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Anticoagulation and its use in haemodialysis

Murni Indrasti
Sub Bag Nefrologi / Hipertensi Bag Penyakit Dalam FK UNDIP/RS Dr Kariadi

Basic clinical dialysis,Georgina Follows Hdx foundation

module

• HEMOSTASIS

hemostasis
• f
BV injury

Agregasi trombosit Konstrisi p.drh

Cascade koagulasi

Hemostasis plug stabil

HEMOSTASIS
1. Hemostasis primer; - vasokonstriksi p.drh - erbentuknya pletelet plug 2. Hemostasis sekunder - aktivasi koagulasi kaskade - deposisi dan stabilisasi fibrin 3. Hemostasis tersier - disolusi fibrin klot - plasminogen aktivasi

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Trombosit berikatan dengan kolagen melalui reseptor colagen spesifik glikoprotein 1a / 2a .Hemostasis primer 1. Kerusakan dd p drh akan memaparkan protein sub endotel kolagen ke subendotel 2.

Hemostasis sekunder Kaskade koagulasi 1.Jalur intrinsik 2.Jalur ekstrinsik Sehingga terbentuk fibrin .

Hemostasis .Hemostasis sekunder. terjadi bersamaan 1.aktivasi kaskade kompleks 2. trombosit segera membentuk plug pd lokasi injury . faktor pembekuan dalam sirkulasi m.Hemostasis primer. Membentuk fibrin strands 3 Fibrin strand memperkuat trombosit plug .

suatu proses degradasi fibrin • Plasmin akan memecah fibrin menyebabkan produksi fragmen dalam sirkulasi yang akan dibersihkan oleh bbg protease atau oleh ginjal dan hati • Plasmin diproduksi dalam bentuk inaktif plasminogen didalam hati.Fibrinolisis. .

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& penggunaan obat anti platelet sering menyebabkan tendensi perdarahan. ada banyak bukti adanya defek pd glikoprotein trombosit reseptor IIb/IIIa thd fibrinogen & glikoprotein (GP) Ib vWF. • Faktor yg menyebabkan trombosis pd penderita HD yaitu : Hipotensi. • Terapi antikoagulan selama HD. malnutrisi .• Perdarahan & trombosis  problem sering terjadi pd HD • Perdarahan terutama disebabkan kelainan trombosit & dinding pembuluh darah walau jml trombosit sering normal. Hiperhomosisteinemi. Disfungsi endotel. inflamasi. • Waktu perdarahan & kadar urea merupakan petunjuk kasar thd perdarahan.

XI. • Pemberian heparin mencegah terjadinya klot. dan menyebabkan inaktifasi dari faktor diatas. XII. • Waktu paruh heparin 30-120 mnt & memanjang dgn adanya disosiasi heparin dari komplek antitrombin III . IX. • Heparin akan berikatan dgn antitrombin III pd sirkulasi & menghambat faktor koagulasi I.• Kontak darah dgn udara pd drip chamber akan menyebabkan terbentuknya klot extrakorporeal diawali dgn timbunan & agregasi trombosit terbentuk tromboksan aII & terjadi aktifasi dari jalur koagulasi intrinsik. terjadi formasi trombin & deposisi fibrin.

turbulence) .Faktor yg berpengaruh terjadinya klot pd ekstrakorporeal : • • • • • Low blood flow High hematocrit High ultrafiltration rate Dialysis access recirculation Intradialytic blood and blood product transfusion • Intradialytic lipid infusion • Use drip chambers (air exposure. foam formation.

1 jam terakhir tanpa heparin . 1 jam terakhir tanpa heparin Heparin minimal : • Priming 2000 unit diikuti 250 unit/jam.Pemberian heparin pd HD : Reguler : • Priming 2000 unit diikuti 1000 unit/jam.

ACT : Activated Clotting Time.Target clotting time during dialysis Routine heparin Tight heparin Desired range Test Reagent Baseline value During dialysis + 80% (120-140) + 80% (200-250) 20-30 At end of dialysis + 40% (85-105) + 40% (170-190) 9-16 Desired range During dialysis + 40% (85-105) + 40% (170-190) 9-16 At end of dialysis + 40% (85-105) + 40% (170-190) 9-16 WBPTT Actin FS Siliceous earth None 60-85 sec ACTa LWCTb 120-150 sec 4-8 min WBPTT : Whole Blood Partial Thromoplastin Time. e. bBaseline values of the LWCT vary greatly depending on how the test is performed . and the baseline value with some methods is much lower. LCWT : Lee-White Clotting Time aThere are various methods of performing the ACT.g 90-120 sec.

