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Fisiología y Fisiopatología de la Hemostasia José Domingo Torres Hernández  Universidad de Antioquia HUSVP
<ul><li>Aquí  </li></ul>
Plaquetas FT Fibrina Pq + FT FT + Fbn Flujo de sangre Pq + FT + Fbn Pq + Fbn
Endotelio <ul><li>Antitrombogénico  Prostaciclina    Heparan sulfato  tPA </li></ul><ul><li>  óxido nítrico </li></ul><ul>...
Factor tisular Colá-geno Trombos Matriz subendotelial Endotelio Músculo liso
adhesión activación secreción Célula  endotelial subendotelio VWF h TSP h colágeno l plaqueta GPlb GPla/lla GPIlb/Illa FG ...
trombina FXI R R GPIb/V/IX secreción IX IXa VIIIa Xa X IXa R FPE Xa II Va trombina trombina trombina trombina trombina tro...
agregación/ reclutamiento de leucocitos Célula  endotelial generación trombina VWF TSP sCD4OL T-cell atracción retracción ...
1. Fase iniciación Iniciación de coagulación
2. Fase de amplificación Plaqueta activada Trombina Protrombina Plaqueta
3. Fase de propagación Fibrinógeno Fibrina Plaqueta activada Protrombina Trombina
Coágulo plaqueta-fibrina R R FPE trombina trombina trombina trombina trombina thrombin trombina fibrinógeno IX IXa VIIIa X...
<ul><li>Plaquetas – Factor V – Factor VIII – Factor XI </li></ul><ul><li>Trombomodulina   TROMBINA   TAFI </li></ul><ul><l...
Fibrinolisis Plasminógeno TAFI
Mecanismos de control de la coagulación  <ul><li>Trombina – factor Xa </li></ul><ul><li>ANTITROMBINA </li></ul><ul><li>Fac...
Mecanismos de control de la coagulación  <ul><li>Trombina + Trombomodulina </li></ul><ul><li>Proteína C – Proteína S </li>...
Mecanismos de control de la coagulación Xa TFPI Xa TFPI Xa TFPI VIIa TF Ca 2+ Ca 2+ +
Plasmina Plasminógeno Fibrinógeno Fibrina
Evaluación Hemostática Preoperatoria Procedimiento mayor Historia sospechosa  de sangrado TP – TTP  Plaquetas Tiempo de sa...
Trastornos Hemostáticos en Hepatopatía  Síntesis disminuida de  factores de la coagulación Anemia Trombocitopenia Disfunci...
Trastornos Hemostáticos en Cirugía Cardíaca Disminución de factores de la coagulación Hemodilución Desnaturalización  Dism...
Sangrado Masivo - Mayor <ul><li>Reemplazo de 1 volumen de sangre en 24 horas </li></ul><ul><li>Reemplazo del 50% volumen s...
Sangrado Quirúrgico - Trauma <ul><li>Sangrado excesivo asociado con morbi-mortalidad y estancia en UCI </li></ul><ul><li>7...
Síndrome de Coagulopatía  Asociada al Trauma <ul><li>Pérdida de sangre y dilución </li></ul><ul><li>Consumo de plaquetas y...
Transfusión en Trauma <ul><li>91%  no requieren </li></ul><ul><li>7% < 10 U </li></ul><ul><li>2%   10 U </li></ul><ul><li...
Causas de Sangrado  Quirúrgico <ul><li>Intraoperatoria </li></ul><ul><li>Problemas técnicos - </li></ul><ul><li>Consumo fa...
Causas de Sangrado Quirúrgico <ul><li>Posoperatoria Temprana ( 0-2 días) </li></ul><ul><li>Problemas técnicos </li></ul><u...
Opciones Terapéuticas <ul><li>Plaquetas si el recuento es < 50,000 </li></ul><ul><li>Plasma fresco congelado si TP o TTP  ...
TXA 2 Trombina ADP
Administración de hemocomponentes en sangrado masivo *Recuento de plaquetas < 50,000 TP o TTP > 1.5 o 1.8 veces el control...
