TRANSFUSIÓN DE HEMODERIVADOS EN EL PACIENTE CON TRAUMA

Presentación del tema: "TRANSFUSIÓN DE HEMODERIVADOS EN EL PACIENTE CON TRAUMA"— Transcripción de la presentación:

1 TRANSFUSIÓN DE HEMODERIVADOS EN EL PACIENTE CON TRAUMA
JAVIER ESTEBAN TORO LÓPEZ RESIDENTE DE ANESTESIA UNIVERSIDAD CES FEBRERO 2011

2 Hemorragia no controlada es rápidamente fatal
Epidemiología Hemorragia no controlada es rápidamente fatal Trauma: 1era causa de muerte entre 1-44 años Mortalidad temprana secundario a Trauma TEC (40-50%) Hemorragia (30-40%) Mortalidad Tardía FOM Crit Care Med 2009; 37:

3 1 /3 de las muertes en el hospital (24 h)
Epidemiología Mayoría exangue a las 48 H 1 /3 de las muertes en el hospital (24 h) 80% muertes en sala de cirugía son por hemorragia no controlada Riesgo de muerte si sangrado es masivo: 50% Crit Care Med 2009; 37:

4 Cirugía control de daño
50% de pacientes hipotensos tienen sangrado quirúrgico Concepto adquirido hace 20 años que disminuyo mortalidad por trauma Desde hace una década no se ha logrado disminuir dicha mortalidad Crit Care Med 2009; 37:

5 Asegurar ventilación adecuada Entrega de oxígeno
Prioridades de manejo Asegurar ventilación adecuada Entrega de oxígeno Control de la hemorragia Perfusión tisular Crit Care Med 2009; 37:

6 Clasificación del shock hemorrágico

7 Crit Care Med 2009; 37:

8 Diagnóstico y monitorización
Evaluar frecuencia cardiaca y presión arterial Saturacion venosa central de oxígeno más sensible para evaluar pérdida aguda de volemia La acidosis metabólica puede ser evaluada por gases arteriales: déficit de bases. Lactato sérico Crit Care Med 2009; 37:

9 Evaluación de la coagulación
TP-INR TPT Plaquetas Fibrinógeno Hemoglobina 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

10 Prevención de sangrado
Hipotensión permisiva hace referencia a la estrategia de reanimación donde la PAS se mantiene entre 80 y 100 mmHg No se aplica en trauma craneoencefálico ni medular donde se debe garantizar adecuada perfusión tisular 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

11 Recomendaciones transfusión glóbulos rojos
El punto de hemoglobina recomendado para transfundir varía entre 6 y 10 g/dL Fisiologicamente: taquicardia, hipotensión, cambios EKG, incremento en el lactato El grado de shock, respuesta hemodinamica al manejo y las pérdidas sanguíneas deben ser integradas a las recomendaciones para transfundir 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

12 Recomendaciones transfusión glóbulos rojos
Transfusión de GR está indicado en pacientes con shock hemorrágico Una estrategia restrictiva de transfusión (<7 g/dL) es igual de eficaz que una estrategia liberal (<10 g/dL) excepto en pacientes con IAM o angina inestable 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

13 Recomendaciones transfusión glóbulos rojos
La decisión de transfundir se basa no sólo en un valor de hemoglobina sino en la evaluación del estado de shock, la respuesta a LEV, duración y grado de la anemia y respuesta fisiológica cardiopulmonar En ausencia de hemorragia aguda la transfusión debe ser administrada unidad a unidad 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

14 Recomendaciones transfusión glóbulos rojos
En pacientes que requieren ventilación mecánica, se debe considerar un valor de hemoglobina <7 g/dL para transfundir Considerar transfundir si Hb <7 g/dL en pacientes críticos estables Considerar transfundir si Hb <7 g/dL en pacientes con enfermedad cardíaca estable 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

