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TRANSFUSI DARAH INTRODUKSI

Warko Karnadihardja Sub Bagian Bedah RSHS/FKUP Bandung 08-07

PENDAHULUAN

The United Kingdom National Blood Transfusion Service dalam masa 50 thn sejak PD II terkumpul 2.5 juta unit darah tiap tahun Kesediaan sebagai donor harus atas dasar sukarela tanpa dibayar Para dokter harus mengetahui indikasi dan bahaya transfusi darah berdasar kompetensi dokter, pertimbangkan untung dan ruginya

SELEKSI DONOR

Dalam keadaan sehat Sukarela, tanpa bayaran Usia : Untuk rata-rata 450 ml darah Lower limit : 17-18 tahun Upper limit : 60 thn untuk yang pertama kali jadi donor 70 thn untuk yang telah terbiasa jadi donor

SELEKSI DONOR
Frekwensi:

2-3 kali dalam setahun tapi ada yang lebih sering tanpa komplikasi HB : Laki-laki 135 g/L Wanita 125 g/L Volume Donasi : Tidak melebihi 13% volume darah Isi kantong 405-495 ml darah rata-rata 450 ml darah BB minimum 47-50 kg

BOTOL BERISI LARUTAN COPPER SULFATE

PENYAKIT DONOR YANG DIHINDARI

Hepatitis B & C HIV-1 & 2 Malaria Syphilis CMV : Cyto Megalo Virus Malignancy

ABC of Transfusion . Edit Marcelle Contreras BMJ 3rd edit.1998

SEROLOGICAL TEST

ABO typing RhD typing Rhc and E typing RhC and K typing an many units Screen for antibodies to red cell antigens HLA typing (only some donor)

ABC of Transfusion . Edit Marcelle Contreras BMJ 3rd edit.1998

A TRIPPLE BAG FOR COLLECTION OF BLOOD

ABC of Transfusion . Edit Marcelle Contreras BMJ 3rd edit.1998

MULTIPLE PACKS FOR COLLECTION OF BLOOD

ABC of Transfusion . Edit Marcelle Contreras BMJ 3rd edit.1998

COLLECTION OF PLATELETS BY APHERESIS FROM A DONOR

ABC of Transfusion . Edit Marcelle Contreras BMJ 3rd edit.1998

ADVERSE EFFECTS

Live leucocytes release cytokines during storage ( IL-1, IL-6, IL-8 & TNF) Reducing the white cell load tenfold in platelet concentrates by simple centrifugation techniques can prevent most non-hemolytic febrile transfusion reaction (NHFTR) by HLA (while cell antibodies) TRALI (Transfusion Related Acute Lung Injury) caused by potent while cell antibodies

ABC of Transfusion . Edit Marcelle Contreras BMJ 3rd edit.1998

ABC of Transfusion . Edit Marcelle Contreras BMJ 3rd edit.1998

AUTO TRANSFUSI (AUTOLOGOUS TRANSFUSION)

Cara: 1. Darah sendiri diambil sebelum operasi elektif : 2-4 units beberapa minggu sebelumnya 2. Sewaktu operasi : intra operative cell salvage Indikasi: Ada bahaya/indikasi allogenic blood Menghindari TRALI/ARDS Menghindari kesalahan administrasi (error) Menghindari immune modulation

KONTRA INDIKASI AUTO TRANSFUSI

Infeksi bakterial aktif Hb awal < 11 g/l Penyakit kardiovaskular yang tak stabil Hipertensi tidak terkontrol

CELL SAVER SYSTEM FOR AUTOTRANSFUSION

CELL SAVER SYSTEM FOR AUTOTRANSFUSION

WHOLE BLOOD

Whole blood dicampur anticoagulant & stabilizer


500 ml = 70 ml presevative + 430 ml whole blood

Dulu dipakai acid citrate dextrose (CPD-A), sekarang dipergunakan phosphate adenin (CPDA) : darah dan eritrosit lebih lama bertahan hidup Dengan temp 4C daya tahan s/d 35 hari dengan CPD-A, untuk sakit berat atau perlu transfusi masif dianjurkan memakai darah usia < 2 minggu Eritrosit dalam whole blood mudah rusak karena ada neutrofil dan sistim proteolitik plasma Leukosit (terutama neutrofil) penyebab banyak efek samping, oleh karena itu di banyak negara leukosit harus dikurangi

