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      Prostacyclin versus Citrate in Continuous Haemodiafiltration: An Observational Study in Patients with High Risk of Bleeding

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          Background: The efficacy and safety of prostacyclin (PGI<sub>2</sub>) and citrate (ACD) anticoagulation were observed and compared during continuous haemodiafiltration. Methods: Mechanically ventilated patients received either the PGI<sub>2</sub> analogue epoprostenol (group A, n = 17) in escalating doses of 4.5–10.0 ng·kg<sup>–1</sup>·min<sup>–1</sup> in combination with heparin (6 IU·kg<sup>–1</sup>·h<sup>–1</sup>) or 2.2% ACD (group B, n = 15). Blood flow was set to match the circuit-filling volume per unit time equal to the intravascular half-life of PGI<sub>2</sub>. Results: Median filter lifetimes were 26 h (interquartile range 16–37) in group A (39 filters) and 36.5 h (interquartile range 23–50) in group B (56 filters; p < 0.01). In group A, 4 patients (23.5%, p < 0.05) had the dose reduced due to hypotension. The final mean dose of PGI<sub>2</sub> was 8.7 ± 2.4 ng·kg<sup>–1</sup>·min<sup>–1</sup>. Four patients in group A (23.5%, p < 0.05) were switched to ACD due to a decrease in platelet count. No bleeding episodes, decrease in platelet count or adverse haemodynamic effects were encountered in group B. The cost of epoprostenol plus low dose heparin (EUR 204.73 ± 53.04) was significantly higher than the cost of ACD-based anticoagulation (EUR 93.92 ± 45.2, p < 0.05). Conclusion: ACD offers longer filter survival, has no impact on platelet count and is less expensive. Increasing the dose of PGI<sub>2</sub> up to the average of 8.7 ng·kg<sup>–1</sup>·min<sup>–1</sup> did not increase the haemodynamic side effects.

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          Most cited references 19

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          Increased total to ionized calcium ratio during continuous venovenous hemodialysis with regional citrate anticoagulation.

          Citrate anticoagulation is commonly used for continuous venovenous hemodialysis (CVVHD) to minimize the risk of bleeding complications. We have previously reported a liver failure patient undergoing citrate-based CVVHD with elevated serum total to ionized calcium ratio. Diminished liver metabolism of citrate with resultant elevated systemic citrate was thought to be the cause. To determine the incidence and clinical significance of an elevated total to ionized calcium ratio during citrate-based CVVHD, 161 patients undergoing citrate-based CVVHD were screened for the presence of an elevated total to ionized calcium ratio (the subset with increased total to ionized calcium ratio comprised the study group). Because all patients in the study group had liver failure, two control groups of patients with normal total to ionized calcium ratios were formed-those without liver failure (control I) and those with liver failure (control II). An elevated total to ionized calcium ratio was detected in 12% of all patients. Thirty-three percent of liver failure patients demonstrated an elevated total to ionized calcium ratio. The study group demonstrated significantly higher mean total calcium levels, significantly lower mean ionized calcium levels, and significantly higher mean total to ionized calcium ratios than controls. As a result, the study group also had significantly increased mean calcium chloride replacement requirements in comparison with controls. The mean calcium to citrate infusion ratio was elevated in the study group in comparison with controls. An elevated total to ionized calcium ratio was associated with increased mortality in comparison with controls. No patients suffered complications from ionized hypocalcemia or elevated serum total calcium. Systemic citrate accumulation as evidenced by an elevated total to ionized calcium ratio occurs commonly in patients requiring CVVHD using citrate-based regional anticoagulation. Observing changes in the total to ionized calcium ratio can aid in early detection of patients with hepatic failure who are unable to appropriately metabolize citrate and will require calcium chloride infusion rates significantly above normal.
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            Citrate pharmacokinetics and metabolism in cirrhotic and noncirrhotic critically ill patients.