15 Recomendaciones transfusión glóbulos rojos en sepsis
Las necesidades de transfusión deben ser establecidas en cada paciente ya que no hay evidencia clara que la transfusión mejore la oxigenación tisular Incrementa Do2 pero usualmente no Vo2 En las primeras 6 horas si SVCo2 <70% 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

16 Recomendaciones transfusión glóbulos rojos en TEC
Se mantiene nivel de hemoglobina <7 g/dL como punto para transfundir en TEC moderado a grave En HSA se debe tomar la decisión de acuerdo a la condición clínica del paciente, no hay soporte que esta medida mejore pronóstico 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

17 Alternativa a la transfusión
La única alternativa práctica en trauma es la de salvar sangre en el intraoperatorio siempre y cuando el sitio de operación no esté contaminado 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

18 Transfusión de plaquetas
Obtener conteo de plaquetas previo Cuando transfundir? Plaquetas < – / mL Disfunción plaquetaria Sangrado anticipado Sangrado en espacio confinado Plaquetas <50.000/mL En TEC < / mL Conteo plaquetario normal con disfunción 2. Transfusion of platelets. If possible, a platelet count should be obtained before transfusion of platelets in a bleeding patient, and a test of platelet function should be done in patients with suspected or drug- induced platelet dysfunction (e.g., clopidogrel). In surgi- cal or obstetric patients with normal platelet function, platelet transfusion is rarely indicated if the platelet count is known to be greater than 100 􏰂 109/l and is usually indicated when the count is below 50 􏰂 109/l in the presence of excessive bleeding. Vaginal deliveries or operative procedures ordinarily associated with limited blood loss may be performed in patients with platelet counts less than 50 􏰂 109/l. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known or suspected platelet dysfunction (e.g., the presence of potent antiplatelet agents, cardiopulmo- nary bypass) and microvascular bleeding.‡ The determination of whether patients with platelet counts between 50 and 100 􏰂 109/l require therapy, in- cluding prophylactic therapy, should be based on the po- tential for platelet dysfunction, anticipated or ongoing bleeding, and the risk of bleeding into a confined space (e.g., brain or eye). When the platelet count cannot be done in a timely fashion in the presence of excessive microvascular bleeding (i.e., coagulopathy), platelets may be given when thrombocytopenia is suspected. When thrombocytopenia is due to increased platelet destruction (e.g., heparin-induced thrombocytopenia, idiopathic thrombocytopenic purpura, thrombotic thrombocytope- nic purpura), prophylactic platelet transfusion is ineffective and rarely indicated. Crit Care Med 2009; 37:

19 Transfusión de plasma fresco congelado
Indicaciones Sangrado masivo, deficiencia factores coagulación, reversa de antagonistas vitamina k y tratamiento de PTT 10-15 ml/kg 3. Transfusion of fresh frozen plasma. If possible, coagulation tests (i.e., PT or INR and aPTT) should be obtained before the administration of FFP in a bleeding patient. Transfusion of FFP is not indicated if PT, INR, and aPTT are normal. FFP transfusion is indicated for (1) cor- rection of excessive microvascular bleeding (i.e., coagu- lopathy) in the presence of a PT greater than 1.5 times normal or INR greater than 2.0, or an aPTT greater than 2 times normal; (2) correction of excessive microvascular bleeding secondary to coagulation factor deficiency in pa- tients transfused with more than one blood volume (ap- proximately 70 ml/kg) and when PT or INR and aPTT cannot be obtained in a timely fashion; (3) urgent reversal of warfarin therapy; (4) correction of known coagulation factor deficiencies for which specific concentrates are un- available; or (5) heparin resistance (antithrombin III defi- ciency) in a patient requiring heparin. FFP is not indicated solely for augmentation of plasma volume or albumin con- centration. Fresh frozen plasma should be given in doses calculated to achieve a minimum of 30% of plasma factor concentra- tion (usually achieved with administration of 10–15 ml/kg FFP), except for urgent reversal of warfarin anticoagula- tion, for which 5–8 ml/kg FFP usually will suffice. Four to five platelet concentrates, 1 unit single-donor apheresis platelets, or 1 unit fresh whole blood§ provide a quantity of coagulation factors similar to that contained in 1 unit FFP. Crit Care Med 2009; 37:

20 Transfusión de crioprecipitado
Indicaciones Fibrinogeno < mg/dL según la posibilidad de sangrado o sangrado en espacio confinado Fibrinogeno < mg/dL en presencia de sangrado microvascular Transfusión masiva, sangrado, sin niveles de fibrinógeno Deficiencias congénitas de fibrinógeno mg/dL 4. Transfusion of cryoprecipitate. If possible, a fi- brinogen concentration should be obtained before the ad- ministration of cryoprecipitate in a bleeding patient. Trans- fusion of cryoprecipitate is rarely indicated if fibrinogen concentration is greater than 150 mg/dl. Transfusion of cryoprecipitate is usually indicated (1) when the fibrinogen concentration is less than 80 –100 mg/dl in the presence of excessive microvascular bleeding, (2) to correct excessive microvascular bleeding in massively transfused patients when fibrinogen concentrations cannot be measured in a timely fashion, and (3) for patients with congenital fibrin- ogen deficiencies. Whenever possible, decisions regarding patients with congenital fibrinogen deficiencies should be made in consultation with the patient’s hematologist. The determination of whether patients with fibrinogen concen- tration between 100 and 150 mg/dl require therapy should be based on the potential for anticipated or ongoing bleed- ing and the risk of bleeding into a confined space (e.g., brain or eye). Bleeding patients with von Willebrand dis- ease should be treated with specific concentrates if avail- able. If concentrates are not available, cryoprecipitate is indicated. Each unit of cryoprecipitate contains 150–250 mg fibrinogen. Each unit of FFP contains 2–4 mg fibrino- gen/ml. Therefore, it should be noted that each unit of FFP delivers the equivalent amount of fibrinogen as 2 units cryoprecipitate.􏰋 Anesthesiology 2006; 105:198 –208

21 Antifibrinolíticos Sulfato de protamina Medicamentos
Recommendations. Periodically check for signs and symptoms of bacterial contamination, TRALI, and hemo- lytic transfusion reactions, including urticaria, hypoten- sion, tachycardia, increased peak airway pressure, hyper- thermia, decreased urine output, hemoglobinuria, and microvascular bleeding. Before instituting therapy for transfusion reactions, stop the blood transfusion and order appropriate diagnostic testing. Anesthesiology 2006; 105:198 –208

22 Monitorización y tratamiento de efectos adversos
Contaminación bacteriana TRALI Infecciones Reacción a la transfusión C. Monitoring and Treatment of Adverse Effects of Transfusions. Adverse effects of transfusions in- clude, but are not limited to, bacterial contamination, transfusion-related acute lung injury (TRALI), transmis- sion of infectious diseases, and transfusion reaction.

23 Contaminación bacteriana
Principal causa de muerte por transfusión Más frecuentemente plaquetas Se relaciona con almacenamiento a grados Bacterial contamination: Bacterial contamination of blood products, most frequently platelets, is the leading cause of death from blood transfusions. The increased risk of bacterial overgrowth is related to a storage tem- perature of above 20 –24° centigrade. Many blood banks are now culturing their platelet concentrates. If a patient develops a fever within 6 h after receiving platelets, sepsis from contaminated platelets may be a possibility. Fiebre 6 horas después de recibir transfusión Anesthesiology 2006; 105:198 –208