Komplikasi pemberian heparin • Lipid.HAT1 : menurunnya jml trombosit dose dependent . Oleh karena supresi aldosteron . menurunkan HDL kolesterol. Heparin mengaktifasi lipoproteinlipase dan meningkatkan trigliserid. • Trombositopeni. Heparin akan menimbulkan terbentuknya antibodi .HAT2 : terbentuknya imunoglobulin G thd heparin/ platelet faktor IV • Pruritus • Hiperkaliemi.

Heparin • Discovered in 1916 by McLean • Anticoagulant found in the liver • Porcine and bovine preparations • Molecular weight = 3000 to 30000 Daltons • Binds to thrombin inhibitor ANTITHROMBIN III > inactivates active Factor X and inhibits conversion of prothrombin to thrombin Basic clinical dialysis.Georgina Follows Hdx foundation module .

– direct access • Cheap • Metabolised naturally by the liver • Acts quickly and effectively on the intrinsic pathway • Reversed quickly and easily by Protamine • Long.Georgina Follows Hdx foundation module .V. established history of use Basic clinical dialysis.Advantages of Heparin • I.

Georgina Follows Hdx foundation module .Disadvantages of Heparin • Bleeding • Hyperlipidaemia • Thrombocytopenia • Allergic reactions • Pruritis • Alopecia • Osteoporosis Basic clinical dialysis.

Rising / falling venous pressure Basic clinical dialysis.Darkened blood .Blood entering venous isolator .Streaks in dialyser .Clots / fibrin rings in chambers .Georgina Follows Hdx foundation module .Assessment of coagulation • Clotting times – APTT (Actual Partial thromboplastin Time) or ACT (Activated Clotting Time) – 120 secs • Observe for signs of clotting .

Georgina Follows Hdx foundation module .Factors affecting coagulation • Blood flow • High haematocrit levels • EPO • Blood transfusion • Intra-dialytic lipid infusion • High UF rate • Type of circuit • Medication Basic clinical dialysis.

Polysulphone more compatible with blood than Cuprophane and Cellulose Basic clinical dialysis.g. • Individual clotting abnormalities • Type of dialyser • Membrane .Synthetic membranes vary.Natural membranes e.Factors affecting coagulation cont. cuprophane – relatively high platelet activation .Georgina Follows Hdx foundation module .

< 150 X l0 9/L • Intracranial haemorrhage • Any active bleeding • Uraemic patients • Heparin free dialysis : flushing the dialyzer with 100ml Nacl 0.9% Every 30-60 minute Basic clinical dialysis.Georgina Follows Hdx foundation module . therapy antiplatelet • Thrombocytopenia.Contraindications for heparin use • Pericarditis • Pre and post surgery. < 48 hour • Following temporary line insertion • Coagulation abnormalities.

Contraindications for heparin use cont.Georgina Follows Hdx foundation module . • Peptic ulcer • Aortic aneurysm • Cerebral aneurysm • Severe liver disease • Hypersensitivity / allergic reactions Basic clinical dialysis.

Standard Heparin (UFH) Dose • bolus dose 2500 U ( 50U/kgBB).Georgina Follows Hdx foundation module . maintenance 1000/jam • atau initial HD: loading dose of 250-500 U followed by infusion rate 250-500. max 2000U •Heparin Free Dialysis • Obtain baseline clotting time • 5000u heparin rinse • High blood flow rate • 100-200 mls saline flush every 30 mins Basic clinical dialysis.

W.• L.M. effective & decreased bleeding risk • Simple – single dose required • Reduced cholesterol and triglyceride levels • Reduced alopecia Disadvantages • Expensive. not use ACT’s Basic clinical dialysis. little thrombin inhibition.Georgina Follows Hdx foundation module . APTT / ACT minimally prolonged. – inhibits Factor X. long half life.H. Advantages • Safe.

BLEEDING & THROMBOSIS Murni Indrasti Sub Bagian Nefrologi-Hipertensi SMF Penyakit Dalam RSUP Dr Kariadi Semarang .

this can mean the loss of 120-250 ml of blood • clotting within an HD circuit can be minimised through aprpropiate use of anticoagulant therapy • periodic anticoagulation is normally given during the dialysis treatment Basic clinical dialysis. the dialysis membran and air in the HD circuit stimulates the clothing cascades • excessive clotting in the dialysis circuit and filter need to be discarded. in adult.Highlight • contact with plastic tubing.Georgina Follows Hdx foundation module .

