III-3-b Liver Transplantation (Henriksson)

III-3-b Liver Transplantation (Henriksson)
Trasplante Hepático B. Å. Henriksson (modificado por A. Martínez) Bengt Åke Henriksson Department of Anaesthesia and Intensive Care Sahlgrenska University Hospital SE Göteborg, Sweden

Función Hepática Metabolismo de la glucosa Síntesis proteica p. ej. factores de la coagulación Metabolización de sustancias endógenas y exógenas “Filtro bacteriano” Among a vast number of functions for the liver, these are important for patients with severe liver disease and undergoing liver transplantation.

Factores de la Coagulación Sintetizados por el Hígado
III-3-b Liver Transplantation (Henriksson) Factores de la Coagulación Sintetizados por el Hígado Factores pro-coagulantes Factores II, VII, IX, X (dependientes de vitamina K) Factores V, VIII, XI, fibrinógeno (Factores VIII y factor vW cuentan además con síntesis extra-hepática) Factores anticoagulantes Antitrombina, proteína C, proteína S

Proteínas con Actividad Fibrinolítica Sintetizadas por el Hígado
III-3-b Liver Transplantation (Henriksson) Proteínas con Actividad Fibrinolítica Sintetizadas por el Hígado Inhibidor 1 del activador de plasminógeno (Plasminogen activator inhibitor 1, PAI-1) α2-antiplasmina Inhibidor de la fibrinolisis activado por trombina (thrombin activated fibrinolysis inhibitor, TAFI)

Hemorragia Masiva y Transfusión
III-3-b Liver Transplantation (Henriksson) Hemorragia Masiva y Transfusión Definición Pérdida equivalente al volumen sanguíneo en un periodo de no más de 24 horas Consecuencias Hipovolemia Carga de citrato Disminución de calcio iónico Acidosis metabólica Hipotermia Incremento de morbilidad y mortalidad Bennett-Guerrero E, Feierman DE, Barclay GR, et al. Preoperative and intraoperative predictors of postoperative morbidity, poor graft function, and early rejection in 190 patients undergoing liver transplantation. Arch Surg 2001; 136: Bennett-Guerrero E et al. Arch Surg 2001; 136: 1177

Estadios de la Enfermedad Hepática
III-3-b Liver Transplantation (Henriksson) Estadios de la Enfermedad Hepática Compensada Dañado pero con función “normal” Descompensada Dañado con función alterada Incremento de INR Incremento de INR y APTT en casos severos During the early stages of liver disease the liver still produces enough coagulation factors and coagulation is normal. Other liver function tests might, however, be abnormal. With increasing liver cell damage INR is increased in mild to moderate liver disease. At this stage, the K-vitamin dependent coagulation factor VII is low because of reduced production and a short plasma half-life (4-6 hours). In the case of severe liver disease, INR has reached high levels and APTT has also increased because of reduced synthesis of the other K-vitamin dependent coagulation factors II (plasma half-life 48 hours), IX (plasma half-life 24 hours) and X (plasma half-life 32 hours). Other coagulation factors such as fibrinogen (plasma half-life hours) and factor V (plasma half-life 12 hours) will be lower than normal in severe liver disease. Coagulation factor VIII usually has normal or supranormal values due to extra-hepatic synthesis. In severe hepatitis, a dysfunctional fibrinogen molecule has been described.

Hipertensión Portal Causas Cirrosis Trombosis de la vena porta Obstrucción del drenaje venoso hepático Consecuencias Dilatación de venas abdominales Hemorragia gastrointestinal y esofágica

Causas de Trasplante Hepático 1
III-3-b Liver Transplantation (Henriksson) Causas de Trasplante Hepático 1 Fallo hepático fulminante Por fármacos o drogas de abuso Vírico Tóxico Circulatorio Criptogénico

Causas de Trasplante Hepático 2
III-3-b Liver Transplantation (Henriksson) Causas de Trasplante Hepático 2 Enfermedad hepática terminal Cirrosis Colangitis esclerosante Alteraciones metabólicas congénitas Enfermedad maligna