Opciones Terapéuticas <ul><li>Factor VIIrh </li></ul><ul><li>Antifibrinolíticos </li></ul><ul><li>Desmopresina </li></ul>
 
Tromboelastografía
Tromboelastografía
Administración de hemocomponentes en sangrado masivo *Recuento de plaquetas < 50,000 TP o TTP > 1.5 o 1.8 veces el control...
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Fisiología Y Fisiopatología de La Hemostasia

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  • N Engl J Med 2008;359:938-49. Copyright © 2008 Massachusetts Medical Society. Hemostasis is the process that maintains the integrity of a closed, high-pressure circulatory system after vascular damage. Vessel-wall injury and the extravasation of blood from the circulation rapidly initiate events in the vessel wall and in blood that seal the breach. Circulating platelets are recruited to the site of injury, where they become a major component of the developing thrombus; blood coagulation, initiated by tissue factor, culminates in the generation of thrombin and fibrin. These events occur concomitantly (Fig. 1A; also see
  • Hemostasis is the process that maintains the integrity of a closed, high-pressure circulatory system after vascular damage. Vessel-wall injury and the extravasation of blood from the circulation rapidly initiate events in the vessel wall and in blood that seal the breach. This new cell-based model considers the involvement of tissue factor–expressing cells and platelets in the hemostatic process and is seen to occur in 3 phases: initiation, amplification, and propagation (Fig 2). The initiation phase occurs on the surface of tissue factor–bearing cells. Thus, vessel injury exposes factor VII to tissue factor and the resulting complex activates coagulation. In the amplification phase, small amounts of thrombin activate platelets as well as factors V, VIII, and XI on the platelet’s surface. In the propagation phase, large amounts of thrombin, sufficient to induce the generation of a fibrin clot on the surface of platelets, are generated. In contrast to the classic cascade model, some plasma components, such as coagulation factor XII, are not incorporated in this model. Because factor XII deficiency is not associated with abnormal bleeding, the intrinsic pathway has been regarded as having only minor importance for in vivo coagulation.
  • La sangre en su estado natural es líquida y el endotelio posee propiedades antitrombogénicas para garantizar la fluidez de la sangre El endotelio produce sustancias antiagregantes plaquetarias y vasodilatadoras como la prostaciclina y el óxido nítrico, en su superficie se deposita heparan sulfato (anticoagulantes naturales), la TM inicia la activación del sistema anticoagulante de la proteína C, produce TFPI que inhibe vía extrínseca de la coagulación y también produce tPA que activa la fibrinolisis Pero cuando sufre una ruptura el vaso sanguíneo, el endotelio adopta un fenotipo protrombótico: libera FvW,
  • Circulating platelets are recruited to the site of injury, where they become a major component of the developing thrombus; blood coagulation, initiated by tissue factor, culminates in the generation of thrombin and fibrin. When the vessel wall is breached or the endothelium is disrupted, collagen and tissue factor become exposed to the flowing blood, thereby initiating formation of a thrombus. Exposed collagen triggers the accumulation and activation of platelets, whereas exposed tissue factor initiates the generation of thrombin, which not only converts fibrinogen to fibrin but also activates platelets. exposure of subendothelial collagen initiates platelet activation; in the other, thrombin — generated by tissue factor derived from the vessel wall or present in flowing blood — is the initiator
  • Al contacto de la plaqueta con el colágeno del subendotelio se activa, y expresa receptores de glucoproteínas que le permitirán la adhesión con el FvW y la TSP sirviendo de puentes entre el colágeno y la plaqueta. Mediante este proceso de activación, las plaquetas emiten seudópodos y secretan agonistas como el ADP y el TxA2 que activan y reclutan nuevas plaquetas, las cuales se agregan y acumulan formando el tapón plaquetario Platelet Secretion Activated platelets release several granule components which modulate functions of interacting platelets and blood and vascular cells. Several secretion products of immobilized platelets stimulate additional circulating platelets which are recruited to form aggregates. The dense bodies of platelets contain important secondary agonists like ADP or serotonin. About 50% of platelet ADP is stored in the dense bodies (storage