Dmytro Khadzhynov1, Christin Schelter2, Ina Lieker3, Alice Mika4, Oliver Staeck5, Hans-H Neumayer6, Harm Peters7, Torsten Slowinski8. 1. Department of Nephrology, Charité Universitätsmedizin Berlin, Charité Campus Mitte, Humboldt University Berlin, D-10117 Berlin, Germany. Electronic address: dmytro.khadzhynov@charite.de. 2. Department of Nephrology, Charité Universitätsmedizin Berlin, Charité Campus Mitte, Humboldt University Berlin, D-10117 Berlin, Germany. Electronic address: christin.baumann@charite.de. 3. Department of Nephrology, Charité Universitätsmedizin Berlin, Charité Campus Mitte, Humboldt University Berlin, D-10117 Berlin, Germany. Electronic address: ina.lieker@charite.de. 4. Department of Nephrology, Charité Universitätsmedizin Berlin, Charité Campus Mitte, Humboldt University Berlin, D-10117 Berlin, Germany. Electronic address: alice.mika@charite.de. 5. Department of Nephrology, Charité Universitätsmedizin Berlin, Charité Campus Mitte, Humboldt University Berlin, D-10117 Berlin, Germany. Electronic address: oliver.staeck@charite.de. 6. Department of Nephrology, Charité Universitätsmedizin Berlin, Charité Campus Mitte, Humboldt University Berlin, D-10117 Berlin, Germany. Electronic address: hans-h.neumayer@charite.de. 7. Department of Nephrology, Charité Universitätsmedizin Berlin, Charité Campus Mitte, Humboldt University Berlin, D-10117 Berlin, Germany. Electronic address: Harm.Peters@charite.de. 8. Department of Nephrology, Charité Universitätsmedizin Berlin, Charité Campus Mitte, Humboldt University Berlin, D-10117 Berlin, Germany. Electronic address: torsten.slowinski@charite.de.
Abstract
BACKGROUND: Systemic citrate accumulation is a complication of regional citrate anticoagulation (RCA) during continuous renal replacement therapy (CRRT). Our objective was to determine the incidence of clinical signs consistent with citrate accumulation in a large and representative cohort of intensive care unit patients undergoing RCA-CRRT. METHODS: Patients treated with RCA-CRRT during 2008-2010 were retrospectively analyzed. Decreased systemic ionized calcium (iCa), increased demand for calcium substitution, elevated total calcium to iCa ratio, and metabolic acidosis were evaluated as indicators for citrate accumulation. RESULTS: In the 3-year period, 1070 patients were treated with RCA-continuous venovenous hemodialysis. Metabolic signs of citrate accumulation occurred in 32 patients (2.99%, 64.5 ± 14.0 years, 65.6% male, Acute Physiology and Chronic Health Evaluation score 34.2 ± 9.7): systemic iCa decreased to 1.01 ± 0.10 mmol/L with a simultaneous increase of the calcium substitution rate to 129% ± 26%, and the mean total calcium to iCa ratio increased to 2.51 ± 0.54. All 32 patients had therapy-resistant shock with severe lactic acidosis (pH 7.20 ± 0.11, lactate 136 ± 61 mg/dL), indicating severe intracellular hypoxia. None of the patients survived. CONCLUSIONS: The incidence of disarrangements consistent with citrate accumulation in patients undergoing RCA-continuous venovenous hemodialysis was low, taking place exclusively in patients with severe lactic acidosis due to multiorgan failure. This suggests that the appearance of citrate accumulation is secondary to a severe failure of cellular respiration.
BACKGROUND: Systemic citrate accumulation is a complication of regional citrate anticoagulation (RCA) during continuous renal replacement therapy (CRRT). Our objective was to determine the incidence of clinical signs consistent with citrate accumulation in a large and representative cohort of intensive care unit patients undergoing RCA-CRRT. METHODS:Patients treated with RCA-CRRT during 2008-2010 were retrospectively analyzed. Decreased systemic ionizedcalcium (iCa), increased demand for calcium substitution, elevated total calcium to iCa ratio, and metabolic acidosis were evaluated as indicators for citrate accumulation. RESULTS: In the 3-year period, 1070 patients were treated with RCA-continuous venovenous hemodialysis. Metabolic signs of citrate accumulation occurred in 32 patients (2.99%, 64.5 ± 14.0 years, 65.6% male, Acute Physiology and Chronic Health Evaluation score 34.2 ± 9.7): systemic iCa decreased to 1.01 ± 0.10 mmol/L with a simultaneous increase of the calcium substitution rate to 129% ± 26%, and the mean total calcium to iCa ratio increased to 2.51 ± 0.54. All 32 patients had therapy-resistant shock with severe lactic acidosis (pH 7.20 ± 0.11, lactate 136 ± 61 mg/dL), indicating severe intracellular hypoxia. None of the patients survived. CONCLUSIONS: The incidence of disarrangements consistent with citrate accumulation in patients undergoing RCA-continuous venovenous hemodialysis was low, taking place exclusively in patients with severe lactic acidosis due to multiorgan failure. This suggests that the appearance of citrate accumulation is secondary to a severe failure of cellular respiration.
Authors: Rinaldo Bellomo; Claudio Ronco; Ravindra L Mehta; Pierre Asfar; Julie Boisramé-Helms; Michael Darmon; Jean-Luc Diehl; Jacques Duranteau; Eric A J Hoste; Joannes-Boyau Olivier; Matthieu Legrand; Nicolas Lerolle; Manu L N G Malbrain; Johan Mårtensson; Heleen M Oudemans-van Straaten; Jean-Jacques Parienti; Didier Payen; Sophie Perinel; Esther Peters; Peter Pickkers; Eric Rondeau; Miet Schetz; Christophe Vinsonneau; Julia Wendon; Ling Zhang; Pierre-François Laterre Journal: Ann Intensive Care Date: 2017-05-04 Impact factor: 6.925
Authors: V Schwenger; D Kindgen-Milles; C Willam; A Jörres; W Druml; D Czock; S J Klein; M Oppert; M Schmitz; J T Kielstein; A Zarbock; M Joannidis; S John Journal: Med Klin Intensivmed Notfmed Date: 2018-03-15 Impact factor: 0.840
Authors: Torsten Slowinski; Stanislao Morgera; Michael Joannidis; Thomas Henneberg; Reto Stocker; Elin Helset; Kirsti Andersson; Markus Wehner; Justyna Kozik-Jaromin; Sarah Brett; Julia Hasslacher; John F Stover; Harm Peters; Hans-H Neumayer; Detlef Kindgen-Milles Journal: Crit Care Date: 2015-09-29 Impact factor: 9.097