Coagulopatía Preoperatoria
III-3-b Liver Transplantation (Henriksson) Coagulopatía Preoperatoria Coagulopatía menos grave Enfermedad hepática maligna Cirrosis biliar primaria Colangitis esclerosante primaria Cirrosis hepática de origen tóxico o vírico Fallo hepático fulminante Coagulopatía grave

Estado de Hipercoagulabilidad Preoperatorio
III-3-b Liver Transplantation (Henriksson) Estado de Hipercoagulabilidad Preoperatorio Puede aparecer en Cirrosis biliar primaria Colangitis esclerosante primaria Enfermedad hepática maligna Ben-Ari Z, Panagou M, Patch D, et al. Hypercoagulability in patients with primary biliary cirrhosis and primary sclerosing cholangitis evaluated by thrombelastography. J Hepatol 1997; 26: Ben-Ari Z et al. J Hepatol 1997; 26: 554

Estado de Hipercoagulabilidad en TEG (Tromboelastografía)
III-3-b Liver Transplantation (Henriksson) Estado de Hipercoagulabilidad en TEG (Tromboelastografía) Hipercoagulabilidad Cirrosis biliar primaria 43% Colangitis esclerosante 28% Cirrosis sin colestasis 5% Ben-Ari Z, Panagou M, Patch D, et al. Hypercoagulability in patients with primary biliary cirrhosis and primary sclerosing cholangitis evaluated by thrombelastography. J Hepatol 1997; 26: Ben-Ari Z et al. J Hepatol 1997; 26: 554

Coagulopatía Durante la Cirugía
III-3-b Liver Transplantation (Henriksson) Coagulopatía Durante la Cirugía Alteraciones preoperatorias relacionadas con la enfermedad hepática Cambios relacionados con el procedimiento quirúrgico Coagulopatía de consumo Incremento de fibrinolisis intraoperatorio Substancias “heparina-like” Transfusión masiva Disfunción del injerto If there is a severe bleeding during surgery, this will cause consumption of coagulation factors as well as thrombocytes. In a study by Himmelreich et al. on ten patients undergoing liver transplantation, there was a significant decrease in thrombocyte count immediately after reperfusion of the grafted liver. Possible explanations for the consumption of the thrombocytes might be intrahepatic sequestration, local thrombin generation and phagocytosis by Kuppfer cells. Furthermore, UW-solution from the reperfused liver was shown to reduce the aggragability of the thrombocytes. In severe liver disease, there are signs of fibrinolysis due to reduced degradation of t-PA. After reperfusion of the grafted liver there is a significant release of t-PA from the grafted liver, transiently increasing the fibrinolysis. Fibrinolysis normally decreases later in the postreperfusion phase of the transplantation. This will be discussed more later. Heparin-like substances are released after reperfusion of the grafted liver and is this discussed later. For restoration of coagulation, it is necessary that the liver starts to produce coagulation factors and degrade anticoagulant substances. If not, the coagulation will deteriorate and it will not be possible to stop bleeding. There are several studies where pre-operative clotting data have been correlated with peri-operative bleeding. Only in a few studies have shown a statistical correlation between the clotting data and peri-operative bleeding. Therefore, it is not possible to predict bleeding from pre-operative clotting data in general. Himmelreich G, Hundt K, Neuhaus P, et al. Decreased platelet aggregation after reperfusion in orthotopic liver transplantation. Transplantation 1992; 53: Himmelreich G et al. Transplantation 1992; 53: 582

Fases del Trasplante Hepático
III-3-b Liver Transplantation (Henriksson) Fases del Trasplante Hepático Fase preanhepática Desde el inicio de la intervención hasta la interrupción del flujo sanguíneo hepático nativo Fase anhepática Hasta la reperfusión del hígado donante Bypass venoso Fase postanhepática Hasta el final de la cirugía