pool), which is released after platelet activation but cannot be refilled. In contrast, the metabolic pool of adenine nucleotides, localized in the cytoplasm but not connected to the dense bodies, is able to synthesize new ADP but cannot be released.13 ADP is predicted to be the prominent amplifier of initial platelet activation.14 There are two important ADP receptors on the platelet surface. The P2Y1-receptor mediates mobilization of Ca2þ and shape change and transient aggregation.15 The P2Y12-receptor is believed to potentiate platelet secretion and to be involved in sustained irreversible aggregation.16 Enzymatic conversion of released ADP to inactive adenosine monophosphate (AMP) by endothelial ecto-ADPase/CD39 limits platelet activation by ADP.17 A lack of the second aggregation wave after collagen stimulation characterizes disorders in ADP-mediated platelet activation. Serotonin (5-hydroxytryptamine, 5-HT), a wellknown strong vasoconstrictor, binds to the Gq-coupled 5HT2A-receptor and amplifies together with ADP the platelet response. In addition, serotonin may play a procoagulant role in augmenting the retention of procoagulant proteins like fibrinogen and thrombospondin (TSP) on the platelet surface.18 The dense tubular system contains a Ca2þ pool which is mobilized during platelet activation. Ca2þ fluxes are central triggers in platelet activation, platelet attraction, and platelet aggregation.19 The a-granules contain large adhesive proteins (vWF, TSP1, vitronectin, fibronectin), mitogenic factors (PDGF, VEGF, TGFb), coagulation factors (factors V, VII, XI, XIII), and protease inhibitors (protein C, PAI-1, TFPI), which are released immediately after platelet activation. Some of the a-granule proteins are synthesized by megakaryocytes (TSP1,20 b-thromboglobulin, platelet factor 4); others are endocytosed from the plasma (immunoglobulins, fibrinogen, vitronectin). Various glycoproteins, for example, P-selectin (CD62P), are exclusively localized on the a-granule membrane of resting platelets. Upon secretion the membrane of the a-granule membrane fuses with the plasma membrane and exposes CD62P on the platelet surface. P-selectin and other activation-dependent glycoproteins, including CD40L, mediate platelet binding to neutrophils and monocytes.21 Leukocytes are able to roll on platelets, which are immobilized on the subendothelium, in a P-selectin–dependent manner
  • Otro elemento clave en la activación plaquetaria es la expresión de receptores de factores de coagulación de tal manera que en s superficie se ensamblará la coagulación con la consiguiente generación de trombina y de fibrina On the surface of the platelet FXIa binds to its receptor GPIb and activates FIX. In contrast to FXa that is readily inhibited by tissue factor pathway inhibitor (TFPI) as soon as it enters the plasma, FIXa, built on TF/FVIIa presenting cells can in addition diffuse to the activated platelets. On the platelet surface the Xase-complex and the prothrombinase-complex have optimal conditions
  • Platelet Aggregation The aggregation of platelets is characterized by the accumulation of platelets into a hemostatic plug (Fig. 3). The central platelet receptor in this process is the GPIIb/IIIa (aIIbb3-integrin) linking activated platelets through fibrinogen bridges. A resting platelet presents 40,000 to 50,000 GPIIb/IIIa complexes on its surface. In its nonactive state this integrin cannot bind soluble ligands like plasma fibrinogen, vWF, TSP, fibronectin, or vitronectin. Only stimulation of a platelet leads to an increase in GPIIb/IIIa molecules, via a-granule exocytosis, and to activation of surfaceexposed GPIIb/IIIa, enabling binding of soluble ligands. On the other hand, immobilized fibrinogen on stimulated platelets serves as an adhesive substrate for resting platelets through GPIIb/IIIa that leads to amplification of primary aggregation.23 Interaction between GPIIb/IIIa and its ligand is associated with molecular conformational changes, resulting in a firm connection. In addition, platelets recruit leukocytes and T-cells into the growing plug. Interactions via Pselectin/PSGL1 or CD40L/CD40 mediate activation of leukocytes which trigger or limit thrombus growth. Circulating platelet-monocyte aggregates are supposed to play a role in enhancing formation of atherosclerotic plaques as well as in graft occlusion after peripheral vascular surgery.31,32 Formation of platelet-leukocyte associates via GPIb on platelets and Mac-1 on leukocytes may be a cause of the phenomenon of rapid clearance of transferred cooled platelets with activated clustered GPIb/V/IX complexes.
