Correspondence

Correction

More on Anticoagulation for Continuous Hemofiltration

N Engl J Med 1998; 338:131-132January 8, 1998

Article

To the Editor:

Hsu et al. (Sept. 4 issue)1 describe a method of regional anticoagulation for continuous venovenous hemofiltration that involves the infusion of a citrate-containing replacement fluid. For over a year we have used a similar technique, in which a replacement fluid containing 15 mmol of disodium citrate per liter is infused at a fixed rate of 2 liters per hour, volume control is achieved by variable ultrafiltration, and the blood-flow rate is set at 60 to 150 ml per minute. This approach achieves metabolic control equivalent to that with lactate-based solutions. Correction of acidosis, however, can be insufficient in cases of severe shock because low hepatic perfusion may compromise the conversion of citrate into bicarbonate. In patients with acidosis due to impaired organ perfusion, we use a solution containing both citrate and bicarbonate (15 mmol of disodium citrate per liter and 10 mmol of sodium bicarbonate per liter).

In addition to reducing the risk of hemorrhage, anticoagulation with citrate for continuous hemofiltration may also offer other advantages. Hypercoagulability may be a new indication for citrate anticoagulation. We achieved a nearly normal filter life by using citrate in patients in whom the extracorporeal system usually clots in less than six hours (despite excessive heparinization) because of high fibrinogen levels and elevated platelet counts. The side effects associated with heparin, such as thrombocytopenia, thrombosis, increased vascular permeability, and hyperlipidemia,2 can be avoided with the use of citrate. In addition, patients with the systemic inflammatory response syndrome might benefit from the inhibition of calcium-mediated activation of inflammatory cells in the extracorporeal circulation.3 For these reasons we are convinced that regional anticoagulation with citrate, performed with modern volume-controlled hemofiltration devices, will replace conventional anticoagulation with heparin within the next decade.

Robert Apsner, M.D.
Wilfred Druml, M.D.
University of Vienna, A-1090 Vienna, Austria

3 References

1. 1

   Hsu C-Y, Palsson R, Niles JL. Continuous hemofiltration. N EnglJ Med 1997;337:713-713
   Web of Science | Medline

2. 2

   Hirsh J, Raschke R, Warkentin TE, Dalen JE, Deykin D, Poller L. Heparin: mechanism of action, pharmacokinetics, dosing considerations, monitoring, efficacy, and safety. Chest 1995;108:Suppl:258S-275S
   CrossRef | Web of Science | Medline

3. 3

   Bohler J, Schollmeyer P, Dressel B, Dobos G, Horl WH. Reduction of granulocyte activation during hemodialysis with regional citrate anticoagulation: dissociation of complement activation and neutropenia from neutrophil degranulation. J Am Soc Nephrol 1996;7:234-241
   Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: We agree with Apsner and Druml that citrate should replace heparin as the anticoagulant in the majority of patients requiring continuous venovenous hemofiltration. Two factors currently limiting the widespread adoption of this approach are the lack of standardized protocols and the lack of commercially available citrate-containing replacement fluids. However, we would like to reiterate that this system is not suitable for the minority of patients who cannot adequately metabolize citrate, a condition that can cause hypocalcemia and exacerbate acidosis.

The first sentence of the second paragraph of our original letter should have read, “In brief, we infuse an isotonic sodium citrate–based replacement fluid proximal to the hemofilter.”

Chi-yuan Hsu, M.D.
Massachusetts General Hospital, Boston, MA 02114

Runolfur Palsson, M.D.
Reykjavik City Hospital, Reykjavik, Iceland

John L. Niles, M.D.
Massachusetts General Hospital, Boston, MA 02114

Citing Articles (7)

Citing Articles

1. 1

   J. Bouchard, F. Madore. (2008) Role of citrate and other methods of anticoagulation in patients with severe liver failure requiring continuous renal replacement therapy. NDT Plus 2:1, 11-19
   CrossRef

2. 2

   H. M. Oudemans-van Straaten, J. P. J. Wester, A. C. J. M. Pont, M. R. C. Schetz. (2006) Anticoagulation strategies in continuous renal replacement therapy: can the choice be evidence based?. Intensive Care Medicine 32:2, 188-202
   CrossRef

3. 3

   Robert Apsner, Diego Gruber, Walter H. Hörl, Gere Sunder-Plassmann. (2004) Parathyroid Hormone Secretion During Citrate Anticoagulated Hemodialysis in Acutely Ill Maintenance Hemodialysis Patients. Anesthesia & Analgesia 99:4, 1199-1204
   CrossRef

4. 4

   Ludwig Kramer, Edith Bauer, Christian Joukhadar, Wolfram Strobl, Alexandra Gendo, Christian Madl, Alfred Gangl. (2003) Citrate pharmacokinetics and metabolism in cirrhotic and noncirrhotic critically ill patients. Critical Care Medicine 31:10, 2450-2455
   CrossRef

5. 5

   Herwig-Ulf Meier-Kriesche, Jeremy Gitomer, Kevin Finkel, Thomas DuBose. (2001) Increased total to ionized calcium ratio during continuous venovenous hemodialysis with regional citrate anticoagulation. Critical Care Medicine 29:4, 748-752
   CrossRef

6. 6

   Wilfred Druml. (1999) Metabolic aspects of continuous renal replacement therapies. Kidney International 56:s72, 56-61
   CrossRef

7. 7

   Herwig-Ulf Meier-Kriesche, Kevin W. Finkel, Jeremy J. Gitomer, Thomas D. DuBose. (1999) Unexpected severe hypocalcemia during continuous venovenous hemodialysis with regional citrate anticoagulation. American Journal of Kidney Diseases 33:4, E8
   CrossRef