Fase Preanhepática Causas de hemorragia Coagulopatía preoperatoria Magnitud de la disección quirúrgica Fibrinolisis (10-20% pacientes) In patients with a high level of adherence and portal hypertension there is often major bleeding during the pre-anhepatic phase In severe liver cirrhosis, many authors have described fibrinolysis ranging from 10-20%. In the study by Kang et al. there was an increase in fibrinolysis during surgery. As will be discussed later, protamine will reduce the fibrinolysis. Kang YG, Lewis JH, Navalgund A, et al. Epsilon-aminocapronic acid for treatment of fibrinolysis during liver transplantation. Anesthesiology 1987; 66: Kang YG et al. Anesthesiology 1987; 66: 766

Fase Anhepática Causas de hemorragia Fibrinolisis Coagulación intravascular diseminada (CID) During the anhepatic phase there is no degradation of t-PA. Due to this, there is increased fibrinolysis during the anhepatic phase. Porte RJ, Bontempo FA, Knot EAR, et al. Systemic effects of tissue plasminogen activator-associated fibrinolysis and its relation to thrombin formation in orthotopic liver transplantation. Transplantation 1989; 47: In liver disease, synthesis of both factors and inhibitors for coagulation and fibrinolysis is disturbed. Because of this, there is a disturbed balance between coagulation and fibrinolysis, which might induce a DIC. In the clinical situation, however, DIC is not a common problem. Porte RJ. Coagulation and fibrinolysis in orthotopic liver transplantation: current views and insights. Semin Thromb Hemost 1993; 19: Porte RJ et al. Transplantation 1989; 47: 978; Porte RJ Semin Thromb Hemost 1993; 19: 191

Fase Postanhepática Causas de hemorragia Fibrinolisis Trombocitopenia Sustancias “heparina-like” Hipotermia After reperfusion of the grafted liver there is a maximum in t-PA concentration in the plasma. When the grafted liver starts to function, there is a gradual decrease in t-PA concentration and the fibrinolysis gradually decreases. Porte RJ, Bontempo FA, Knot EAR, et al. Systemic effects of tissue plasminogen activator-associated fibrinolysis and its relation to thrombin formation in orthotopic liver transplantation. Transplantation 1989; 47: In a study by Himmelreich et al. on ten patients undergoing liver transplantation, there was a significant decrease in thrombocyte count immediately after reperfusion of the grafted liver. Possible explanations for consumption of the thrombocytes might be intrahepatic sequestration, local thrombin generation and phagocytosis by Kuppfer cells. Furthermore, UW-solution from the reperfused liver was shown to reduce the aggregability of the thrombocytes. Himmelreich G, Hundt K, Isenberg C, et al. Thrombocytopenia and platelet dysfunction in orthotopic liver transplantation. Semin Thromb Hemost 1993; 19: After reperfusion of the grafted liver there are heparin and heparin-like substances that affect coagulation. The origin of these substances will be discussed later. Kettner SC, Gonano C, Seebach F, et al. Endogenous heparin-like substances significantly impair coagulation in patients undergoing orthotopic liver transplantation. Anesth Analg 1998; 86: Porte RJ et al. Transplantation 1989; 47: 978; Himmelreich G et al. Semin Thromb Hemost 1993; 19: 209; Kettner SC et al. Anesth Analg 1998; 86: 691

Fibrinolisis Cirrosis por hepatitis B Fase postanhepática + 5 min Figura izquierda: natural Figura derecha: adición de 30 l de análogo de lisina a la muestra This slide shows TEGs from a liver transplantation on a patient with liver cirrhosis due to hepatitis B. After reperfusion there are signs of fibrinolysis. The TEG shows a slightly increased r, MA and the TEG shows rapid lysis of the clot. After addition of a lysine analogue (30 μl ε-amino-capronic acid to 330 μl blood) there is a normal TEG. This indicates that the coagulation is normal and that the coagulopathy is caused by increased fibrinolysis.