  • INITIATION of coagulation: INICIACIÓN de la coagulación
  • Prothrombin: Protrombina Thrombin: Trombina Platelet: Plaqueta Activated Platelet: Plaqueta Activada
  • The concerted actions of coagulation factors on the platelet surface lead to a burst of thrombin formation, so that a stable fibrin clot can be formed
  • La integralidad y funcionamiento del sistema hemostático lo tenemos que traducir a la clínica, una de estas situaciones es durante la evaluación preoperatoria Patients undergoing surgery should have a bleeding history taken. This should include detail of previous surgery and trauma, a family history, and detail of anti-thrombotic medicatio n. Patients with a negative bleeding history do not require routine coagulation screening prior to surgery. The APTT should be designed to detect bleeding disorders due to deficiencies of factors VIII, IX, and XI and inhibitors of the intrinsic and common pathway factors (including lupus anticoagulant and therapeutic anticoagulants) . Inevitably, it also detects deficiency of factor XII. PT prolongation should detect important deficiencies (or rarely inhibitors) of factors II, V, VII and X . Its main use is for anticoagulant monitoring and detection of acquired bleeding disorders (especially disseminated intravascular coagulation, liver disease and vitamin K deficiency). T de sangría is the only in vivo haemostasis test available. It is used to test for defects of platelet-vessel wall interaction and should detect inherited or acquired disorders of platelet function, von Willebrand disease (VWD) and abnormalities of vessel wall integrity. Medications (aspirin and other nonsteroidal anti-inflammatory drugs), severe renal failure, thrombocytopenia, paraproteinaemia and severe anaemia. Similarly, the bleeding time may be within the normal range in VWD, platelet storage pool disorder and in aspirin users, but increased perioperative bleeding may still occur
  • Reduced/defective synthesis of Vit K dependent clotting factors; low-grade DIChyperfibrinolysis; anemia, thrombocytopenia (hypersplenism and marrow depression); platelet dysfunction; note impaired synthesis of anticoagulant factors may preserve hemostasis Consider prophylactic tranexamic acid if high risk and no prothrombotic history or TEG. Assess coagulation clinically before treatment (cannulation sites, surgical field): treat clinical coagulopathy according to TEG and laboratory data (blood products, antifibrinolytic, protamine). Maintain normothermia. If intractable coagulopathy consult hematologist and consider FVIIa by local protocol
  • During extracorporeal circulation, a decrease of coagulation factors and platelets as well as an activation of fibrinolysis can be observed. These changes in hemostasis can partially be explained by hemodilution because of the need to prime the extracorporeal circulation . Further contributing causes to the decrease in plasma coagulation factors are the activation and denaturation of these proteins by artificial surfaces and contact to air bubbles , particularly in certain types of oxygenators During cardiopulmonary bypass, a decrease of the platelet count and platelet dysfunction can regularly be observed. In addition to the hemodilution caused by the priming volume of the system, adhesion, activation, and the mechanical destruction of platelets occurs because of contact with artificial surfaces of the bypass circuit .34,35 In addition, extracorporeal circulation induces a decrease in ADP and collagen-induced platelet aggregation . Platelet dysfunction can persist after cessation of cardiopulmonary bypass for a prolonged period. Surgical trauma and inflammation are the main causes of intravascular tissue factor expression. In addition to increased tissue factor expression on the surface of monocytes, further sources of this activator of factor VII have been reported in the context of cardiac surgery. During cardiopulmonary bypass, it has been demonstrated Hypothermia is commonly used during cardiac surgery to prolong the ischemia tolerance of the patient.
