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Hemostasis Shaina Eckhouse 10/12/2010. Objectives Biology of Hemostasis Congenital Hemostasis Defects Aquired Hemostasis Defects Hypercoagulable States.

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Presentation on theme: "Hemostasis Shaina Eckhouse 10/12/2010. Objectives Biology of Hemostasis Congenital Hemostasis Defects Aquired Hemostasis Defects Hypercoagulable States."— Presentation transcript:

1 Hemostasis Shaina Eckhouse 10/12/2010

2 Objectives Biology of Hemostasis Congenital Hemostasis Defects Aquired Hemostasis Defects Hypercoagulable States Venous thromboembolism Transfusion Evaluation of the Surgical Patient at Hemostatic Risk

3 Name that Movie

4 Biology of Hemostasis Complex process that prevents or terminates blood loss from a disrupted intravascular space Major physiologic events Vascular constriction Platelet plug formation Fibrin formation fibrinolysis

5 Biology of Hemostasis Vascular Constriction Initial vascular response to injury Vasoconstriction linked to platelet plug formation TXA2 ET 5-HT Bradykinin & Fibrinopeptides

6 Biology of Hemostasis Platelet Function K circulating platelets ~30% sequestered in the spleen Thrombopeptin, IL-1, IL-6 mediate platelet production

7 Biology of Hemostasis Platelets play an integral role in: Formation of a hemostatic plug Contributes to thrombin formation

8 Biology of Hemostasis VC + platelet plug formation = PRIMARY HEMOSTASIS Reversible Not associated with secretion

9 Biology of Hemostasis

10 Intrinsic Pathway All the components leading to the fibrin clot formation are intrinsic to the circulating plasma Elevated PTT associated with an abnormality in the intrinsic clotting pathway

11 Biology of Hemostasis Extrinsic Pathway Requires exposure of tissue factor on the surface of the injured vessel wall Starts with Factor VII Abnormality of the extrinsic pathway is associated with an elevated PT

12 Biology of Hemostasis

13 Fibrinolysis = lysis of the fibrin clot Plasminogen Plasmin degrades fibrin, Factor V and VIII Plasminogen plasmin by several activatorstPA, (kalikrein increases release of tPA), uPA, factor XII Plasminogen levels rise due to exercise, venous occlusion, and anoxia Breakdown of the clot permits restoration of blood flow and fibrin clot in vessel wall may be replaced with collagen Antithrombin III Binds and inhibits thrombin and factors IX, X, XI Protein C Vitamin K-dependent Degrades fibrinogen and factors V and VIII Protein S Vitamin K-dependent Protein C cofactor

14 Biology of Hemostasis How do SCDs work? The squeeze stimulates the release of tPA from the endothelial cells of vessels. Induction of fibrinolysis. (tPA is selective for fibrin-bound plasminogen and converts to plasmin; therefore, fibrinolysis occurs mostly at the site of clot formation.)

15 Name that movie

16 Congenital Hemostatic Defects Coagulation Factor Deficiencies Hemophilia Factor VIII deficiency = Hemophilia A Sex-linked recessive Both prolonged aPTT and PT Need level to be 100% pre-op and 30% post-op Crosses placenta Hemophiliac Joint No aspiration; ice; ROM exercises, factor VIII concentrate or cryoprecipitate Factor IX deficiency = Hemophilia B/Christmas Disease Sex-linked recessive Need level 50% pre-operatively Prolonged aPTT and normal PT Tx-factor IX concentrate or cryoprecipitate

17 Congenital Hemostatic Defects von Willibrands Disease MOST COMMON congenital bleeding disorder Low levels of vWF variable decrease in Factor VIII due to loss of the carrier protein vWF is necessary for normal platelet aggregation; therefore deficiency presents in a similar fashion to platelet disorders Prolonged bleeding time, possible abnormal PTT, normal PT Types- I-partial quantitative deficiency (AD) II-qualitative defect (AD) III-total deficiency (AR) Txintermediate purity factor VIII or DDAVP (Type I or II only)

18 Congenital Hemostatic Defects Platelet disorders Glanzmanns thrombocytopeniadeficiency in GIIbIIIa receptor of platelets; therefore, platelets cannot bind to each other Tx-platelets Bernard SoulierGp1b receptor deficiency; therefore, platelets cannot bind collagen via vWF Tx-platelets

