Khadzhynov Dmytro, Dahlinger Annette, Schelter Christin, Peters Harm, Kindgen-Milles Detlef, Budde Klemens, Lehner Lukas Johannes, Halleck Fabian, Staeck Oliver, Slowinski Torsten
1Department of Nephrology, Charité, Universitätsmedizin Berlin, Berlin, Germany. 2Department of Anesthesiology, University Hospital Duesseldorf, Heinrich-Heine-University, Berlin, Germany.
Crit Care Med. 2017 Sep;45(9):e941-e946. doi: 10.1097/CCM.0000000000002501.
Citrate accumulation is a major complication of regional citrate anticoagulation during continuous renal replacement therapy. We studied the prediction of citrate accumulation during continuous veno-venous hemodialysis with regional citrate anticoagulation by initial lactate concentrations and lactate kinetics.
A retrospective follow-up analysis from a cohort of critically ill patients.
Mixed medical-surgical ICUs at a university hospital.
All adult patients with acute kidney injury and treated with regional citrate anticoagulation-continuous veno-venous hemodialysis during a 3-year period (n = 1,070) were included in this retrospective study and screened for metabolic signs of citrate accumulation.
None.
The frequency of citrate accumulation during the first 48 hours of therapy was 2.26%. In patients with initial normal lactate (< 2.2 mmol/L), elevated lactate (≥ 2.2 to < 4 mmol/L), or severe hyperlactatemia (≥ 4 mmol/L), the frequency of citrate accumulation was 0.77%, 2.70%, and 6.33%, respectively. Receiver operating characteristics-area under the curve of initial lactate concentration was 0.789 for the prediction of citrate accumulation. Optimal cutoff from receiver operating characteristics (2.39 mmol/L) showed strong negative prediction (99.28%), but weak positive prediction (5.21%). The slope intercept of lactate kinetics over 48 hours was positive and significantly higher in patients with citrate accumulation compared to those without (+0.2 vs -0.006 mmol/L/hr; p < 0.001). In patients with initial severe hyperlactatemia (≥ 4 mmol/L), the median calculated lactate clearance at 6, 12, and 18 hours was 24.0%, 48.1%, and 59.4% in the nonaccumulation group. These clearance rates were significantly higher at each time-point compared to patients with citrate accumulation (-9.8%, -20.5%, and 2.3%, respectively; p < 0.001 for each time-point). The highest receiver operating characteristics-area under the curve for citrate accumulation was observed for 12-hour values of lactate clearance (area under the curve = 0.839; 95% CI, 0.751-0.927) with an optimal cut-off value of 24.3%.
Risk of citrate accumulation during regional citrate anticoagulation in a well-selected cohort of patients is low even in case of initial severe hyperlactatemia. Lactate kinetics rather than initially elevated lactate concentration should be considered in assessing the risk of citrate accumulation.
枸橼酸盐蓄积是连续性肾脏替代治疗期间局部枸橼酸盐抗凝的主要并发症。我们通过初始乳酸浓度和乳酸动力学研究了局部枸橼酸盐抗凝的连续性静脉-静脉血液透析期间枸橼酸盐蓄积的预测情况。
对一组危重症患者进行回顾性随访分析。
一所大学医院的内科和外科混合重症监护病房。
本回顾性研究纳入了在3年期间内所有患有急性肾损伤并接受局部枸橼酸盐抗凝-连续性静脉-静脉血液透析治疗的成年患者(n = 1070),并对枸橼酸盐蓄积的代谢体征进行筛查。
无。
治疗的前48小时内枸橼酸盐蓄积的发生率为2.26%。初始乳酸正常(<2.2 mmol/L)、乳酸升高(≥2.2至<4 mmol/L)或严重高乳酸血症(≥4 mmol/L)的患者中,枸橼酸盐蓄积的发生率分别为0.77%、2.70%和6.33%。初始乳酸浓度预测枸橼酸盐蓄积的受试者工作特征曲线下面积为0.789。受试者工作特征曲线的最佳截断值(2.39 mmol/L)显示出较强的阴性预测能力(99.28%),但阳性预测能力较弱(5.21%)。48小时内乳酸动力学的斜率截距为正值,与未发生枸橼酸盐蓄积的患者相比,发生枸橼酸盐蓄积的患者斜率截距显著更高(+0.2 vs -0.006 mmol/L/小时;p < 0.001)。在初始严重高乳酸血症(≥4 mmol/L)的患者中,非蓄积组在6、12和18小时计算的乳酸清除率中位数分别为24.0%、48.1%和59.4%。与发生枸橼酸盐蓄积的患者相比,这些清除率在每个时间点均显著更高(分别为-9.8%、-20.5%和2.3%;每个时间点p < 0.001)。乳酸清除率12小时值预测枸橼酸盐蓄积的受试者工作特征曲线下面积最高(曲线下面积 = 0.839;95%CI,0.751 - 0.927),最佳截断值为24.3%。
在精心挑选的患者队列中,即使初始存在严重高乳酸血症,局部枸橼酸盐抗凝期间枸橼酸盐蓄积的风险也较低。在评估枸橼酸盐蓄积风险时,应考虑乳酸动力学而非初始升高的乳酸浓度。