  • UNCONTROLLED hemorrhage, and by way of consequence, massive transfusion (MT) is a frequent complication of trauma and surgery. MT is commonly defined as the replacement of one blood mass in a period of 24 hr . A dynamic definition of MT, such as the transfusion of four or more red cell concentrates within one hour when ongoing need is foreseeable,1 or the replacement of 50% of the total blood volume within three hours , is more relevant in the acute clinical setting. Massively transfused patients will show evidence of defective hemostasis in a high percentage of cases More recently, it has been shown that abnormalities of the prothrombin time (PT) and of the activated partial thromboplastin time (aPTT) occur after the transfusion of 12 units of PRBC and that thrombocytopenia develops after the transfusion of 20 units . The deficiency in fibrinogen concentration develops earlier than any other hemostatic abnormality when plasma-poor red cell concentrates and colloid plasma substitutes are used for the replacement of major blood loss. al. showed that a concentration of fibrinogen of 1.0 g·L–1 was reached when the blood loss was 1.42 times the calculated blood volume and that blood losses in excess of two blood volumes caused the deficiency of prothrombin, factor V, platelets and factor VII, in this order. Thus, it appears logical to consider that coagulopathy after MT can be a problem resulting from a combined deficit of platelets and fibrinogen . Only marked prolongations of the PT or aPTT (1.5 and 1.8 times higher than control when the fibrinogen level is low and normal respectively) are likely to be significant from a clinical perspective
  • In major surgery for liver diseases, as well as in cardiac surgery, excessive blood loss is associated with increased mortality, morbidity, and intensive care stay. Approximately 75% to 90% of intraoperative and early postoperative bleeding is due to technical factors. However, in some cases either acquired or congenital coagulopathies may favor, if not directly cause, surgical hemorrhage. Uncontrolled bleeding leads to a combination of hemodilution, hypothermia, consumption of clotting factors, and acidosis, which in turn exert their own negative influences over the clotting process to further exacerbate the problem in a vicious bloody circle
  • Consumption of coagulation factors and platelets, seen in the past as DIC, is now thought to be highly localized at the site of injury. In this view, millions of endothelial microtears create enough exposure of tissue factor on the surfaces of normally subendothelial smooth-muscle cells and fibroblasts to bind out most of the factor VII. The generation of thrombin at these many sites of injury leads to its binding to thrombomodulin on adjacent normal endothelial cells with the activation of protein C.25 Reduced local thrombin concentrations at sites of injury lead to thin fibrin strands with high surface-to-volume ratios and prevent the activation of the thrombin-activated fibrinolysis inhibitor (TAFI). At the same time, low vascular flow leads to the release of tissue plasminogen activator (tPA) from intact endothelial cells. The consequence of these last three effects is increased fibrinolysis . In trauma patients, two major mechanisms are responsible for the occurrence of DIC. The first relates to the nature and to the importance of tissue trauma. The second relates to shock and tissue anoxia. Brain injury is associated with a particularly high incidence of coagulopathy. Regarding the importance of tissue trauma, in the absence of massive head injury and pre-existing disease, life-threatening coagulopathy was associated with a pH of less than 7.10, a temperature of less than 34°C, an injury severity score greater than 25, and a systolic blood pressure of less than 70 mmHg. When all risk factors were present, the incidence of coagulopathy was 98%. When tissue anoxia is avoided and surgical trauma is controlled, the occurrence of DIC may remain low despite MT.
