Jia-Neng Tan1,2, Sabrina Wong Peixin Haroon1,2, Amartya Mukhopadhyay2,3, Titus Lau1,2, Tanusya M Murali1,2, Jason Phua2,3, Zong-Yao Tan4, Nicholas Lee4, Horng-Ruey Chua1,2. 1. 1 Division of Nephrology, University Medicine Cluster, National University Hospital, Republic of Singapore. 2. 2 Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Republic of Singapore. 3. 3 Division of Respiratory and Critical Care Medicine, University Medicine Cluster, National University Hospital, Republic of Singapore. 4. 4 National University of Singapore High School of Mathematics and Science, Republic of Singapore.
Abstract
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.
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 illpatients 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-ionizedcalcium >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 illpatients. Serum lactate surveillance may help preempt issues with citratetoxicity.
Entities:
Keywords:
acute kidney injury; citrate toxicity and intolerance; continuous renal replacement therapy; critical care; hemodialysis; hyperlactatemia; intensive care unit; lactate and shock; regional citrate anticoagulation
Authors: Matthias Klingele; Theresa Stadler; Danilo Fliser; Timo Speer; Heinrich V Groesdonk; Alexander Raddatz Journal: Crit Care Date: 2017-11-29 Impact factor: 9.097