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Continuous hemodialysis with citrate anticoagulation and standard dialysate for managing acute kidney injury in patients with moderate to severe hyponatremia-A retrospective study.
Acta Anaesthesiologica Scandinavica 2021 July
BACKGROUND: The safety of continuous veno-venous hemodialysis (CVVHD) with citrate-calcium anticoagulation for acute kidney injury (AKI) with coincident hyponatremia remains unclear. We aimed to explore the feasibility of CVVHD with standard dialysate and citrate-calcium anticoagulation in hyponatremic critically ill AKI patients.
METHODS: Thirty-seven of the 493 critically ill AKI patients requiring CVVHD and admitted to our intensive care unit during a 10-year period had hyponatremia (<130 mmol/L) and were included in this retrospective study. All patients received CVVHD with citrate-calcium anticoagulation and standard commercial dialysate and plasma sodium concentrations were frequently controlled until death or CVVHD discontinuation. Clinical data, mortalities and cases of central pontine myelinolysis within one-year follow-up were recorded.
RESULTS: Median plasma sodium concentration was 127 (IQR 124-129) mmol/L at CVVHD initiation. CVVHD duration was median 3 (IQR 1.5-5.5) days and the mean daily sodium load of the trisodium citrate solution during the first 3 days of CVVHD was 1754 (SD 730) mmol. The plasma sodium concentration increased a median 8 (IQR 5-10) mmol/L during the first 24 hours of CVVHD and excessively high plasma sodium correction (>8 mmol/L/24 h) was observed in 18 (48.6%) patients. However, increased mortality in association to rapid plasma sodium correction was not observed in this study.
CONCLUSIONS: CVVHD using standard citrate-calcium anticoagulation effectively increased plasma sodium concentration in this study. However, excessively high plasma sodium correction was observed in half of the patients and the sodium load provided by the standard citrate anticoagulation solutions was substantial.
METHODS: Thirty-seven of the 493 critically ill AKI patients requiring CVVHD and admitted to our intensive care unit during a 10-year period had hyponatremia (<130 mmol/L) and were included in this retrospective study. All patients received CVVHD with citrate-calcium anticoagulation and standard commercial dialysate and plasma sodium concentrations were frequently controlled until death or CVVHD discontinuation. Clinical data, mortalities and cases of central pontine myelinolysis within one-year follow-up were recorded.
RESULTS: Median plasma sodium concentration was 127 (IQR 124-129) mmol/L at CVVHD initiation. CVVHD duration was median 3 (IQR 1.5-5.5) days and the mean daily sodium load of the trisodium citrate solution during the first 3 days of CVVHD was 1754 (SD 730) mmol. The plasma sodium concentration increased a median 8 (IQR 5-10) mmol/L during the first 24 hours of CVVHD and excessively high plasma sodium correction (>8 mmol/L/24 h) was observed in 18 (48.6%) patients. However, increased mortality in association to rapid plasma sodium correction was not observed in this study.
CONCLUSIONS: CVVHD using standard citrate-calcium anticoagulation effectively increased plasma sodium concentration in this study. However, excessively high plasma sodium correction was observed in half of the patients and the sodium load provided by the standard citrate anticoagulation solutions was substantial.
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