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Anticoagulation in CRRT

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Title: Aspen, Colorado Author: BRADLEY A WARADY, MD Description: Aspen Talk, July, 1998 Last modified by: Timothy E. Bunchman Created Date: 7/3/1997 7:31:28 AM – PowerPoint PPT presentation

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Title: Anticoagulation in CRRT


1
Anticoagulation in CRRT
Timothy E. BunchmanProfessorPediatric
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
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.
5
Heparin ProtocolsBenefit and Risks
  • 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

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)

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

9
(Ca 0.4 x citrate rate 60 mls/hr)
(Citrate 1.5 x BFR 150 mls/hr)
Pediatr Neph 2002, 17150-154
(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)

10
Complications of CitrateMetabolic 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 CitrateCitrate 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!

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

13
Citrate Heparin LM Hep
Hoffbauer R et al. Kidney Int. 1999561578-1583.
14
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 lt 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) ACTs
    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
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