A brief introduction to principles of Anticoagulation in Hemodialysis, CRRT

1. Anticoagulation in Hemodialysis
DR. ORIBA DAN LANGOYA
RESIDENT INTERNAL MEDICINE,
DEPT. OF INTERNAL MEDICINE, MAKERERE UNIVERSITY

2. INTRODUCTION
• An ever increasing number of patients with established
RF are dependent on hemodialysis (HD) to sustain their
lives
• HD has very few absolute contraindications and so is the
default therapy of all forms of renal replacement
therapy (RRT).
• Long-term patient survival in incident HD patients of all
age groups has increased gradually during the past 20
years
• Adequate anticoagulation in hemodialysis procedures
relies on knowledge of hemostasis

3. Key components of the hemodialysis system.

4. Coagulation Cascade

5. HEMOSTATIC ABNORMALITIES INRENAL
INSUFFICIENCY
• Uremia can lead to increased bleeding tendency due
to PLT dysfunction
• Thrombosis can occur at increased rates in Dialysis,
PE, Vascular access thrombosis.
• Pts with Chronic renal failure have a high
prevalence of systemic inflammation & diffuse
endothelial damage
• Activation of platelets and monocytes has also been
detected
• Hypercoagulability increases as renal function declines

6. ACTIVATION OF THE COAGULATION
CASCADE IN THE EXTRACORPOREAL
CIRCUIT
• HD causes turbulent blood flow & high shear rates
• In HD, Gran & Plt coaggregation an effect which is membrane
dependent
• Co-aggregation is followed by activation of both cell types.
• On adhesion to artificial surfaces, granulocytes release the
contents of their granules
• Clotting on artificial surfaces is thought to mainly occur via the
intrinsic (contact activation)

7. ASSESSING BLEEDING RISK
• Severe thrombocytopenia (platelet count of <20,000 x 109/L
• Evidence of active bleeding
• Active intracranial or extradural hemorrhage
• Use of systemic anticoagulants
• Uremic pericarditis
• Coagulation factor VII or VIII deficiency

8. Standard-risk patients
• Both UFH and LMWH protocols are effective
• Unfractionated heparin – Dialysis units in many regions, use UFH for
anticoagulation during hemodialysis (HD). Cal-Heparine.
• We administer a bolus of 2000 units at the beginning of dialysis,
followed by a continuous infusion of 500 units per hour.
• This infusion is usually turned off 60 minutes before the end of the
dialysis session
• If clotting develops, then we stop 30 minutes before the termination
of dialysis.

9. Unfractionated Heparin
• Affects conversion of Heparin is
exerted through affecting
conversion of Fibrinogen to
Fibrin.
• Mediated by Xa as well as Iia
• It acts by activating plasma
antithrombin III
• The Heparin-ATIII complex then
to and inactivates clotting
factors. (Xa,IIa, Ixa, XIIIa)
• Intrinsic and Common Pathways

10. Low-molecular-weight heparins
• Comprise a mixture of anionic glucose-aminoglycans with a smaller
size (molecular weight: 4–8 kDa)
• Antithrombin/LMWH complexes have less affinity to thrombin
• LWMH) are the preferred initial treatment for many thromboembolic
disorders but are renally excreted and relatively contraindicated in
patients with renal failure because of concerns of increased bleeding
risks

12. Patients with heparin-induced
Thrombocytopenia
• 2 forms of heparin-induced thrombocytopenia (HIT),
• Only one of which is clinically significant (type 2):
• HIT type II is a clinically significant condition resulting from
antibodies to PF4 complexed to UFH, referred to as "HIT
antibodies" or "PF4/heparin antibodies.

13. Schematic diagram showing no-heparin regimen in
hemodialysis

14. Summary
• HD and CRRT) are typically delivered with some form of
anticoagulation
• Patients on chronic HD are generally prothrombotic.
• Standard-risk patients – We treat standard-risk patients
(who are not at higher risk for bleeding or thrombosis) with
either UFH or LMWH.
• Patients at high risk for bleeding – Patients at high risk for
bleeding are treated with the "no-heparin" method
• Patients with recurrent filter thrombosis – Patients at
standard risk for bleeding who have recurrent filter
thrombosis should have their UFH or LMWH increased.

15. CAL HEPARIN
INPUTS FROM THE Physician