            To investigate pharmacokinetics and metabolism of sodium citrate in critically ill patients. To determine the risk of citrate accumulation in the setting of liver dysfunction (cirrhosis, hepatorenal syndrome). Prospective cohort study. Intensive Care Unit, Department of Medicine IV, University Hospital Vienna. Consecutive critically ill cirrhotic (n = 16) and noncirrhotic patients (n = 16). Infusion of sodium citrate (0.5 and calcium chloride (0.17 for 2 hrs. Analysis of serial arterial blood samples. Total body clearance of citrate was normal in noncirrhotic critically ill patients but significantly reduced in cirrhotic patients (710 vs. 340 mL/min, p =.008). Citrate peak concentrations and concentration over time were increased by 65% and 114% in cirrhotic patients (p <.001), respectively; volumes of distribution were similar. Net metabolic changes were quantitatively similar, with pH and plasma bicarbonate concentrations increasing more slowly in cirrhotic patients. No citrate-related side effects were noted. Citrate clearance could not be predicted by standard liver function tests and was not appreciably influenced by renal function and Acute Physiology and Chronic Health Evaluation II scores. This first systematic study on citrate pharmacokinetics and metabolism in critically ill patients confirms a major role of hepatic citrate metabolism by demonstrating reduced citrate clearance in cirrhotic patients. Pharmacokinetic data could provide a basis for the clinical use of citrate anticoagulation in critically ill patients. Provided dose adaptation and monitoring of ionized calcium, citrate anticoagulation seems feasible even in patients with decompensated cirrhosis. Metabolic consequences of citrate infusion were not different between groups in this study but may be more pronounced in prolonged infusion.
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              Regional citrate anticoagulation in continuous venovenous hemofiltration in critically ill patients with a high risk of bleeding.

              Systemic heparinization is associated with a high rate of bleeding when used to maintain patency of the extracorporeal circuit during continuous renal replacement therapy (CRRT) in critically ill patients. Regional anticoagulation can be achieved with citrate, but previously described techniques are cumbersome and associated with metabolic complications. We designed a simplified system for delivering regional citrate anticoagulation during continuous venovenous hemofiltration (CVVH). We evaluated filter life and hemorrhagic complications in the first 17 consecutive patients who received this therapy at our institution. Blood flow rate was set at 180 ml/min. Ultrafiltration rate was maintained at 2.0 liters/hr and citrate-based replacement fluid (trisodium citrate 13.3 mM, sodium chloride 100 mM, magnesium chloride 0.75 mM, dextrose 0.2%) was infused proximal to the filter to maintain the desired fluid balance. Calcium gluconate was infused through a separate line to maintain a serum-ionized calcium level of 1.0 to 1.1 mM. All patients were critically ill and required mechanical ventilation and vasopressor therapy. Systemic heparin anticoagulation was judged to be contraindicated in all of the patients. A total of 85 filters were used, of which 64 were lost because of clotting, with a mean life span of 29.5 +/- 17.9 hours. The remaining 21 filters were discontinued for other reasons. Control of fluid and electrolyte balance and azotemia was excellent (mean serum creatinine after 48 to 72 hr of treatment was 2.4 +/- 1.2 mg/dl). No bleeding episodes occurred. Two patients, one with septic shock and the other with fulminant hepatic failure, developed evidence for citrate toxicity without a significant alteration in clinical status. Nine patients survived (52.9%). Our simplified technique of regional anticoagulation with citrate is an effective and safe form of anticoagulation for CVVH in critically ill patients with a high risk of bleeding.

                Author and article information

                Blood Purif
                Blood Purification
                S. Karger AG
                September 2005
                04 October 2005
                : 23
                : 4
                : 325-329
                Department Anaesthesia and Intensive Care, University Hospital Kralovske Vinohrady, Prague, Czech Republic
                87770 Blood Purif 2005;23:325–329
                © 2005 S. Karger AG, Basel

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                Figures: 1, Tables: 1, References: 21, Pages: 5
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