REANIMACIÓN CONTROL DAÑO EN TRAUMA: MANEJO EN URGENCIAS

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1 REANIMACIÓN CONTROL DAÑO EN TRAUMA: MANEJO EN URGENCIAS
MAYLA ANDREA PERDOMO AMAR Urgentóloga Hospital Pablo Tobón Uribe Docente UPB – CES - UdeA

2

3 INTRODUCCION TRAUMA: problema salud pública.
5 millones personas mueren/ año. Mortalidad temprana: TEC: 40-50% Hemorragia: 20-40% Mortalidad tardía: FOM 7-9%, asociada transfusión masiva 65%. Shaz BH. Anesth Analg. 2009;108:1760 –8

4 MORTALIDAD POR HEMORRAGIA
Muerte prehospitalaria en % de los casos. Heridos en combate: 7% Heridos civiles: 2% > 20 unidades de GRE: Mortalidad 50% Kauvar DS et al. Impact of Hemorrhage on Trauma Outcome: An Overview of Epidemiology, Clinical Presentations, and Therapeutic Considerations. J Trauma. 2006;60:S3–S11.

5 DEFINICIONES PERDIDA MASIVA DE SANGRE Pérdida sanguínea:
Por lo menos el 100% del volúmen sanguíneo en 24 horas. 50% en 3 horas. 150cc/min ó 1.5cc/min/kg en 20 minutos. Massive bleeding occurs in a small subgroup of trauma patients and is defined as blood loss of at least 100% of the blood volume within 24 h, at least 50% within 3 h, or 150 ml/min or 1.5 ml/min/kg over 20 min [4]. Massive blood loss is necessarily associated with severely impaired hemostasis. In simple terms, to achieve clot formation and thus stop bleeding, sufficient amounts of thrombin and substrate are required Dietmar F. Current Opinion in Anesthesiology. 2009;22:

6 DEFINICIONES TRANSFUSIÓN MASIVA
10 o más unidades de GRE en 24 horas. (aprox. total volúmen sanguíneo). 10 o más unidades de GRE en 6 horas, 6 o mas u en 12 horas. 50 unidades de hemoderivados en las primeras 24 horas. Pediatría: transfusión de un volúmen sanguíneo de GRE en 24 horas. (edad x 1GRE). Massive transfusion portends a high-mortality rate in patients with trauma. Those who received 10 or more red blood cell (RBC) units in their hospital stay (2.6% of all patients with trauma) had a mortality rate of 39% and patients who received 50 or more units of blood products in the first 24 h (0.6% of all patients with trauma) had a mortality rate of 57% in two separate retrospective studies.12,13 Massive transfusion is commonly defined as transfusion of 10 or more RBC products (which approximates the total blood volume of a recipient) within 24 h14; other definitions include 10 or more RBC products within the initial hospital stay or within 6 h, six or more RBC units within 12 h, or 50 or more blood products in the first 24 h.12,15,16 In pediatric patients, massive transfusion is defined as transfusion of one blood volume of RBC products in 24 h. The number of RBC products in one blood volume is approximately equal to one RBC product multiplied by the patient’s age in years; for example, a 4 yr old is massively transfused after four RBC products. Shaz BH. Anesth Analg. 2009;108:1760 –8

7 DEFINICIONES COAGULOPATÍA EN TRAUMA
Síndrome de sangrado no quirúrgico en mucosas, superficies serosas, heridas, accesos vasculares, continuan sangrando posterior a controlar sangrados vasculares. Depresión profunda de proteínas de coagulación, plaquetas al igual que en situaciones donde los productos de la coagulación pueden estar presentes pero no funcionan. The coagulopathy of trauma is a syndrome of nonsurgical bleeding from mucosal lesions, serosal surfaces, and wound and vascular access sites, the tissue oozing that continues after identifiable vascular bleeding has been controlled. It occurs in the presence of profoundly depressed concentrations of blood coagulation proteins and platelets but also in situations where the normal clotting factors are present but do not work. Recent clinical and laboratory studies now permit a comprehensive view of the coagulopathy associated with severe injury Hess JR. J Trauma. 2006;60:S12-S19.