  • Las indicaciones aprobadas por la FDA para el f VIIrh son Para el sangrado quirúrgico y la coagulopatía asociada al trauma no está aprobado pero con base en informes de la literatura de reporte de casos y serie de casos
  • Reagent-supported thromboelastometry with the rotation thrombelastography (e.g. ROTEM) is a whole blood assay that evaluates the visco-elastic properties during blood clot formation and clot lysis. A hemostatic monitor capable of rapid and accurate detection of clinical coagulopathy within the resuscitation room could improve management of bleeding after trauma. ROTEMis a point-ofcare device that rapidly detects systemic changes of in vivo coagulation in trauma patients, and it might be a helpful device in guiding transfusion. Diagnosis of coagulopathy can be made clinically but coagulation monitoring is essential to directed care . Thrombelastography is a whole blood coagulation technique providing information on the initiation of coagulation, propagation kinetics, fibrin–platelet interaction, clot firmness and fibrinolysis [7,8]. Recently, the modified rotation thrombelastogram analyzer (ROTEM; Pentapharm, Munich, Germany) has overcome some of the limitations of classic thrombelastography, such as the long observation time when coagulation is not initiated by biochemical agonists and the susceptibility to vibrations and mechanical shocks. Moreover, by using an electronic pipette reproducibility and performance have increased. Also, depending on the parameters measured, ROTEM results are available as quickly as 10 min from commencement, and therefore ROTEM may be used as a point-of-care device to monitor hemostasis, as previously shown in various clinical setting of coagulation disorders, such as liver transplantation and cardiac surgeryFibrinolysis was evaluated by measuring D-dimer levels (Asserachrom; D-DI, Diagnostica Stago). We defined trauma coagulopathy at admission as an INR spontaneously&gt; 1.6 and/or an APTT &gt; 60 s and/or a platelet count&lt; 100.109 L)1 and/or a fibrinogen less than 1 g L)1. Decreases in CT as well as CFT suggested that initiation of coagulation (CT) as well as its propagation (CFT) may be sensitive to trauma. furthermore, MCF and CA were significantly decreased in the trauma group and that effect was even more pronounced in the coagulopathic patients in whom a significant platelet decrease was observed (Table 1). MCF has been reported to be dependent on platelet function and count [26,27] and it is probably also dependent on dilution or consumption of coagulation factors. impact of vibration or mechanical stress on the results.16 TEG measures the entire process of the clotting cascade, from initial clot formation through complete clot lysis. Currently, the initial results of a TEG are available in 10 minutes to 15 minutes, excluding fibrinolysis data, whereas PT and PTT, because of the logistical restraints of hospital laboratories, require 45 minutes to 60 minutes. An abnormal R time, the time to clot initiation, relates to the concentration of clotting factor, and a reduced MA, maximal clot strength, indicates a deficiency in number and/or function of platelets. Platelet function and number affect the kinetics of clot formation and therefore are also reflected in the -angle. Treatment based on these “decision trees” has resulted in significant reductions of 45% and 76% in blood product use . Differences in interpretation of the TEG between studies seem to be a factor in the determination of the coagulation status. Decisions concerning blood transfusions are often made empirically in the emergency and operating room because of the lack of a fast and reliable method to test a patient’s coagulation status .20 A rapid TEG would provide information upon which physicians could develop a transfusion protocol that would best suit each patient’s hemostatic needs. In addition, presently available data, such as platelet counts and hematocrit, with appropriate interpretation may support TEG findings to provide adequate guidelines. The risk of viral infection, immunosuppression, and microcirculatory damage combined with the high costs of blood transfusions warrant the development of such a system
