Dipergunakan pada Hemodialisis sejak 1960-an

Tujuan yang diharapkan adalah memberikan

dosis seoptimal mungkin untuk mencegah
terjadinya pembekuan pada extracorporeal
sirkuit dan meminimalisir resiko komplikasi
perdarahan



Faktor pencetus pembekuan extracorporeal sirkuit :
a. Low blood flow
b. High hematokrit
c. High ultrafiltration rate
d. Dyalisis access recirculation
e. Intradialytic blood and blood product transfusion
f. Intradialytic lipid infusion
g. Use of drip chambers (air exposure,foam formation,turbulence)

Penilaian koagulasi selama Dialisis
Visual inspeksi, tanda-tandanya :
1. Extremely dark blood
2. Shadows or black streaks in the dialyzer
3. Foaming with subsequent clot formation in drip chambers and venous
trap
4. Presence of clots at the arterial side header

Tekanan extracorporeal sirkuit
Tampilan Dialiser setelah dialisis
Pengukuran volume residual dialiser

Koagulasi pada pasien dialisis
Dapat terjadi 5-10% selama 3-4 jam sesi dialisis
Resiko kehilangan darah hingga 100-150ml
Mengurangi luas permukaan membran dialiser volume
dialiser
Mengurangi adekuasi hd
Penggunaan jenis membran juga akan meningkatkan aktivasi
koagulasi mis. Cellulose (cuprophane)
Pertimbangan penggunaan antikoagulasi berbeda-beda
AS ------- Unfractioned heparin
European Union ----------- low molecular weight heparin


Unfractionated Heparin
Inaktivasi faktor-faktor pembekuan terutama faktor Xa
Membentuk komplek heparin-trombin-antitrombin
aktifitas antitrombin (heparin dgn 18 sakarida)
Half life : 30 menit - 2 jam
Dapat diberikan rutin pada pasien yang tidak mempunyai
resiko perdarahan
Ada 2 cara :
a. Bolus 2000 IU (3-5 mnt) drip 1000 IU/jam
b. Bolus 3000-4000 IU ; diulang jika perlu 1000-2000 IU

Unfractionated Heparin
Dihentikan 30-60 mnt sebelum akhir dialisis
Target ACT 200-250 detik (angka normal 90-140 detik)
Efek samping : gatal, alergi, osteoporosis, hiperlipidemia (
aktivitas lipoprotein lipase hipertrigliserida),
trombositopenia dan perdarahan
Heparin Induce Trombositopenia (HIT)
HIT 1 non imun , dapat kembali normal
HIT 2 antibodi terhadap heparin-platelet faktor 4 kompleks ,
tidak dapat kembali normal

ANTIKOAGULAN
1. Antikoagulan rutin
a. Kontinyu
b. Bolus berulang
2. Heparinisasi minimal
(resiko perdarahan sedang)
3. Dialisis bebas heparin
(resiko perdarahan besar)


ANTIKOAGULAN
Resiko perdarahan sedang
o perkarditis
o riwayat perdarahan kurang
dari 48 jam
o setelah pemasangan
tunneled catheter kurang dari
24 jam
o pembedahan minor kurang
dari 72 jam
o pembedahan mata dan
pembedahan besar dalam 3-7
hari
Resiko perdarahan tinggi
o bleeding diathesis
o penyakit dengan
gangguan faktor
pembekuan
o perdarahan aktif
o pembedahan mata dan
pembedahan besar
kurang dari 72 jam
o perdarahan intrakranial
kurang dari 7 hari
Heparinisasi Minimal
Heparin diberikan bolus 500 unit setiap 30 menit, untuk
mencapai target ACT 150-200 detik

Dapat juga dengan teknik bolus heparin 5-10 unit/kg,
dilanjutkan tanpa heparin atau infus sangat pelan 250-500
unit/jam. Jika nilai ACT menurun atau terlihat pembekuan
darah, maka bolus heparin 500 unit dapat diberikan diantara
infus kontinyu
Dialisis Bebas Heparin