Fibrinolisis Plasminogen t-PA PAI-1 Plasmin Fibrin FDP Sintetizados por el hígado Plasminógeno TAFI α2-antiplasmina PAI-1 Metabolizados por el hígado t-PA _ TAFIa α2-anti plasmina _ + _ Normally there is a balance between synthesis of t-PA in endothelial cells and degradation of t-PA in the liver. In severe liver disease and especially during the anhepatic phase the degradation of t-PA is reduced. This leaves an excess for fibrinolysis, even if liver-synthesised factors are reduced due to the liver disease. Nesheim M. Thrombin and fibrinolysis. Chest 2003; 124: 33S-9S. During the anhepatic phase there is a gradual increase in t-PA. After reperfusion there is also an increase in t-PA due to release of t-PA that might be synthesised in the liver vascular endothelial cells. During the post-anhepatic phase, the Trasplanted liver metabolises t-PA and synthesizes plasminogen, PAI-1 and antiplasmin with decreased fibrinolysis and restoration of the normal balance between coagulation and fibrinolysis. TAFI seems to be of minor importance. + Nesheim M Chest 2003; 124: 33S

Regulación de la Fibrinolisis
III-3-b Liver Transplantation (Henriksson) Regulación de la Fibrinolisis Estimulación t-PA Inhibición (regulación a la baja) TAFIa Inhibidor tipo 1 del activador de plasminógeno (Plasminogen activator inhibitor type-1, PAI-1) α2-antiplasmina Normally there is a balance between synthesis of t-PA in endothelial cells and degradation of t-PA in the liver. In severe liver disease and especially during the anhepatic phase, the degradation of t-PA is reduced. This leaves an excess for fibrinolysis, even if the liver synthesised factors are reduced due to the liver disease. Nesheim M. Thrombin and fibrinolysis. Chest 2003; 124: 33S-9S. During the anhepatic phase, there is a gradual increase in t-PA. After reperfusion there is also an increase in t-PA due to release of t-PA that might be synthesised in the liver vascular endothelial cells. During the post-anhepatic phase the Trasplanted liver metabolises t-PA and synthesizes plaminogen, PAI-1 and antiplasmin with decreased fibrinolysis and restoration of the normal balance between coagulation and fibrinolysis. TAFI seems to be of minor importance. Nesheim M Chest 2003; 124: 33S

Actividad de t-PA y PAI-1 Durante la Cirugía
III-3-b Liver Transplantation (Henriksson) Actividad de t-PA y PAI-1 Durante la Cirugía Actividad t-PA Actividad PAI 20 40 60 80 10 20 30 40 IU/ml AU/ml The coagulation abnormalities occuring after the revascularization of the graft is what many call the postreperfusion coagulopathy and his so-called postreperfusion coagulopathy is a matter of controversy Some investigators have interpretated it as DIC and some others as primary fibrinolysis and some others believe that both occur Most investigators agree on accelerated fibrinolysis being the predominant feature anyway Here is a study by Robert Porte in Pittsburgh who has shown that in patients with hyperfibrinolysis - t-PA activity levels increse markedly during the anhepatic phase with an explosive increase immediately after the revascularization. Later in the neohepatic phase, t-PA hyperactivity gradually disappears - PAI-1 activity shows a pattern inverse that of t-PA with only minimal activity left at the peak of t-PA -The highest FgDP levels prallel the peak in t-PA while the highest FbDP levels occur somewhat later Porte RJ, Bontempo FA, Knot EAR, et al. Systemic effects of tissue plasminogen activator-associated fibrinolysis and its relation to thrombin formation in orthotopic liver transplantation. Transplantation 1989; 47: Prean An Postan- fase hepática Prean An Postan- fase hepática Porte RJ et al. Transplantation 1989; 47: 978