24 TRALI LESIÓN PULMONAR AGUDA QUE OCURRE EN LAS 6 HORAS SIGUIENTES A LA TRANSFUSIÓN CON UNA CLARA RELACIÓN TEMPORAL A LA TRANSFUSIÓN Incidencia 1:5000 2 modelos fisiopatológicos: anti HLA I y II Edema pulmonar no cardiogénico Hipoxia Fiebre Disnea TRALI: Transfusion-related acute lung injury is noncar- diogenic pulmonary edema resulting from immune reactiv- ity of certain leukocyte antibodies a few hours after trans- fusion. Signs and symptoms will appear 1–2 h after transfusion and are in maximum force within 6 h. Hypoxia, fever, dyspnea, and even fluid in the endotracheal tube may occur. There is no specific therapy other than stopping transfusion and instituting critical care supportive measures. Most patients recover in 96 h, although TRALI is one of the top three most common causes of transfusion related deaths. Transfusion-Related Acute Lung Injury Transfusion-related acute lung injury (TRALI) is a potentially life-threatening complication of allogeneic blood transfusion manifested typically by dyspnea, tachypnea, fever, and hypo- tension and may result in severe hypoxemia, requirement for mechanical ventilation, and eventual progression to the acute respiratory distress syndrome." It has been estimated to occur in 0.04% to 0.16% of patients transfused, and some studies estimate an incidence as high as 1 in 5000 blood product transfusions. This complication has been identified as the third leading cause of transfusion-related mortality. Despite the increasing recognition that TRALI represents an impor- tant clinical syndrome, it remains underreported, and accu- rate estimates of its incidence are not available .P Furthermore the etiologic factors and pathophysiology of TRALI remain poorly understood." Now, TRALI is the leading cause of transfusion-related mortality, even though it is probably still underdiagnosed and underreported." Two different etiologies have been proposed: a single antibody-medicated event, involving anti-HLA class I and class II, or antigranulocyte antibodies; and a two-event model, which includes the clinical condition of the patient resulting in pulmonary endothelial activation and neutrophil sequestration. The second event is the transfusion of a bio- logic response modifier (lipids or antibodies) in the blood component that activates primed neutrophils. Based on the fact that TRALI is now the leading cause of transfusion-associated mortality, the National Heart, Lung, and Blood Institute convened a working group to identify areas of research needed in TRALI.25 The working group identified the immediate need for a common definition and thus developed the clinical definition of TRALI. The major concept is that TRALI is defined as new acute lung injury occurring during or within 6h after a transfusion, with a clear temporal relationship to the transfusion. Also, another important concept is that acute lung injury temporally associ- ated with multiple transfusions can be TRALI because each unit of blood or blood component can carry one or more of he possible causative agents: antileukocyte antibody, bio- logically active substances, and other yet-unidentified agents. This group recommended that all future studies utilize the new TRALI definition and proposed that clinicians can diagnose and report TRALI cases to the blood bank. Importantly, researchers can use this TRALI definition to determine accurate incidence, pathophysiology, and strate- gies to prevent this leading cause of transfusion-associated mortality.