KOMPLIKASI PEMBERIAN STORAGE WHOLE BLOOD

Efek Metabolik ATP makin PH kerusakan sel kebocoran K+ Fungsi Hb ok ATP afinitas thd O2 Perubahan sel eritrosit konsentrate tidak secepat whole blood Mikroagregat Terdiri atas pecahan : platelet-leukosit fibrin + thrombosis yang makin lama disimpan semakin banyak ( q > 170 m) Perlu mikrofilter sewaktu transfusi Fresh whole blood tidak menimbulkan akibat diatas

POTENTIAL PROBLEMS FROM INFUSION OF MICROAGGREGATES


Impaired pulmonary gas exchange (ARDS) Microcirculatory dysfunction Depression of RES function Depression of fibronection levels Febrile reactions Activation of the haemostatic system Activation of the complement system Unnecessary antigenic stimulation Release of vasoactive substances
JP Isbister in Ohs Intensive Care Manual, 5th edition, 2003

POTENTIAL HAZARDS OF MASSIVE AND RAPID BLOOD TRANSFUSION


Impaired oxygen transport MIcroaggregates * Fluid overload Defective red cell function * Impaired haemoglobin function * Disseminated intravascular coagulation (DIC) * Acute respiratory distress syndrome (ARDS) * Multiorgan dysfunction syndrome (MODS) *

JP Isbister in Ohs Intensive Care Manual, 5th edition, 2003

POTENTIAL HAZARDS OF MASSIVE AND RAPID BLOOD TRANSFUSION


Haemostatic Failure Dilution Depletion Decreased production Disseminated intravascular coagulation (DIC) * Metabolic disturbances Electrolyte and metabolic disturbances* Hyperkalaemia or delayed hypokalaemia Sodium overload * Acid-base disturbances* Citrates toxicity * Hypothermia *

JP Isbister in Ohs Intensive Care Manual, 5th edition, 2003

POTENTIAL HAZARDS OF MASSIVE AND RAPID BLOOD TRANSFUSION


Vasoactive reactions Kinin activation* Damaged platelets and granulocytes* Serological incompatibility Impaired reticuloendothelial function*

JP Isbister in Ohs Intensive Care Manual, 5th edition, 2003

MECHANISM BY WHICH RED CELLS MAY BE HAEMOLYSED BEFORE OR FOLLOWING TRANSFUSION


Immune destruction Donor red cell serological incompatibility Acute incompatible blood transfusion Delayed haemolytic transfusion reaction High-titre haemolysis in the donor plasma Interdonor incompatibility Destruction of donor red cells without detectable antibodies Non-Immune destruction Transfusion in correctly stored or outdated blood Inadvertently frozen blood Infected blood Mechanical destruction, e.g. infused under pressure

Clinical consequences of the storage lesion


Fever Neutrophili a Flushing Capillary leak TRALI/ARD S MOF Other adverse Effects of leukocytes

Plasma Damage/activatio n Of plasma proteins Cytokines

Kinins complement coagulation

Hypotensio n flushing anxiety GIT symptoms Pain

Buffy coat Microaggreg ates

Procoagula nts
Thrombosis Chemical metabolic and physical Red cells Haemolysis

Thrombosis ?ARDS RES blockade microvascu lar pathology

Bilirub in LDH iron

Acidos K+, Na+, NH4+ Hypothermi a glucose plasticizers

Post-transfusion survival and efficacy

Jaundic e

COLLOIDS DAN PRODUK DARAH

Warko Karnadihardja

COLLOIDS

Plasma expander, pengaruh tekanan hidrostatik dan osmotik Dua group Komponen plasma Human albumin Fresh frozen plasma Fraksi plasma protein Larutan immunoglobumin (gamma globulin) Cryoprecipitate Factor VIII Factor IX Factor VII Semi Sintetik Gelatin (Hydrolized bovine collagen) Dextran (Polysaccharides) Hydroxyethyl starch (HES)

VOLUME DISTRIBUTION OF COLLOID, SALINE AND GLUCOSE


Colloid

Saline

Glucose

Plasma (31) Interstitial Compartment (101) Blood Cells (21)

Intracellular Compartment (301)

Grocott Mpw, Mythen MG, Clinical anesthesiology, 1999

POLYDISPERSITY OF COLLOID MOLECULAR SIZE

Semi-permeable membrane

Increased molecular size Prolonged intravascular retention less particles Decreased volume expansion

Decreased molecular size Shortened intravascular retention many particles Increased volume expansion