Fármacos Antifibrinolíticos
III-3-b Liver Transplantation (Henriksson) Fármacos Antifibrinolíticos Inhibidor de la proteasa sérica Aprotinina Análogos de lisina Ácido tranhexámico Ácido ε-aminocaproico For more detailed information on antifibrinolytic drugs see reference: Mannucci PM. Hemostatic drugs. N Engl J Med 1998; 339: Aprotinin is extracted from bovine lungs and can cause hypersensitivity reactions after repeated administration. At a lower dose (>50 KIU/ml) it acts by forming an inactive complex with plasmin and thereby preventing degradation of fibrin. This complex formation is reversible. At a higher dose (>200 KIU/ml) it forms a reversible complex with kallikrein that prevents conversion of factor XII to XIIa. It thereby inhibits blood coagulation induced by contact with foreign surfaces such as in the venous bypass. In a multi-centre study, the efficacy of aprotinin on bleeding and transfusion during orthotopic liver transplantation has been shown Porte RJ, Molenaar IQ, Begliomini B, et al. Aprotinin and transfusion requirements in orthotopic liver transplantation: a multicentre randomised double-blind study. EMSALT Study Group. Lancet 2000; 355: The lysine analogue binds reversibly to plasminogen. thereby blocking the binding of plasminogen to fibrin and conversion to plasmin. A small study has shown that tranexamic acid reduced intraoperative bleeding by 50% and there was less need for blood transfusion This shows an effect equal to aprotinin but the data needs to be confirmed by a larger study. Boylan JF, Klinck JR, Sandler AN, et al. Tranexamic acid reduces blood loss, transfusion requirements, and coagulation factor use in primary orthotopic liver transplantation. Anesthesiology 1996; 85: ; discussion 30A-31A. Mannucci PM N Engl J Med 1998; 339: 245; Porte RJ et al. Lancet 2000; 355: 1303; Boylan JF et al. Anesthesiology 1996; 85: 1043

Fármacos Antifibrinolíticos
III-3-b Liver Transplantation (Henriksson) Fármacos Antifibrinolíticos Plasminogen Plasmin Fibrin FDP Inhibidor de la proteasa sérica Aprotinina Origen bovino Análogos de lisina Ácido tranhexámico Ácido ε-aminocaproico Aprotinina Análogos de lisina _ For more detailed information on antifibrinolytic drugs see reference: Mannucci PM. Hemostatic drugs. N Engl J Med 1998; 339: Aprotinin is extracted from bovine lungs and can cause hypersensitivity reactions after repeated administration. At a lower dose (>50 KIU/ml) it acts by forming an inactive complex with plasmin and thereby preventing degradation of fibrin. This complex formation is reversible. At a higher dose (>200 KIU/ml) it forms a reversible complex with kallikrein that prevents conversion of factor XII to XIIa. It thereby inhibits blood coagulation induced by contact with foreign surfaces such as in the venous bypass. In a multi-centre study, the efficacy of aprotinin on bleeding and transfusion during orthotopic liver transplantation has been shown Porte RJ, Molenaar IQ, Begliomini B, et al. Aprotinin and transfusion requirements in orthotopic liver transplantation: a multicentre randomised double-blind study. EMSALT Study Group. Lancet 2000; 355: The lysine analogue binds reversibly to plasminogen. thereby blocking the binding of plasminogen to fibrin and conversion to plasmin. A small study has shown that tranexamic acid reduced intraoperative bleeding by 50% and there was less need for blood transfusion This shows an effect equal to aprotinin but the data needs to be confirmed by a larger study. Boylan JF, Klinck JR, Sandler AN, et al. Tranexamic acid reduces blood loss, transfusion requirements, and coagulation factor use in primary orthotopic liver transplantation. Anesthesiology 1996; 85: ; discussion 30A-31A. _ + Mannucci PM N Engl J Med 1998; 339: 245

Aprotinina en el Trasplante Hepático
III-3-b Liver Transplantation (Henriksson) Aprotinina en el Trasplante Hepático p = 0,02 p = 0,03 Dosis alta Dosis en bolo 2 x 106 KIU/20 min Perfusión continua 1 x 106 KIU/h Dosis baja Perfusión continua 0,5 x 106 KIU/h Placebo ml p = 0,04 p = 0,02 A double-blind, randomised, placebo-controlled, multi-centre trial (6 liver transplant centres). 137 patients were included. They received high dose (n=46), regular-dose (n=43) or placebo (n=48). Bleeding was reduced by 60% in the high-dose group and 44% in the regular-dose group compared to the control group. Transfusion was reduced by 37% in the high-dose group and 20% in the regular-dose group compared to the control group. Thromboembolic complications occurred in two patients in the high-dose group and two patients in the control group but none in the regular-dose group. Thirty-day mortality was equal in all groups (6.5%, 4.7% and 8.3%). Porte RJ, Molenaar IQ, Begliomini B, et al. Aprotinin and transfusion requirements in orthotopic liver transplantation: a multicentre randomised double-blind study. EMSALT Study Group. Lancet 2000; 355: Porte RJ et al. Lancet 2000; 355: 1303

