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 DialisisVisual 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 dialisisDapat 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 HeparinInaktivasi 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 HeparinDihentikan 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.

RegionalHeparin / 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

RegionalCITRATE

PROBLEMSToo complex to be a routine method-maybe in bleeding

pt Requires two infusion pumps and two infusion sol’ns Risk of life threatening Low or High CalciumHypernatraemia a risk if using hypertonic NaCitrate -

use low Na dialysateMetabolic alkalosis - from metabolism of citrate

ADVANTAGESBleeding complications reduced compared to low dose

heparin Improves biocompatibility - reduced granulocyte

activationReduced deposition of blood components on dialysis

membrane compared to UFH or LMWH Simplified protocols being developed