1. Anticoagulation in CRRT
Timothy E. Bunchman Professor Pediatric Nephrology & Transplantation

2. Anti-Coagulation What is best? Can you run anticoagulation free?
Having no anticoagulation shortens circuit life
Will you use Heparin?
Patient bleeding
Platelet count (HIT)
Will you use Citrate?
Citrate lock
Metabolic alkalosis

3. Anticoagulation free Protocols
Classically occur in patients with MODS with abnormal clotting parameters
Usually these patient are given ample amount of platelet infusions and coagulation factors
This excessive amount of volume adds to greater need for ultrafiltration
Final affect is clotting

4. Mehta,RL. Regional Citrate anticoagulation for CAVHD in
Heparin or Citrate
(Mehta data)
Saline Flushes
Filter Life (hours)
Citrate
Heparin
Mehta,RL. Regional Citrate anticoagulation for CAVHD in
critically ill patients . Kidney Int, 38; , 1990.

5. Heparin Protocols Benefit and Risks
Benefits
Heparin infusion prior to filter with post filter ACT measurement
Bolus with units/kg Infuse at units/kg/hr
Adjust post filter ACT secs
Risks
Patient Bleeding
Unable to inhibit clot bound thrombin
Ongoing thrombin generation
Activates - damages platelets / thrombocytopenia

6. Citrate: How does it work
Clotting is a calcium dependent mechanism; chelating calcium within blood will inhibit clotting
Adding citrate to blood will bind the free calcium (ionized) calcium in the blood thus inhibiting clotting
Common example of this is blood banked blood

7. Citrate: Mechanism of Action
(Thanks to Peter Skippen)
Citrate as CPD is the anticoagulant used to collect and store blood for transfusion. Every bloodbank to my knowledge uses it. IT WORKS!
As you can see from this slide, the effects of citrate on the ionized calcium levels in the blood are dose related. The body easily handles the citrate load by metabolism, particularly in the liver, but virtually everywhere as a substrate for the citric acid cycle (Krebs Cycle).

8. Citrate: Advantages No need for heparin
Commercially available solutions exist (ACD-citrate-Baxter)
Less bleeding risk
Simple to monitor
Many protocols exist

9. ACD-A/Normocarb Wt range 2.8 kg – 115 kg
(Ca = 0.4 x citrate rate
60 mls/hr)
(Citrate = 1.5 x BFR
150 mls/hr)
Pediatr Neph 2002, 17:
(BFR = 100 mls/min)
Normal Saline Replacement Fluid
Calcium can be infused in 3rd lumen of triple lumen access if available.
Normocarb Dialysate
ACD-A/Normocarb Wt range 2.8 kg – 115 kg
Average life of circuit on citrate 72 hrs (range hrs)

10. Complications of Citrate: Metabolic alkalosis
Metabolic alkalosis due to
citrate converts to HCO3 (1 mmol of citrate converts to 3 mmols of HCO3)-major cause
Solutions contain 35 meq/l HCO3-minor cause
NG losses-minor cause
TPN with acetate component-minor cause
Rx metabolic alkalosis by addition of an acid load = Normal Saline (pH 5.4)

11. Complications of Citrate: “Citrate Lock”
Seen with rising total calcium with either a sustained or dropping patient ionized calcium
Essentially delivery of citrate exceeds hepatic metabolism and CRRT clearance
Rx of “citrate lock”
Decrease or stop citrate for minutes then restart at 70% of prior rate
Patients receiving multiple blood products receive additional citrate that may not be accounted for!

12. What is the best anticoagulant
None
Heparin
Standard
Low molecular weight
Citrate

13. Citrate Heparin LM Hep
Hoffbauer R et al. Kidney Int. 1999;56:

14. Heparin or Citrate? (M Golberg RN et al, Edmonton PCRRT 2002)
Heparin circuits
13 patients with 45 filters
hrs average length of circuit
Citrate circuits
16 patients with 51 filters
hrs average length of circuit
(p < 0.001)

15. Filter clot free survival at fixed time intervals according to method of anticoagulation
citrate
heparin
(data from Sheldon Tobe)

16. ppCRRT- Anticoagulation
Center, Patient and Circuit Demographics
Data collected from 1/1/01 through 10/31/03
HepACG only: 3 centers (1 CVVH, 2 CVVHD)
CitACG only: 2 centers
HepACG changed to CitACG: 2 centers
138 patients total
18208 hours of CRRT circuit time
230 hepACG circuits (52%) (9468.hrs)
158 citACG circuits (36%) (6545 hrs)
54 noACGcircuits (12%) (2185 hrs)

17. ppCRRT: Anticoagulation
(Brophy et al, submitted)

18. ppCRRT: Anticoagulation
43/158 citACG vs 58/230 hepACG clotted (NS)
9 pts (hepACG) had systemic bleeding; 4 led to hepACG discontinuation
1 pt (hepACG) developed Thrombocytopenia leading to hepACG discontinuation
No systemic bleeding side effects were reported with citACG; 4 pts developed alkalosis and 2 pts with hepatic failure developed citrate lock.
No correlation between circuit survival and (1) mean hepACG rate (2) #ACT/hour or (3) # ACT’s less 180 seconds

19. Summary Many protocols exist for anticoagulation
All have risk and benefit
Heparin with protamine has been used but adds to potential complications and work at bedside

20. Conclusion Choice of anticoagulation is best decided locally
For the benefit of the bedside staff who do the work come to consensus and use just one protocol
Having the “protocol” changed per whim of the physician does not add to the the care of the child but subtracts due to additional confusion and work at bedside