CID Durante el Trasplante Hepático
III-3-b Liver Transplantation (Henriksson) CID Durante el Trasplante Hepático Causas Coagulación Activación de la coagulación Aclaramiento reducido de factores activados Niveles bajos de anticoagulantes sintetizados por el hígado (antitrombina III y proteína C) Fibrinolisis Niveles elevados de t-PA Niveles bajos de PAI-1 sintetizado por el hígado Mueller MM, Bomke B and Seifried E. Fresh frozen plasma in patients with disseminated intravascular coagulation or in patients with liver diseases. Thromb Res 2002; 107 Suppl 1: S9-17. Mueller MM et al. Thromb Res 2002; 107 Suppl 1: S9

Cambios en las Plaquetas
III-3-b Liver Transplantation (Henriksson) Cambios en las Plaquetas Causas de trombocitopenia Déficit de trombopoyetina Hiperesplenismo Reperfusión del injerto hepático Sangrado masivo Causas de trombocitopatía Disminución de la agregación plaquetaria tras la reperfusión del injerto hepático Thrombopoeitin is synthesised in the liver and in severe liver disease the level of thrombopoeitin is lower. Portal hypertension is associated with hypersplenism and thrombocytopenia. In a study by Himmelreich et al. on ten patients undergoing liver transplantation, there was a significant decrease in thrombocyte count immediately after reperfusion of the grafted liver. Possible explanations for the consumption of the thrombocytes might be intrahepatic sequestration, local thrombin generation and phagocytosis by Kuppfer cells. Furthermore, UW-solution from the reperfused liver was shown to reduce the aggragability of the thrombocytes. Himmelreich G, Hundt K, Isenberg C, et al. Thrombocytopenia and platelet dysfunction in orthotopic liver transplantation. Semin Thromb Hemost 1993; 19: Himmelreich G et al. Semin Thromb Hemost 1993; 19: 209

Substancias “Heparina-like”
III-3-b Liver Transplantation (Henriksson) Substancias “Heparina-like” Origen exógeno y endógeno Eliminadas por el hígado No todas son revertidas con protamina These substances have multiple origins. Possible origins are heparin from the donor, heparin from heparin-coated tubes in the venous bypass and small heparin-like substances (i.e. heparan sulfate) from the donor liver. This cartoon is from a patient Trasplanted because of a primary schlerosing cholangitis. The coagulation profile on the TEG at start of surgery showed a slight hyper-coagulation. During surgery there was a moderate bleeding. The TEG during the anhepatic phase showed signs of a slight hypo-coagulation but after reperfusion of the grafted liver the TEG showed a straight line as shown in the figure. A sample with heparinase added showed a almost normal TEG, indicating sufficient amounts of coagulation factors and no signs of severe fibrinolysis. Since the patient was not bleeding, no therapy was given. Four hours later the TEG was normal without any therapy since the liver had degraded the heparin-like substances. Kettner SC, Gonano C, Seebach F, et al. Endogenous heparin-like substances significantly impair coagulation in patients undergoing orthotopic liver transplantation. Anesth Analg 1998; 86: Original Heparinasa Kettner SC et al. Anesth Analg 1998; 86: 691

Hipotermia (< 35ºC) Disminución reversible de la coagulación INR y APTT prolongados Tiempo de sangrado prolongado Síntesis reducida de tromboxano A2 en las plaquetas Respuesta vasoconstrictora a la lesión reducida Eddy VA, Morris JA, Jr. and Cullinane DC. Hypothermia, coagulopathy, and acidosis. Surg Clin North Am 2000; 80: Eddy VA et al. Surg Clin North Am 2000; 80: 845

Citrato Sódico Anticoagulante Quelante de Ca2+ Metabolizado en el hígado Na3H5C6O7 + [O] Na+ + 3HCO3- + 3CO2 +H2O