  • Hyper-coagulable trace Shortened r-time/CT Increased α angle &amp; k Hyper-fibrinolytic trace Prolonged r-time/CT Decreased α angle &amp; k Decreased MA/MCF Hypo-coagulable trace Prolonged r-time/CT Decreased α angle &amp; k Decreased MA/MCF
  • Transcript of "Fisiología Y Fisiopatología de La Hemostasia"

    1. 1. Fisiología y Fisiopatología de la Hemostasia José Domingo Torres Hernández Universidad de Antioquia HUSVP
    2. 2. <ul><li>Aquí </li></ul>
    3. 3. Plaquetas FT Fibrina Pq + FT FT + Fbn Flujo de sangre Pq + FT + Fbn Pq + Fbn
    4. 4. Endotelio <ul><li>Antitrombogénico Prostaciclina Heparan sulfato tPA </li></ul><ul><li> óxido nítrico </li></ul><ul><li>Trombomodulina TFPI </li></ul><ul><li>Protrombogénico FvW FT PAI - 1 </li></ul>
    5. 5. Factor tisular Colá-geno Trombos Matriz subendotelial Endotelio Músculo liso
    6. 6. adhesión activación secreción Célula endotelial subendotelio VWF h TSP h colágeno l plaqueta GPlb GPla/lla GPIlb/Illa FG CD62P TSP ADP TxA 2 activación atracción GPVI/ Fc  Flujo
    7. 7. trombina FXI R R GPIb/V/IX secreción IX IXa VIIIa Xa X IXa R FPE Xa II Va trombina trombina trombina trombina trombina trombina trombina trombina Fibrinógeno fibrina GPIb/V/IX PAR1, PAR4 GPIIb/IIIa VWF Activación Plaquetaria
    8. 8. agregación/ reclutamiento de leucocitos Célula endotelial generación trombina VWF TSP sCD4OL T-cell atracción retracción coágulo/ Expulsión microvesículas / activación de leucocitos, Cels-T y cels endoteliales colágeno sCD4OL activación subendotelio sCD4OL sCD4OL sCD4OL sCD62P sCD62P CD62P CD62P sCD4OL sCD62P sCD62P CD62P leucocito cel T
    9. 9. 1. Fase iniciación Iniciación de coagulación
    10. 10. 2. Fase de amplificación Plaqueta activada Trombina Protrombina Plaqueta
    11. 11. 3. Fase de propagación Fibrinógeno Fibrina Plaqueta activada Protrombina Trombina
    12. 12. Coágulo plaqueta-fibrina R R FPE trombina trombina trombina trombina trombina thrombin trombina fibrinógeno IX IXa VIIIa Xa X IXa IXa VWF IX Xa IXa X VIIIa Xa trombina trombina trombina FXI IX IXa VIIIa Xa X IXa IXa VWF IX Xa IXa X VIIIa X FXI R R FPE R R FPE Va X R R FPE Va II R R FPE Va II X IX IXa IXa Xa R R FPE Va II VWF thrombin Xa XI fibrinógeno FXI trombina FXI
    13. 13. <ul><li>Plaquetas – Factor V – Factor VIII – Factor XI </li></ul><ul><li>Trombomodulina TROMBINA TAFI </li></ul><ul><li>Fibrinógeno Fibrina </li></ul>
    14. 14. Fibrinolisis Plasminógeno TAFI
    15. 15. Mecanismos de control de la coagulación <ul><li>Trombina – factor Xa </li></ul><ul><li>ANTITROMBINA </li></ul><ul><li>Factor VIIa – IXa – XIa – XIIa </li></ul>
    16. 16. Mecanismos de control de la coagulación <ul><li>Trombina + Trombomodulina </li></ul><ul><li>Proteína C – Proteína S </li></ul><ul><li>Factor Va Factor VIIIa </li></ul>
    17. 17. Mecanismos de control de la coagulación Xa TFPI Xa TFPI Xa TFPI VIIa TF Ca 2+ Ca 2+ +
    18. 18. Plasmina Plasminógeno Fibrinógeno Fibrina
    19. 19. Evaluación Hemostática Preoperatoria Procedimiento mayor Historia sospechosa de sangrado TP – TTP Plaquetas Tiempo de sangría Historia altamente sospechosa de defecto hemostático mayor TP – TTP Plaquetas Agregometría plaquetaria Fibrinógeno – TT Factor VIII - IX Factor XIII Tiempo de lisis de la euglobulina