8 DEFINICIONES CIRUGÍA DE CONTROL DAÑO EN TRAUMA
Rápido control quirúrgico de la hemorragia, contaminación, evitar daños adicionales para restaurar fisiología normal . DAMAGE CONTROL (U.S. Navy) Capacidad de ganar control inicial de un barco dañado, bajo fuego y mantenerlo en movimiento de regreso al puerto para el reparo definitivo… Tieu BH, Holcomb JB. World J Surg. 2007;3:

9 DEFINICIONES REANIMACIÓN CONTROL DAÑO EN TRAUMA Fase de resuscitación.
Dos componentes: Reanimación hipotensiva Reanimación hemostática Tieu BH, Holcomb JB. World J Surg. 2007;3: .

10 1. REANIMACIÓN HIPOTENSIVA
“Actuales consideraciones implican limitar o retardar la reanimación con líquidos endovenosos preoperatorios en aquellos pacientes con sangrados no controlados aún si están hipoperfundidos, manteniendo presión menor a la normal, hasta controlar la fuente del sangrado” Fowler R, Pepe PE. Current Opinion in Anesthesiology. 2002;15:173-78

11 REANIMACIÓN CONTROL DAÑO EN TRAUMA
REANIMACIÓN HIPOTENSIVA “Cualquier intento de subir la presión antes de que el cirujano haya corregido un sangrado activo, llevara a que la sangre siga perdiéndose” Dr. Walter P. Cannon, 1920 Primera Guerra Mundial Dutton RP. Low pressure resuscitation from hemorrhagic shock. W&W. 2004:19-30

12 REANIMACIÓN CONTROL DAÑO EN TRAUMA
2. REANIMACIÓN HEMOSTÁTICA Empleo de componentes sanguíneos tempranamente en la fase de reanimación para restaurar la perfusión, coagulación, minimizando el uso de cristaloides. Previene dilución de factores de la coagulación. Uso de GRE, PFC, plaquetas, crioprecipitado, tratar la coagulopatía. Tieu BH, Holcomb JB. World J Surg. 2007;3:

13 POR QUÉ REALIZAR REANIMACIÓN CONTROL DAÑO EN TRAUMA?

14 COAGULOPATÍA EN TRAUMA
8% del trauma en general 25% en trauma severo Factores predictores: ISS >25 pH <7.10 T° <34°C PAS <70 mm Hg Sin factores 1% Un factor 10-40% 4 factores 98% Cosgriff en 1997 definió 4 factores mayores de riesgo para desarrollar coagulopatía. Early trauma-induced coagulopathy (ETIC) is a new paradigm of trauma-induced coagulopathy as an early and primary event. Other terms which have been applied to the early trauma-associated coagulopathy are “acute traumatic coagulopathy” and more recently “acute coagulopathy of trauma-shock.”20 ETIC has yet to be supported by large prospectively designed studies, but data in three large retrospective trials support the concept of ETIC. These trials identified a prolonged prothrombin time (PT), which occurs early after trauma in up to 25% of patients, as a predictor of mortality. First, MacLeod et al.21 analyzed a trauma registry database and demonstrated that an abnormal PT independently predicted a 35% increase in the likelihood of mortality. Second, Brohi et al.22 retrospectively analyzed PT, partial thromboplastin time (PTT), and thrombin time, in conjunction with other clinical data and demonstrated that ETIC was associated with significantly higher mortality. Finally, a retrospective analysis of a German trauma database demonstrated that an increase in PT was predictive of increased mortality. The authors subsequently proposed a prognostic model based on age, Glascow Coma Scale (GCS), Injury Severity Score, base excess, and PT to more precisely predict mortality.23 Each of these studies attempted to control for factors known to increase mortality. MacLeod et al.21 showed the prolonged PT to be independent of the presence of head injury, time from injury or the presence of shock. Brohi et al.22 were able to control for the amount of fluid resuscitation in their helicopter-transported trauma cohort. The German study controlled for similar factors that were found in the study by Macleod et al.23 Therefore, trauma registry data has demonstrated that an increased PT predicts an increase in mortality and occurs early after trauma in a wider range of patients than was originally believed. Cosgriff N . J Trauma 1997, 42:857-86 Hess JR. J Trauma. 2006;60:S12-S19

