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Anticoagulation in CRRT . Timothy E. Bunchman Professor Pediatric Nephrology & Transplantation. 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)
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Anticoagulation in CRRT Timothy E. BunchmanProfessorPediatric Nephrology & Transplantation
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
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
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; 976-978, 1990.
Benefits Heparin infusion prior to filter with post filter ACT measurement Bolus with 10-20 units/kg Infuse at 10-20 units/kg/hr Adjust post filter ACT 180-200 secs Risks Patient Bleeding Unable to inhibit clot bound thrombin Ongoing thrombin generation Activates - damages platelets / thrombocytopenia Heparin ProtocolsBenefit and Risks
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
Citrate: Mechanism of Action • (Thanks to Peter Skippen)
Citrate: Advantages • No need for heparin • Commercially available solutions exist (ACD-citrate-Baxter) • Less bleeding risk • Simple to monitor • Many protocols exist
(Ca = 0.4 x citrate rate 60 mls/hr) (Citrate = 1.5 x BFR 150 mls/hr) Pediatr Neph 2002, 17:150-154 (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 24-143 hrs)
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)
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 10-30 minutes then restart at 70% of prior rate • Patients receiving multiple blood products receive additional citrate that may not be accounted for!
What is the best anticoagulant • None • Heparin • Standard • Low molecular weight • Citrate
Citrate Heparin LM Hep Hoffbauer R et al. Kidney Int. 1999;56:1578-1583.
Heparin or Citrate?(M Golberg RN et al, Edmonton PCRRT 2002) • Heparin circuits • 13 patients with 45 filters • 29.4 + 23 hrs average length of circuit • Citrate circuits • 16 patients with 51 filters • 49.1 + 26 hrs average length of circuit • (p < 0.001)
Filter clot free survival at fixed time intervals according to method of anticoagulation citrate heparin (data from Sheldon Tobe)
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)
ppCRRT: Anticoagulation (Brophy et al, submitted)
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
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
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