• To gain understanding of any contraindications to heparin uses. • To gain understanding of heparin. Basic clinical dialysis.Aims and objectives • To gain understanding of the mechanisms involved in the clotting process and coagulation assessment. its administration. • To gain understanding of any alternatives to heparin usage. advantages and disadvantages.Georgina Follows Hdx foundation module .

Introduction Blood comes into contact with extrinsic factors during haemodialysis. Basic clinical dialysis.Georgina Follows Hdx foundation module . •Both of these methods are prescribed and can be altered to tailor each patients needs. Administration of heparin • Bolus dose at the beginning of dialysis •Continuous infusion during dialysis. Heparin is the most commonly used anticoagulant during dialysis.

Meningkatnya waktu paruh LMW heparin .Penyakit imun (SLE) .Obat-obatan misal : mycophenolate.Perdarahan pd penderita dialisis • • • • Inadekwat dialsysis Anemi Hb < 9 Trombositopeni .Post plasma varesis hilangnya faktor pembekuan . ciclophospamide .Heparin pd HD . azathioprine.Sepsis (DIC) .Gangguan sumsum tulang • Koagulopati .

koagulasi • Pd penderita dgn warfarin diberikan terapi FFP (BB 80 4 unit FFP). resusitasi pasien • Ambil darah utk crossmed & pem. dosis maksimum 50 mg dlm 10 mnt sisanya diberikan dlm per-infus dlm 8 jam • Pd penderita disfungsi trombosit diberikan Desmopresin (DDAVP) DDAVP akan memobilisasi faktor VIII & vWF jaringan dari endotel • Perbaikan anemi dgn transfusi sampai Hb 9 • Tingkatkan dosis dialisis pd penderita dgn dialisis tak adekwat .Penatalaksanaan perdarahan akut serius pd penderita HD • Stop HD. vit K 10-20 mg i.v • Pd penderita trombosit < 50.v tiap 100 unit heparin.000 diberikan TC • Pd penderita dgn heparin diberikan protamin 1 mg i.

Penatalaksanaan perdarahan AV vistula post dialisis • Diberikan kompres es • Bila masih berdarah diberikan DDAVP Cara pemberian DDAVP • DDAVP i.v 0.5 • Waktu paruh faktor VIII plasma 5-8 jam & vWF 8-10 jam • DDAVP bisa menyebabkan vasodilatasi & akan tetapi hipotensi berkurang dgn pemberian infus lambat selama 30 menit • Dosis ulangan diberikan 12-24 jam setelah dosis awal .3 gr/kg dlm 50cc NaCL 0.

Penatalaksanaan perdarahan dari CVC • • • • • Berikan tekanan lokal (dgn es) Kalau perlu dijahit Bila perdarahan msh berlanjut diberikan DDAVP Evaluasi RW pd hematom yg besar & pd hemotorax Rawat pasien .

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GROUP WORK A patient complains of loss of hair over the past couple of months. what would you do?? A patient has just completed dialysis and you notice that the kidney is very dark. but still no change.Georgina Follows Hdx foundation module . What would you do?? Basic clinical dialysis. She has minimal heparin on dialysis. The patient is already on high doses of heparin.

Basic clinical dialysis. • Non-thrombogenic membranes.Future • Coating of elements of circuit with active heparin. • Heparinised coated cartridges capable of removing heparin infused into the extra corporeal circuit.Georgina Follows Hdx foundation module .

QUESTION??? • Which pathway is initiated during haemodialysis? Basic clinical dialysis.Georgina Follows Hdx foundation module .

The Coagulation Cascade Vascular Constriction Platelet plug formation Formation of blood clots Basic clinical dialysis.Georgina Follows Hdx foundation module .

The Coagulation Cascade Vascular Constriction Platelet plug formation Formation of blood clots Basic clinical dialysis.Georgina Follows Hdx foundation module .

•The coagulation cascade then occurs by using thrombin – an enzyme that converts fibrinogen into fibrin. This forms a mesh trapping the formed elements of blood – thus forming a CLOT. Basic clinical dialysis.Extrinsic pathway • Damaged tissue – thromboplastin released – initiates formation of prothrombinase in presence of Factor X and calcium ions.Georgina Follows Hdx foundation module .