15 COAGULOPATÍA TEMPRANA EN TRAUMA
Coagulopatía traumática aguda, Coagulopatía aguda del trauma – shock. Evento primario, 25% pacientes. Teorías: Generación de factor tisular conduce incremento formación trombina patrón de CID + Fibrinolisis alterada. vascular contraction and platelet plug formation followed Coagulation normally begins with an immediate by activation of thrombin and formation of a fibrin clot in conjunction with initial impairment of fibrinolysis.29 Subsequently, extra fibrin is removed by secondary fibrinolysis. At present, it appears that there are two possible theories regarding ETIC: 1) tissue factor generation leads to increase thrombin generation and ultimately a disseminated intravascular coagulopathy (DIC)-like pattern with altered fibrinolysis and 2) tissue hypoperfusion leads to activation of protein C and systemic anticoagulation. DIC is a predictor of acute respiratory distress syndrome, MOF, and death in patients with trauma.30 The diagnosis of DIC is based on clinical symptoms (presence of bleeding and organ dysfunction) and laboratory results (elevated fibrinogen degradation products [FDP], low platelet count, low fibrinogen, and increased PT).31 The trigger for thrombin formation is tissue factor binding to factor VII resulting in activation of the coagulation cascade. Extensive activation of blood coagulation with impaired fibrinolysis results in the generation and deposition of fibrin, resulting in microvascular thrombi and subsequent development of multiple organ dysfunction syndrome.31 Gando et al.30,31 reported that trauma patients with DIC had lower platelet counts, PT, fibrinogen, antithrombin, and 2 plasmin inhibitor levels and higher FDP and tissue factor levels than non-DIC patients with trauma during the first 4 days after trauma. In addition, they Plaquetas, TP, fibrinógeno, PDF, antitrombina SDRA, FOM, Muerte Spahn DR. Br J Anaesth. 2005; 95: Shaz BH. Anesth Analg. 2009;108:1760-8

16 COAGULOPATÍA TEMPRANA INDUCIDA POR TRAUMA
Vía Proteína C - Trombomodulina An abnormal coagulation status is frequently present early after major trauma at admission to the emergency department (ED) and is associated with a five-fold increase in mortality [10,11–13]. Traditionally, acute traumatic coagulopathy has been thought to be due to consumption of coagulation factors, dilution from intravenous fluid therapy, hypothermia and metabolic acidosis. It has recently been shown, however, that none of these factors is initially responsible for the acute traumatic coagulopathy [12,13]. These factors become significant only in the later phase of traumatic coagulopathy. Studies by Brohi et al. [11–14] have described an early and previously unknown acute traumatic coagulopathy before any of the above-mentioned traditional causes of traumatic coagulopathy were present. It has been shown that tissue injury and hypoperfusion followed by the activation of the anticoagulation thrombomodulin protein C pathway plays the central role in the pathogenesis of acute traumatic coagulopathy. As a result of overt activation of protein C, acute traumatic coagulopathy is characterized by coagulopathy in conjunction with hyperfibrinolysis (Fig. 1). Protein C is activated through a thrombin-dependent reaction, with thrombomodulin and the endothelial protein C receptor. Once protein C is being activated (aPC), it exerts its profound anticoagulant effects by irreversibly inactivating factors Va and VIIIa (coagulopathy). This reaction is augmented by the cofactor protein S, and serves to limit continued thrombin production. In addition to its direct inhibition of fibrin formation, aPC resolves already formed clots through its derepression of fibrinolysis. aPC directly inhibits plasminogen activator inhibitor 1 (PAI-1), which usually serves to limit tissue plasminogen activator (t-PA) activity. Without the limitation of PAI-1, t-PA is free to enhance the conversion of plasminogen to plasmin and thereby enhance fibrinolysis (hyperfibrinolysis). The activation of the thrombomodulin protein C pathway has clinical significance; high thrombomodulin and low protein C plasma levels were associated with increased mortality, blood transfusion requirements, acute renal injury and reduced ventilator-free days early after trauma [11–14]. demonstrated that patients with DIC had higher levels of plasminogen activator inhibitor-1 (PAI-1) activity, which inhibits fibrinolysis, potentially resulting in microvascular thrombi, which correlated with increased MOF.30 Gando et al.31 suggested that DIC is associated with systemic inflammatory response syndrome and the subsequent development of MOF. The second theory was proposed by Brohi et al.32 who, in a prospective study of 208 trauma patients, measured prothrombin fragment (coagulation activation), fibrinogen, soluble thrombomodulin (coagulation inhibition), protein C activity (coagulation inhibition), PAI-1 activity (inhibitor of fibrinolysis), and d-dimers (fibrinolysis) as well as PTT, PT, and BD (a measure of the degree of tissue hypoperfusion). The authors correlated these laboratory coagulation values to clinical factors and demonstrated prolongation of PT and PTT when both the BD and prothrombin fragment were high. In addition, they demonstrated that thrombomodulin increases and protein C decreases (theoretically because it is activated) in relation to the BD and mortality. They suggested that the cause of ETIC is systemic anticoagulation via inhibition of the coagulation cascade by activated protein C. In subsequent publications from the same patient cohort, the author determined that traumatic brain injury must be paired with hypoperfusion (defined as increased BD) to result in coagulopathy, and both complement and endothelial activation are correlated with hypoperfusion and coagulopathy.33–35 Brohi et al.20 concluded that the mechanism of acute trauma-induced coagulopathy is the activation of anticoagulant and fibrinolytic pathways through the thrombomodulin-protein C pathway. Evento primario y temprano Theusinger OM. Current Opinion in Anaesthesiology. 2009;11:

17 TRIADA DE LA MUERTE: CIRCULO VICIOSO HEMORRAGIA
Acidosis Hipotermia Hemodilución: COAGULOPATÍA SECUNDARIA Tieu BH at al. World J Surg 2007; 31:1055–1064

18 COAGULOPATIA EN TRAUMA: INTERVENCIÓN
Spahn DR et al. Br J Anaesth 2005; 95: 130–9

19 Simplemente devuélvale al paciente la sangre que perdió…
Cuál es la forma ideal para la reanimación del paciente severamente traumatizado con sangrado masivo? Simplemente devuélvale al paciente la sangre que perdió… Paciente en reanimación

20 Dar sangre total o Transfundir para mimificarla.
Animales: mejora función miocárdica. Operations Iraqi Freedom: mejora la sobrevida Sangre total fresca: < h, 22 grados. Dar sangre total o Transfundir para mimificarla. Beekley MA. Crit Care Med. 2008;36(S):S267-S274

21 COMPARACIONES SANGRE TOTAL 500cc Hcto 38-50%
Plaquetas – Fact coagulación actividad 100%. Fibrinógeno 1500mg. 1GRE + 1PFC + 1 plaquetas + 1 Criopr. Volúmen 660cc Hcto 29%. Plaquetas Fact coagulación actividad 65% Fibrinógeno 750mg. Beekley MA. Crit Care Med. 2008;36(S):S267-S274

22 REANIMACIÓN CONTROL DAÑO
Transfusión temprana de plasma fresco congelado y plaquetas con las primeras unidades de glóbulos rojos, minimizando el uso de cristaloides, en pacientes que requieren transfusión masiva para aumentar la sobrevida. Reanimación control daño Holcomb JB. J Trauma. 2007;62:

23 REANIMACIÓN CONTROL DAÑO
Cirugía control de daños. Hipotensión permisiva. (PAS 90mm hg) Reconocimiento y prevención de la hipotermia. Disminución de la acidosis. Corrección inmediata de la coagulopatía. Inicio en urgencias, continuar en cirugía y UCI. Alec C. Crit Care Med 2008 Vol. 36, No. 7 (Suppl.)