    20. 20. Trastornos Hemostáticos en Hepatopatía Síntesis disminuida de factores de la coagulación Anemia Trombocitopenia Disfunción plaquetaria Hiperfibrinolisis primaria CID Síntesis disminuida de factores anticoagulantes Aumento niveles de factor von Willebrand, factor VIII, fibrinógeno
    21. 21. Trastornos Hemostáticos en Cirugía Cardíaca Disminución de factores de la coagulación Hemodilución Desnaturalización Disminución recuento y función plaquetas Hemodilución Desnaturalización Aumento de la fibrinolisis Secundario a activación de la coagulación Generación aumentada de trombina Expresión aumentada del FT Uso de heparina y protamina Hipotermia Uso previo de antiplaquetarios y anticoagulantes
    22. 22. Sangrado Masivo - Mayor <ul><li>Reemplazo de 1 volumen de sangre en 24 horas </li></ul><ul><li>Reemplazo del 50% volumen sanguíneo total en 3 horas </li></ul><ul><li>1.5 ml/Kg/min en 20 min </li></ul>
    23. 23. Sangrado Quirúrgico - Trauma <ul><li>Sangrado excesivo asociado con morbi-mortalidad y estancia en UCI </li></ul><ul><li>75-90% hemorragia por factores técnicos </li></ul><ul><li>Coagulopatías heredadas o adquiridas </li></ul>
    24. 24. Síndrome de Coagulopatía Asociada al Trauma <ul><li>Pérdida de sangre y dilución </li></ul><ul><li>Consumo de plaquetas y factores de coagulación </li></ul><ul><li>Disfunción plaquetaria por hipotermia </li></ul><ul><li> de actividad de factores de coagulación por acidosis e hipotermia </li></ul><ul><li>Fibrinolisis aumentada </li></ul>
    25. 25. Transfusión en Trauma <ul><li>91% no requieren </li></ul><ul><li>7% < 10 U </li></ul><ul><li>2%  10 U </li></ul><ul><li>Resucitación con GR:Plasma: Plaquetas </li></ul><ul><li>Hcto 29% Plaquetas 88K Actividad factor coagulación 65% </li></ul><ul><li>Plasma AB </li></ul>
    26. 26. Causas de Sangrado Quirúrgico <ul><li>Intraoperatoria </li></ul><ul><li>Problemas técnicos - </li></ul><ul><li>Consumo factores de coagulación </li></ul><ul><li>Fibrinolisis aumentada </li></ul><ul><li>Hemodilución </li></ul><ul><li>Hipotermia </li></ul><ul><li>Acidosis </li></ul><ul><li>Sobredosis de heparina </li></ul>
    27. 27. Causas de Sangrado Quirúrgico <ul><li>Posoperatoria Temprana ( 0-2 días) </li></ul><ul><li>Problemas técnicos </li></ul><ul><li>Trombocitopenia - Trombocitopatía </li></ul><ul><li>Defecto leve heredado de coagulación </li></ul><ul><li>Postoperatoria Tardía (2-7 días) Trombocitopenia – Trombocitopatía </li></ul><ul><li>Deficiencia de vitamina K </li></ul><ul><li>Falla multiorgánica </li></ul>
    28. 28. Opciones Terapéuticas <ul><li>Plaquetas si el recuento es < 50,000 </li></ul><ul><li>Plasma fresco congelado si TP o TTP  1.5 veces control </li></ul><ul><li>Crioprecipitado si fibrinógeno < 150 mg% </li></ul>
    29. 29. TXA 2 Trombina ADP
    30. 30. Administración de hemocomponentes en sangrado masivo *Recuento de plaquetas < 50,000 TP o TTP > 1.5 o 1.8 veces el control Fibrinógeno < 150 mg/dL Presencia de Sangrado Clínico Pruebas de Coagulación Anormales Si No Si Transfunda según resultados Solo si el riesgo hemorrágico es muy alto No Re-evalue Busque otra causa No hay indicación Desconocido Transfusión guiada por probabilidad clínica de defecto hemostático específico No hay indicación
    31. 31. Opciones Terapéuticas <ul><li>Factor VIIrh </li></ul><ul><li>Antifibrinolíticos </li></ul><ul><li>Desmopresina </li></ul>
    32. 33. Tromboelastografía
    33. 34. Tromboelastografía
    34. 35. Administración de hemocomponentes en sangrado masivo *Recuento de plaquetas < 50,000 TP o TTP > 1.5 o 1.8 veces el control Fibrinógeno < 150 mg/dL Presencia de Sangrado Clínico Pruebas de Coagulación Anormales Si No Si Transfunda según resultados Solo si el riesgo hemorrágico es muy alto No Re-evalue Busque otra causa No hay indicación Desconocido Transfusión guiada por probabilidad clínica de defecto hemostático específico No hay indicación
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