25 TRALI Anesthesiology 2006; 105:198 –208
Popovsky et al. [40] first popularized the immune-mediated model of TRALI in According to this model, donor antibodies, and less frequently recipient antibodies, cause an immune reaction targeting leukocyte antigens. Soluble circulating antibody–antigen complexes activate comple- ment in lung, promoting neutrophil influx. Accumulation of neutrophils leads to microvascular damage and extravasa- tion of proteinaceous fluid into the alveoli and interstitium, similar to pathogenic models of ARDS. This sequence of events produces the clinical signs and symptoms of TRALI (Fig. 1). The observation that recipient antibodies are found in association with TRALI far less often than donor anti- bodies is consistent with a dose-dependent effect of leu- kocytes, reflecting a far larger leukocyte pool in the recipient compared with the leukocyte dose in transfused blood. Lung injury mimicking TRALI has been reproduced in animal models. Seeger et al. [49] used an ex vivo rabbit lung model in which rabbit lungs were perfused with plasma containing antibody against the 5b neutrophil antigen and neutrophils expressing the 5b antigen. Following infusion, significant increases in vascular perme- ability and pulmonary artery pressure occurred in the experimental lungs. In addition, neutrophils from the experimental group demonstrated higher levels of arachi- donic acid and lipoxygenase product release. In a similar experiment, Hicks et al. [15] injected mice expressing the major histocompatibility complex class H-2d with anti-H2d monoclonal antibodies. The mice developed hypothermia, pulmonary edema, alveolar protein leak, and lung mono- nuclear infiltrates. These experiments established proof-of- principle that leukocyte–antibody interactions can produce physiologic responses consistent with TRALI. In human studies, Popovsky and Moore demonstrated in 1985 [39] a relationship between the presence of antibody in transfused blood and the development of TRALI symp- toms in transfusion recipients. They investigated 22,292 transfused patients and identified 36 cases of TRALI. Pre- transfusion patient sera and donor sera were tested for neutrophil antibodies, lymphocytotoxic antibodies, and HLA specificity. Donor neutrophil antibodies were identi- fied in 89% of cases, lymphocytotoxic antibodies in 72% of cases, and HLA-specific antibodies in 65% of suspected TRALI cases [39]. Since the Popovsky study, other reports have identified specific anti-HLA class I and anti-neutrophil antibodies in TRALI, including anti-HLA-A2 [4], anti-NB1 [4, 25], anti- 5b [71] anti-HNA 1a [30], and anti-monocyte antibodies [22]. Anti-HLA class II antibodies have also been impli- cated [8, 18, 33, 42]. One interesting case report described TRALI developing in only the transplanted lung of a pa- tient who had received a single lung transplant [6]. The patient’s allograft lung had HLA B44 antigen and the blood donor had anti-HLA B44 antibody. Presumably, few leu- kocytes remained from the lung donor, suggesting that the other HLA antigen-containing tissues, such as pulmonary endothelium, could be involved in the pathogenesis of TRALI. Another human study by Palfi et al. [35] implicated antibodies from multiparous female blood donors. In a randomized, double-blind, crossover study, 100 patients requiring transfusion were randomly assigned to receive two units of FFP, with only one of the two units donated from a multiparous donor. A significant decrease in the PaO2:FiO2 ratio was noted after the transfusion from the multiparous donor unit but not after the nonparous donor unit [35]. Since multiparity is associated with an increased frequency of antibodies [36], a possible explanation for the difference is the presence of antibodies in multiparous donor blood. The main criticism of Popovsky’s model of TRALI is that not all cases of TRALI are associated with a detectable antibody, and only a small fraction of antibody-containing blood products are associated with TRALI [17]. These observations suggest that the conditions required for TRALI are more complex and stringent than simply the presence of anti-leukocyte antibodies in transfused blood. An alterna- tive model of the pathogenesis of TRALI involves several concurrent factors. Silliman’s Two-Hit Model In 1992, Silliman et al. [52] proposed the ‘‘two-hit’’ model of TRALI. In this model, the first hit is a physiologic insult that activates pulmonary endothelium and promotes prim- ing and adhesion of neutrophils. The second hit is an event that activates neutrophils, causing release of cytotoxic factors and endothelial damage with capillary leakage (Fig. 1). It has been hypothesized [57] that the first hit may include a number of comorbid conditions such as sepsis, cardiac disease, trauma, or hematologic malignancy. The second hit involves exposure to biologically active agents from transfused blood. The concept of the second hit being from blood products derives from the observations that the age of stored blood correlates positively with likelihood of transfusion reactions [14], and that potentially responsible biologically active agents in blood products increase in concentration with time of storage [55, 57]. Silliman et al. [55, 56] tested the two-hit hypothesis using animal models. In a perfused rat lung model, neu- trophils in the pulmonary circulation were activated by LPS. Subsequent exposure to blood products transfused on the day of outdate produced significant increases in pul- monary artery pressure and pulmonary edema compared with exposure to fresh blood or fresh frozen plasma. Both hits (LPS and aged blood products) were necessary to produce the physiologic effects [55]. In addition, Silliman et al. [52] demonstrated that stored blood components, but not fresh blood, were capable of priming neutrophil NADPH oxidase in vitro. Plasma at the day of outdate or fresh plasma was added to primed neu- trophils and respiratory burst was measured. Only day-of- outdate plasma primed NADPH oxidase [52], suggesting that substances present only in aging stored blood can activate neutrophils. Silliman et al. [53] subsequently identified a possible priming agent as lysophosphatidylch- oline (Lyso-PC). In clinical studies correlating these results, TRALI pa- tients’ post-transfusion serum was found to have a 2.1-fold increase in neutrophil priming activity compared with pretransfusion serum or control plasma [54]. The lack of priming activity in the pretransfusion serum of TRALI patients implied that transfusion was required to initiate neutrophil priming. Other studies have also demonstrated increased NADPH oxidase activity in the serum of TRALI patients [26]. The two-hit model of TRALI proposed by Silliman is appealing in that it requires the convergence of two specific sets of conditions, the relatively low probability of which might account for the relative rarity of TRALI. However, neither the precise nature of the physiologic conditions required for the first hit nor the exact nature of the factors in blood constituting the second hit, be they lysoPC, anti- bodies, or other factors, are as yet well understood. As such, the ability to predict TRALI or prevent its occurrence in individual patients remains a goal for further research. Recently, Kopko et al. [22] in an attempt to explain cases of TRALI not attributable to known antibodies, theorized that monocyte activation, with resultant cytokine production, occurs in TRALI [49]. Although not proven, the ultimate culprit may be monocytes, and not solely neutrophils. It has yet to be resolved whether a unifying theory, such as this one, can resolve the mechanism of TRALI. Alternatively, TRALI may be a mix of diseases with one commonality, i.e., lung damage. Anesthesiology 2006; 105:198 –208