24 QUIÉN DEBE TRANSFUNDIRSE?
CLINICA Lesión penetrante. Lesiones combate. Amputaciones proximales. Hemorragia tórax. Lesión abdominal + hipotensión. Pulso radial ausente/débil. PARACLÍNICA Exceso de base -6. INR > 1.5 PAS <90mmHg lesiones combate. PAS <110mmHg civiles. Hb < 11mg/dl. T <35-36 grados C. Beekley MA. Crit Care Med. 2008;36(S):S267-S274

25 CÚANDO HACERLO? REACTIVA/ TRADICIONAL
Secuencial: cristaloides… GRE… PFC… plaquetas. Hipotensos a pesar cristaloides, 6u GRE, coagulopatía lab’s, sangrando. ANTICIPADA Control daño: MILITAR, Iraq, Afganistán. muerte sangrado Inicio simultáneo componentes sanguíneos. Evitar hemodilución. Resolver coagulopatía. Plaquetas menor o en pactes con TEC, prolongación del Tp/TPT mayor 1.5, hb menor 7, pero tardan los resultados y el paciente ya esta coagulopático, no mejora y muere. Holcomb JB. Ann of Surgery. 2008;248:

26 CÓMO REALIZARLA?

27 Identificación temprana del paciente.
Minimizar cristaloides: 5-8lts/24h Transfusión PFC 1: GRE 1: disminuye la mortalidad. Pacientes que requieren resuscitación continua: Protocolo Transfusión masiva 6 GRE – 6 PFC – 6 plaquetas – 6 Crioprecipitado. recommendations of an international consensus conference Based on (1) previous civilian clinical studies, (2) the on early massive transfusion for trauma,51 and (3) considerable experience in the current war, we think patients at high risk for coagulopathy can be readily identified at admission and prompt simultaneous treatment of hypothermia, acidosis, and coagulopathy initiated. Hypothermia, an independent factor for increased mortality in trauma patients, was an earlier focus for active prevention and treatment,52–54 but application of training and equipment recommendations of the Committee on Tactical Combat Casualty Care and the Joint Theater Trauma System has made it an uncommon finding.55 Acidosis significantly impairs the thrombin generation rates, critical to optimal coagulation function56 and is thus aggressively managed by use of THAM and volume loading with blood components once hemostasis is obtained, with restoration of a normal blood lactate, base deficit, or pH as the ultimate goal. Damage control resuscitation as a structured intervention begins immediately after rapid initial assessment in the ED and progresses through the OR into the ICU. All efforts are directed toward this goal by repeated point of care testing and the use of multiple blood products and drugs readily available in theater, albeit in new ratios and amounts. Compared with civilian practice, damage control resuscitation efforts are largely completed in the OR, with little resuscitation required in the ICU. Achieving this goal quickly in the OR may allow a shift from limited damage control surgery to earlier definitive surgical interventions, including sophisticated limb salvage techniques, and improved outcomes. In the severely injured casualty, damage control resuscitation consists of two parts and is initiated within minutes of arrival in the ED. First, resuscitation is limited to keep blood pressure at approximately 90 mm Hg, preventing renewed bleeding from recently clotted vessels.15,17,39,57–62 Second, intravascular volume restoration is accomplished by using thawed plasma as a primary resuscitation fluid in at least a 1:1 or 1:2 ratio with PRBCs.8,10,48–50 Our initial clinical experience shows these ratios decrease mortality in similarly injured casualties (Borgman MA, et al. unpublished data). Recombinant FVIIa is occasionally used along with the early units of red cells and as required throughout the resuscitation. For casualties who will require continued resuscitation, the blood bank is notified to activate the massive transfusion protocol and deliver to the operating room 6 units of plasma, 6 units of PRBCs, 6 packs of platelets, and 10 units of cryoprecipitate stored in individual coolers.50 The most severely injured of this group also receive fresh warm whole blood as a resuscitative fluid.47,63 Holcomb JB.J Trauma.2007;62: Malone DL. J Trauma.2006;60(S):S91-6

28 CUÁNTO TRANSFUNDIR?

29 CUÁNTO TRANSFUNDIR? No estudios aleatorizados, controlados.
4 estudios observacionales. Maegele et al: Rango 1:1 reduce mortalidad. Duchesne: 1:<2 reduce mortalidad 17%vs43%. Kasnuk, Scalea: rango 1:1 no efecto mortalidad. Shahriar Z. Academic Emergency Medicine.2009;16:371–378.

