/L, respectively, versus 7% in those with peak lactate ≤4 mmol/L ( P ≤ .001), despite comparable citrate load and effluent rates across all categories. On multivariate analysis, hyperlactatemia and hyperbilirubinemia predicted CI ( P ≤ .01), which was associated with increasing calcium infusion requirement. Higher peak lactate from >4 to >7 mmol/L predicted CI with graded increase in odds ratio and specificity from 59% to 87%, but the corresponding negative predictive value from 93% to 87%. Area under nonparametric receiver operating characteristic curve for peak lactate and CI was 0.78. Conclusion: Hyperlactatemia predicts CI during RCA-CVVH with reasonable discriminatory performance in critically ill patients. Serum lactate surveillance may help preempt issues with citrate toxicity.

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Low bicarbonate replacement fluid normalizes metabolic alkalosis during continuous veno-venous hemofiltration with regional citrate anticoagulation

Annals of Intensive Care ◽

10.1186/s13613-021-00850-4 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Paul Köglberger ◽

Sebastian J. Klein ◽

Georg Franz Lehner ◽

Romuald Bellmann ◽

Andreas Peer ◽

...

Keyword(s):

Critically Ill ◽

Critically Ill Patients ◽

Metabolic Alkalosis ◽

Base Excess ◽

Kidney Injury ◽

Regional Citrate Anticoagulation ◽

Citrate Anticoagulation ◽

Future Studies ◽

Replacement Fluid ◽

Retrospective Comparative Study

Abstract Background Metabolic alkalosis is a frequently occurring problem during continuous veno-venous hemofiltration (CVVH) with regional citrate anticoagulation (RCA). This study aimed to evaluate the effectiveness of switching from high to low bicarbonate (HCO3−) replacement fluid in alkalotic critically ill patients with acute kidney injury treated by CVVH and RCA. Methods A retrospective-comparative study design was applied. Patients who underwent CVVH with RCA in the ICU between 09/2016 and 11/2017 were evaluated. Data were available from the clinical routine. A switch of the replacement fluid Phoxilium® (30 mmol/l HCO3−) to Biphozyl® (22 mmol/l HCO3−) was performed as blood HCO3− concentration persisted ≥ 26 mmol/l despite adjustments of citrate dose and blood flow. Data were collected from 72 h before the switch of the replacement solutions until 72 h afterwards. Results Of 153 patients treated with CVVH during that period, 45 patients were switched from Phoxilium® to Biphozyl®. Forty-two patients (42 circuits) were available for statistical analysis. After switching the replacement fluid from Phoxilium® to Biphozyl® the serum HCO3− concentration decreased significantly from 27.7 mmol/l (IQR 26.9–28.9) to 25.8 mmol/l (IQR 24.6–27.7) within 24 h (p < 0.001). Base excess (BE) decreased significantly from 4.0 mmol/l (IQR 3.1–5.1) to 1.8 mmol/l (IQR 0.2–3.4) within 24 h (p < 0.001). HCO3− and BE concentration remained stable from 24 h till the end of observation at 72 h after the replacement fluid change (p = 0.225). pH and PaCO2 did not change significantly after the switch of the replacement fluid until 72 h. Conclusions This retrospective analysis suggests that for patients developing refractory metabolic alkalosis during CVVH with RCA the use of Biphozyl® reduces external HCO3− load and sustainably corrects intracorporeal HCO3− and BE concentrations. Future studies have to prove whether correcting metabolic alkalosis during CVVH with RCA in critically ill patients is of relevance in terms of clinical outcome.

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