Grocott Mpw, Mythen MG, Clinical anesthesiology, 1999

SCHEMATIC OF TECHNIQUE FOR MEASUREMENT OF THE COP 50:COP 10 RATIO


Pore size 50 kDa

Pore size 10 kDa

P1

P2

Saline

Colloid

Saline

Colloid

Grocott Mpw, Mythen MG, Clinical anesthesiology, 1999

TRALI VS ARDS
Transfusion related acute lung injury

Potentially fulminant compliaction of blood transfusion, charactered by Acute respiratory distress Arise within hours of blood transfusion Recovery usually within 48 hours, usually with full recovery different with ARDS Pathophysiology of TRALI: the presence of leuco agglutinins activate complement C5a promotes neutrophil aggregation squestration in the lung microvasculature endothelial damage intestinal edema TRALI can continue to post transfusion ARDS

CLINICAL GUIDELINES FOR BLOOD

Red cell transfusions Hb < 100g/L, unless there are specific indications Appropriate when Hb 70-100 g/L, and supported by the need to relieve clinical sign and symptoms and prevent significant morbidity and mortality Appropriate when Hb < 70 g/L, but lower threshold levels may be in pts who are asymptomatic and/or when specific therapy is available

PLATELET TRANSFUSIONS

May benefit pts with platelet deficiency or dysfunction

PLATELET TRANSFUSIONS
Prophylaxis Bone marrow failure when PLT < 10 x 10 g/L without risk factors for bleeding or PLT < 20 x 10 g/L in the presence of risk factors To maintain PLT > 50 x 10 g/L in pts undergoing surgery or invasive procedures In qualitative platelet function disorders and setting (PLT count is not a realible indicator for transfusion)

PLATELET TRANSFUSIONS
Bleeding patients In any hemorrhaging patient in whom thrombocytopenia secondary to marrow failure When PLT < 50 x 10 9/L in the context of massive hemorrhage/transfusion and PLT < 100 x 10 g/L in the presence of diffuse microvascular bleeding

PLATELET TRANSFUSIONS

Is not appropriate in

Thrombocytopenia is due to immune mediated destruction Thrombotic thrombocytopenia purpura and hemolytic uremic syndrome Uncomplicated cardiac bypass surgery

FRESH FROZEN PLASMA-1


There are few specific indication, but its use may be appropriate: 1. For replacement of single factor deficiencies where a specific or combined factor concentrate is not available 2. For immediate reversal of warfarin induced anti bleeding and use in addition to vit IC and factor IX concentrate 3. For treatment of multiple coagulation deficiencies in DIC

FRESH FROZEN PLASMA-2


For treatment of inherited deficiencies of coagulation inhibitors in pts undergoing high risk procedures where a specific factor concentrate is unavailable 5. In the presence of bleeding and abnormal coagulation parameters following massive transfusion or cardiac bypass surgery or in pts with liver disease
4.

IMMUNOGLOBULIN

Treatment or prevention of infection in pts with proven hypogammaglobulinemia (IV/IM) I.V. immunoglobulin for treatment of some autoimmune disorders Idiophatic thrombocytopenic purpura Autoimmune polyneuropathy Etc

FACTOR CONCENTRATES

Increasing number of plasma protein concentrates Some prepared from Donor plasma Recombinant technology Factor VIII & IX concentrates-hemophilia Antithrombin III : Thrombophilia due to AT III deficiency Controversial in other AT III repleted (DIC, MODS) rFVIIa : recombinant activated Panhemostatic agent Wide range of hemostatic disorders

RECOMBINANT ACTIVATED FACTOR VII (rFVIIa)

Originaly developed for hemophiliac pts Because FVIIa is dependent on tissue factor (TF), its clinical use is safe from a thrombosis-inducing and its use is now being panhemostatic agent FVIIa initiates coagulation pathway only when complexed to the sites of injury For hemostatic disorder : massive blood transfusion, liver disease, uremia, severe thrombocytopenia and platelets disorders

RECOMBINANT HUMAN ACTIVATED PROTEIN C


Has Anti thrombotic Anti-inflammatory Profibrinolytic properties Likely to have a role in the treatment severe sepsis

METHODS

Retrospective reviewed records combat support hospitals in Iraq january 2004-Oktober 2005 M : 5.334 trauma pts civilianand military Massive transfusion > 10 units PRC in 24 hours 365 (6.8%) : requires massive transfusion 117 (32%) : received rFVIIa 67 : complete record blood transfusion 17 : received rFVIIa early 44 : received rFVIIa late Perkins JQ et al : J Trauma, 2007, 62: 1095-1101