30 Retrospectivo, 246 pacientes
Conclusiones: “pacientes con trauma por combate que requieran transfusión masiva, relaciones altas 1PFC : 1.4 GRE, se asocian a mejoría en la sobrevida por disminución de la hemorragia. En términos prácticos, PTM deben utilizar rangos 1PFC:1GRE en pacientes coagulopáticos con lesiones traumáticas”. Methods: We performed a retrospective chart review of 246 patients at a US Army combat support hospital, each of who received a massive transfusion (>10 units of RBCs in 24 hours). Three groups of patients were constructed according to the plasma to RBC ratio transfused during massive transfusion. Mortality rates and the cause of death were compared among groups. Results: For the low ratio group the plasma to RBC median ratio was 1:8 (interquartile range, 0:12–1:5), for the medium ratio group, 1:2.5 (interquartile range, 1:3.0 –1:2.3), and for the high ratio group, 1:1.4 (interquartile range, 1:1.7–1:1.2) ( p < 0.001). Median Injury Severity Score (ISS) was 18 for all groups (interquartile range, 14 –25). For low, medium, and high plasma to RBC ratios, overall mortality rates were 65%, 34%, and 19%, (p < 0.001); and hemorrhage mortality rates were 92.5%, 78%, and 37%, respectively, (p < 0.001). Upon logistic regression, plasma to RBC ratio was independently associated with survival (odds ratio 8.6, 95% confidence interval 2.1–35.2). Conclusions: In patients with combatrelated trauma requiring massive transfusion, a high 1:1.4 plasma to RBC ratio is independently associated with improved survival to hospital discharge, primarily by decreasing death from hemorrhage. For practical purposes, massive transfusion protocols should utilize a 1:1 ratio of plasma to RBCs for all patients who are hypocoagulable with traumatic injuries J Trauma. 2007;63:805–813.

31 J Trauma. 2007;63:805–813. Methods: We performed a retrospective
chart review of 246 patients at a US Army combat support hospital, each of who received a massive transfusion (>10 units of RBCs in 24 hours). Three groups of patients were constructed according to the plasma to RBC ratio transfused during massive transfusion. Mortality rates and the cause of death were compared among groups. Results: For the low ratio group the plasma to RBC median ratio was 1:8 (interquartile range, 0:12–1:5), for the medium ratio group, 1:2.5 (interquartile range, 1:3.0 –1:2.3), and for the high ratio group, 1:1.4 (interquartile range, 1:1.7–1:1.2) ( p < 0.001). Median Injury Severity Score (ISS) was 18 for all groups (interquartile range, 14 –25). For low, medium, and high plasma to RBC ratios, overall mortality rates were 65%, 34%, and 19%, (p < 0.001); and hemorrhage mortality rates were 92.5%, 78%, and 37%, respectively, (p < 0.001). Upon logistic regression, plasma to RBC ratio was independently associated with survival (odds ratio 8.6, 95% confidence interval 2.1–35.2). Conclusions: In patients with combatrelated trauma requiring massive transfusion, a high 1:1.4 plasma to RBC ratio is independently associated with improved survival to hospital discharge, primarily by decreasing death from hemorrhage. For practical purposes, massive transfusion protocols should utilize a 1:1 ratio of plasma to RBCs for all patients who are hypocoagulable with traumatic injuries J Trauma. 2007;63:805–813.