26 Infecciones Anesthesiology 2006; 105:198 –208
Infectious diseases: Another major adverse effect of transfusion therapy is the transmission of infectious agents. For the past 20 yr, transfusion-induced hepatitis and autoimmune deficiency syndrome were dominant concerns regarding allogeneic blood administration. These infectious risks are now rare. One of the major reasons for the decrease in blood-borne infections has been the use of nucleic acid technology. The human immunodeficiency virus, hepatitis C virus, and West Nile virus can now be detected by this technology. To date, malaria, Chagas disease, severe acute respiratory syn- drome, and variant Creutzfeldt-Jakob disease cannot be detected. Anesthesiology 2006; 105:198 –208

27 Reacción a la transfusión
Fiebre Brote Urticaria Hipotensión Taquicardia Hemoglobinuria Sangrado microvascular Hemolítica No hemolítica Transfusion reaction: General anesthesia may mask the symptoms of both hemolytic and nonhemolytic transfusion reactions. Signs of hemolytic reactions in- clude hypotension, tachycardia, hemoglobinuria, and microvascular bleeding, but these may be erroneously attributed to other causes in the anesthetized patient. The most common signs of a nonhemolytic transfusion reaction in awake patients include fever, chills, or urti- caria. However, these signs may not be detectable dur- ing anesthesia. The consultants and ASA members strongly agree that checking for signs and symptoms of a transfusion reac- tion should periodically be done in the anesthetized patient. The consultants agree and the ASA members strongly agree that urine output and color should be assessed. Both the consultants and ASA members agree that peak airway pressure should be assessed to monitor for transfusion reactions. Anesthesiology 2006; 105:198 –208

28 Reacción a la transfusión
Anesthesiology 2006; 105:198 –208

29 Anesthesiology 2006; 105:198 –208

30 TRALI VIGILAR SIGNOS Y SINTOMAS CONTAMINACIÓN HEMÓLISIS
En todo paciente… TRALI VIGILAR SIGNOS Y SINTOMAS CONTAMINACIÓN Recommendations. Periodically check for signs and symptoms of bacterial contamination, TRALI, and hemo- lytic transfusion reactions, including urticaria, hypoten- sion, tachycardia, increased peak airway pressure, hyper- thermia, decreased urine output, hemoglobinuria, and microvascular bleeding. Before instituting therapy for transfusion reactions, stop the blood transfusion and order appropriate diagnostic testing. HEMÓLISIS Anesthesiology 2006; 105:198 –208