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Citrate pathophysiology and metabolism

Mehran Monchi1

  • 1Intensive care deparment, Centre Hospitalier de Melun, Melun, F-77000, France.

Transfusion and Apheresis Science : Official Journal of the World Apheresis Association : Official Journal of the European Society for Haemapheresis
|January 12, 2017
PubMed

Insights

Citrate anticoagulation effectively prevents bleeding during extracorporeal circuits by chelating calcium. However, it can cause hypocalcemia, leading to QT prolongation and hypotension, especially in patients with cirrhosis.

Area of Science:

  • Nephrology
  • Hematology
  • Critical Care Medicine

Background:

  • Citrate anticoagulation is a widely used method in extracorporeal circuits, offering an alternative to heparin.
  • It functions by chelating ionized calcium, thereby inhibiting the coagulation cascade.
  • Citrate anticoagulation is associated with reduced activation of leukocytes and platelets.

Purpose of the Study:

  • To evaluate the efficacy and safety of citrate anticoagulation in extracorporeal circuits.
  • To investigate the impact of citrate on patient anticoagulation and bleeding risk.
  • To explore the metabolic fate and potential toxic effects of citrate, particularly in patients with renal impairment or liver cirrhosis.

Main Methods:

  • Review of existing literature on citrate anticoagulation in extracorporeal circuits.
  • Analysis of citrate pharmacokinetics and its clearance mechanisms, including the citric acid cycle (Krebs cycle).
  • Examination of citrate's effects on ionized calcium levels, coagulation parameters, and potential adverse events like hypocalcemia and QT interval prolongation.

Main Results:

  • Citrate effectively achieves anticoagulation in extracorporeal circuits without increasing the patient's bleeding risk.
  • Citrate anticoagulation demonstrates a reduced activation of leukocytes and platelets compared to other anticoagulation methods.
  • Citrate clearance via the citric acid cycle is unaffected by renal failure but is significantly reduced (by approximately 50%) in patients with cirrhosis.
  • Toxic citrate effects are primarily linked to a decrease in plasma ionized calcium, with clinical signs of hypocalcemia and hypotension observed below 0.9 mmol/L.

Conclusions:

  • Citrate anticoagulation is a safe and effective method for extracorporeal circuits, minimizing bleeding complications.
  • Patient factors, particularly liver cirrhosis, can significantly impair citrate metabolism, increasing the risk of toxicity.
  • Close monitoring of ionized calcium levels is crucial to prevent adverse events such as QT prolongation and hypotension in patients undergoing citrate anticoagulation.

Keywords:
AnticoagulationCitrateExtra corporeal circuitsPharmacodynamicsToxicity

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