32 Prospectivo, observacional 415 pacientes
Conclusión: pacientes que requieren transfusión de más de 8 u de sangre, la relación PFC >1: GRE 1.5, disminuye la Mortalidad (52%) , pero aumenta el riesgo de SDRA. Conclusions: In patients requiring >8 units of blood after serious blunt injury, an FFP:PRBC transfusion ratio >1: 1.5 was associated with a significant lower risk of mortality but a higher risk of acute respiratory distress syndrome. The mortality risk reduction was most relevant to mortality within the first 48 hours from the time of injury. These results suggest that the mortality risk associated with an FFP:PRBC ratio <1:1.5 may occur early, possibly secondary to ongoing coagulopathy and hemorrhage. This analysis provides further justification for the prospective trial investigation into the optimal FFP:PRBC ratio required in massive transfusion practice., Patients who received transfusion products in >1:1.50 FFP:PRBC ratio (high F:P ratio, n 102) versus <1: 1.50 FFP:PRBC ratio (low F:P, n 313) required significantly less blood transfusion at 24 hours (16 9 units vs units, p ). Crude mortality differences between the groups did not reach statistical significance (high F:P 28% vs. low F:P 35%, p ); however, there was a significant difference in early (24 hour) mortality (high F:P 3.9% vs. low F:P 12.8%, p ). Cox proportional hazard regression revealed that receiving a high F:P ratio was independently associated with 52% lower risk of mortality after adjusting for important confounders (HR 0.48, p , 95% CI 0.3– 0.8). A high F:P ratio was not associated with a higher risk of organ failure or nosocomial infection, however, was associated with almost a twofold higher risk of acute respiratory distress syndrome, after controlling for important confounders. J Trauma. 2008;65:986 –993

33 Retrospectivo, 133 pacientes.
Conclusión: datos sugieren relación PFC 1:GRE 1, reduce la coagulopatía, pero esto no se puede trasladar a un beneficio de sobrevida. Mayores estudios clinicos son necesarios antes de recomendar el uso de rutina de PFC 1: GRE 1 en el paciente exsanguinado por trauma. Conclusion: Although our data suggest that 1:1 FFP:RBC reduced coagulopathy, this did not translate into a survival benefit. Our findings indicate that the relationship between coagulopathy and mortality is more complex, and further clinical investigation is necessary before recommending routine 1:1 in the exsanguinating trauma patient. J Trauma. 2008;65:261–271

34 REANIMACIÓN CONTROL DAÑO
TIEMPO de INICIO No definido RELACIÓN GRE:PFC:PLAQ:CRIOPRECIPITADO No está claramente definida Debe iniciarse de forma temprana en el paciente.

35 PROTOCOLO DE TRANSFUSIÓN MASIVA

36 PROTOCOLO DE TRANSFUSIÓN MASIVA
1. Define: institución Severidad del trauma Notificación rápida y efectiva a los servicios: Cirugía, laboratorio, banco de sangre, anestesia Preparación de productos sanguíneos Cantidad Intervalos Paquetes Recursos y necesidades del paciente Shaz BH. Anesth Analg. 2009;108:1760 –8

37 PROTOCOLO DE TRANSFUSIÓN MASIVA
Protocolo de Transfusión masiva. Grady Memorial Hospital/Emory University Shaz BH. Anesth Analg. 2009;108:1760 –8

38 ALGORITMO: RCD Tieu BH, Holcomb JB. World J Surg. 2007;3:

39 ALGORITMO: RCD Tieu BH, Holcomb JB. World J Surg. 2007;3:

40 TERAPIA TRANSFUSIONAL COAGULOPATIA POSTERIOR A CONTROL DAÑO
Sangrado y coagulación: HB : 7 – 9 mg/dl PFC : Sangrado masivo o coagulopatía (TP o TPT mas 1.5 veces el control 15ml/kg PLT: o en TEC politraumatizado. 4 a 8 U Fibrinógeno: Sangrado + fibrinogeno menor 1g/l. 1U/10kg Spahn D et al. European Guideline. Crit Care. 2007;11(1):R17

41 CONCLUSIONES Trauma principal causa
de muerte a nivel mundial: hemorragia. Reanimación control daño empieza: identificar el paciente en riesgo de morir por sangrado. Control quirúrgico del sangrado: precoz. Administrar GRE: PFC: plaquetas: crioprecipitado. Evitar hipotermia y acidosis. Minimizar el uso de cristaloides.

42 GRACIAS!! “La clave del éxito es tener siempre una postura excepcional ante la vida”