Bilas sirkuit dialisis dengan NaCL 0,9% yang telah dicampur
heparin 3000-5000 unit
Bilas dan keluarkan cairan tersebut diatas (jangan dimasukkan ke
dalam tubuh pasien)
Gunakan secepat mungkin aliran darah (Qb 250 ml/mnt)
Bilas sirkulasi dialisis tiap 15-30 menit dengan NaCl 0,9% sebanyak
25-200 ml untuk mencegah pembekuan di jalur arteri
Naikkan laju ultrafiltrasi untuk mengeluarkan NaCl ekstra
Perhatikan dialiser dan awasi tekanan vena dengan hati-hati untuk
mendeteksi tanda-tanda awal pembekuan darah
Hindari pemberian tranfusi darah
Naikkan UF goal
Dialisis Bebas Heparin

HD selama 2-3 jam
Penggunaan membran polysulfone (lowest
trombogenicity)


Low Molecular Weight Heparin(LMWH)
Depolymerised fractions of heparin obtained by chemical or enzymatic
treatment of UFH
Anionic glycosaminoglycans
2 - 9 kDa but mostly around 5kDa ie 15 saccharide units
less coagulation inhibitory
LMWH binds with antithrombin III to inhibit factor Xa, but mostly (50-70%) does
not have the second binding sequence needed to inhibit thrombin due to
smaller size/length
Affinity to Xa vs Thrombin is 2.5-3 to 1
Only cleared by renal/dialysis mechanisms
Can be monitored by Anti-Factor Xa activity in plasma
Administered into venous limb as cleared by hi-flux membrans

Low Molecular Weight Heparin(LMWH)
Convenience of single administration
less dialysis membrane associated clotting, fibrin deposition
and cellular debris
Less non specific binding
Less binding to platelets- less platelet dysfunction
Less binding to endothelium- fewer interactions between von
Willebrand factor, platelets and endothelium
Minor beneficial changes in lipid profile LDL/VLDL//HDL Heparin
Lower K - heparin induces inhibition of mineralocorticoid metabolism
reduced adrenal aldosterone secretion. Less aldosterone inhibition
with LMWH
Cost disadvantage


Low Molecular Weight Heparin(LMWH)
Because of high bioavailability and predictable effect monitoring
may not be required.
Anti-Xa Testing may be used for
monitoring of effect during/end dialysis
ensure no accumulation at beginning of next dialysis - to
adjust dose in subsequent dialyses



Low Molecular Weight Heparin(LMWH)
The findings of a meta-analysis showed that LMW heparin and
unfractionated heparin were similarly safe and effective in
preventing extracorporeal circuit thrombosis
11 studies included
No significant differences in terms of bleeding or thrombosis



Safety and efficacy of low molecular weight heparins forhemodialysis in patients
with end-stage renal failure: a metaanalysis of randomized trials. Lim W; Cook
DJ; Crowther MA J Am Soc Nephrol 2004 Dec;15(12):3192-206.

Regional
Heparin / Protamine

Infuse Heparin into arterial line (coming out of patient)
Infuse Protamine into venous return line
Technically difficult, no significant advantage over low dose
heparin
Protamine has shorter half life than heparin, also R.E. system
frees heparin from protamine-heparin complex therefore
increased risk of bleeding 2-4 hrs post dialysis
1 mg protamine neutralises 90-115 USP U heparin
Not in HITS!!
No longer a recommended technique

Regional
Heparin / Protamine


Regional
CITRATE
Infusion of iso-osmotic trisodium citrate or hypertonic
trisodium citrate into arterial side of circuit - binds ionised
calcium and inhibits clotting cascade
Citrate-calcium complex partly removed by dialyser
Needs or is Enhanced by calcium (and Mg) free dialysate
Infuse 5% CaCl into venous return at 0.5ml/min
May need low-bicarb Dialysate to avoid alkalosis if daily dialysis
Frequent measures of plasma calcium eg 2hrly

Regional
CITRATE

PROBLEMS
Too complex to be a routine method-maybe in bleeding pt
Requires two infusion pumps and two infusion solns
Risk of life threatening Low or High Calcium
Hypernatraemia a risk if using hypertonic NaCitrate - use low Na
dialysate
Metabolic alkalosis - from metabolism of citrate

ADVANTAGES
Bleeding complications reduced compared to low dose heparin
Improves biocompatibility - reduced granulocyte activation
Reduced deposition of blood components on dialysis membrane
compared to UFH or LMWH
Simplified protocols being developed