Hipocalcemia Cambios rápidos en el Ca2+ iónico Alargamiento del intervalo QT Arritmias ventriculares Fallo cardiaco Bushinsky DA and Monk RD. Electrolyte quintet: Calcium. Lancet 1998; 352: Bushinsky DA, Monk RD Lancet 1998; 352: 306

Monitorización de la Coagulación
III-3-b Liver Transplantation (Henriksson) Monitorización de la Coagulación Pruebas de laboratorio APTT INR Fibrinógeno Plaquetas Dímeros-D Monitorización “a pie de cama” TEG, RoTEG Sonoclot The results from laboratory tests are delayed by minutes, and in such a dynamic situation as a liver transplantation they are not reliable when they arrive. Therefore other tests of coagulation has been investigated. In this situation, the TEG, RoTEG and Sonoclot have been shown to be helpful. They are “Site of care” monitors, easy to evaluate and also useful for in vitro tests of treatment.

Pruebas de Laboratorio
III-3-b Liver Transplantation (Henriksson) Pruebas de Laboratorio Límites sugeridos durante la cirugía Hemoglobina ~ 10 g/dL TP, APTT <1.5 veces el valor normal (o INR <1.6) Plaquetas >50 x 103 /mm3 Fibrinógeno >80 mg/dL British Committee for Standards in Haematology: Blood transfusion task force. Transduction for massive blood loss. Clin Lab Haematol 1988; 10: British Committee for Standards in Haematology: Blood transfusion task force Clin Lab Haematol 1988; 10: 265

TEG Coagulation Fibrinolysis α° MA r These are the criteria for treatment presented in Pittsburgh. Despite the correlation between APTT, fibrinogen and thrombocyte count, one has to keep in mind that the coagulation in the patient starts with complex formation of TF/FVIIa, whereas the TEG it starts with contact activation via FXII. In the clinical situation, however, the TEG is of great help in monitoring coagulation. Kang YG, Martin DJ, Marquez J, et al. Intraoperative changes in blood coagulation and thrombelastographic monitoring in liver transplantation. Anesth Analg 1985; 64: r corresponds to APTT MA corresponds to fibrinogen levels in blood and thrombocyte count Alpha angle corresponds to thrombocyte count Criterios de tratamiento r = tiempo de reacción >15 min MA = amplitud máxima < 40 mm α° = ángulo alfa < 40° Kang YG et al. Anesth Analg 1985; 64: 888

Terapia PFC 12 mL/kg (3-4 unidades) Plaquetas 1 unidad / 10 kg Crioprecipitado/Fibrinógeno (equivalente a 1-2 g de fibrinógeno) Aprotinina rFVIIa Thrombocytes can be prepared using different methods. One unit is usually from one donor and it is common that some units are mixed together in one pack. According to a generally agreed-upon standard, one pack contains about 300 x 109 thrombocytes. One pack of thrombocytes transfused into an adult person increases thrombocytes in the blood by about 30 x 109 /L. One gram of fibrinogen given to an adult person increases the fibrinogen level by about 0.5 g/L. British Committee for Standards in Haematology: Blood transfusion task force. Transduction for massive blood loss. Clin Lab Haematol 1988; 10: British Committee for Standards in Haematology: Blood transfusion task force Clin Lab Haematol 1988; 10: 265

rFVIIa Estudio piloto 80 μg/kg de rFVIIa al inicio de la intervención 6 pacientes de estudio comparados con 12 controles pareados Pacientes Controles Valor de p CH Total (U) 3 (0-5) 9 (4-40) 0,002 PFF (U) 1 (0-7) 8 (2-35) 0,011 CP (U) 0 (0-5) 5 (0-15) 0,24 FC (g) 0 (0-2) 0,63 This is a small pilot study and there is a multi-centre study running. Look for the results in the literature! Hendriks HG, Meijer K, de Wolf JT, et al. Reduced transfusion requirements by recombinant factor VIIa in orthotopic liver transplantation: a pilot study. Transplantation 2001; 71: Hendriks HG et al. Transplantation 2001; 71: 402

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