19 Name that movie

20 Acquired Hemostatic Defects Anticoagulation Heparinpotentiates ATIII action Reversed with administration of protamine (1mg protamine for every 100u heparin received) Follow aPTT want x upper limit of nl (60-90) Does not cross placental barrier Lovenoxpotentiates ATIII and inhibits both thrombin and Factor Xa more reliable therapeutic anticoagulation can be achieved Drug effect can be determined by anti-Xa assay No definitive reversal Warfarin (Coumadin) Inhibits Vitamin K synthesis Reversed by FFP or Vitamin K administration Follow INR/PT

21 Acquired Hemostatic Defects Why do we bridge with heparin or Lovenox when initially starting Coumadin? Protein C and S are inhibited before factors II, VII, IX and X which makes the patient relatively hypercoaguable for 5-7 days

22 Acquired Hemostatic Defects Antiplatelet Medications AsprinPlatelet cyclooxygenase is irreversibly inhibited ; decreases TXA2 which promotes platelet aggregation Plavix (Clopidogrel)ADP receptor antagonist Pentoxifyllineinhibits platelet aggregation and decreases viscosity of blood; used in treatment of peripheral arterial disease

23 Acquired Hemostatic Defects Heparin Induced Thrombocytopenia 2/2 antiplatelet Ab (IgG) that results in platelet destruction Platelet count falls to <100K or by <50% in 5-7 days if first exposure or in 1-2 days if re-exposure High incidence of platelet aggregation and thrombosis (white clot) If suspected STOP heparin Start alternate anticoagulation (lepirudin or argatroban)

24 Acquired Hemostatic Defects Disseminated Intravascular Coagulation Systemic process producing both thrombosis and hemorrhage Exposure of blood to procoagulants Formation of fibrin in the circulation Fibrinolysis Depletion of clotting factors end-organ damage Dx= decreased platelets, prolonged PT and aPTT, low fibrinogen, high fibrin split products, high D-dimer Treat the underlying disease (sepsis, trauma, burns, malignancy)

25 Acquired Hemostatic Defects Thrombocytopenia MOST COMMON abnormality of hemostasis Variety of etiologies (ITP, TTP, HUS, SLE, lymphoma, secondary hypersplenism, portal HTN, uremia…) In setting of massive transfusionexchange of 1L of blood volume (~11units) decreases platelet count from 250K to 80K. Associated impaired ADP- stimulated aggregation if >10units of blood transfused.

26 Name that movie

27 Hypercoagulable States Factor V Leiden Deficiency MOST COMMON congenital hypercoagulable disorder AD Leiden variant of Factor V cannot be inactivated by Protein C Increased risk for DVT, spontaneous abortion Tx = heparin or warfarin

28 Hypercoagulable States AT-III deficiency Spontaneous venous thrombosis Heparin does not work on these patients unless pretreated by FFP Tx: AT-III concentrated Antiphospholipid Antibody Syndrome Presence of lupus anticoagulant that bind to phospholipids and proteins on the cell membrane an interfere with clotting; HOWEVER, associated with thrombosis and habitual abortions (prolonged PTT in the face of a hypercoagulable state) Tx: Heparin, coumadin

29 Hypercoagulable States Amicar Aminocaproic acid Inhibits fibrinolysis by inhibiting plasmin Indications: DIC, persistent bleeding following CPB, thrombolytic overdose Aprotinin Inhibits fibrinolysis by inhibiting activation of plasminogen to plasmin

30 Name that movie

31 Venous thromboembolism DVT and PE Virchows triad = stasis, endothelial injury, hypercoagulability Treatment for DVT 1 st = warfarin x 6months 2 nd = warfarin x 1year 3 rd or significant PE = lifetime warfarin Greenfield filters For patients with contraindications to anticoagulation Documented PE while on anticoagulation Free-floating iliofemoral clot IVC or femoral DVT Patients who have undergone previous pulmonary embolectomy PE most commonly caused by DVT in iliofemoral region

32 Name that movie

33 Transfusion PRBCs 1unit=~250mL Storage life ~35days 1unit increases Hgb by 1 and Hct by 3 Fever without hemolysis is the most common transfusion reaction (1 in 6,000) Usually recipient antibody reaction against WBCs in donor blood Acute Hemolytic reactions occur 1 in 35,000 Caused by ABO incompatibility or Ab mediated usually from human error (Ab in recipient binding to surface Ag on donor RBC) Sx=hypotension, fever, dyspnea, chest pain, low back pain Tx=fluids, diuretics, HCO3, histamine blockers, pressors

34 Transfusion Platelets billion in 50mL plasma Can be stored for ~7 days (viability declines after 3 days) Each platelet concentration should raise circulating platelets by >5,000 (4-6 pack of platelets shound increase platelets by 20-30K) Febrile nonhemolytic reactions more common than with PRBCs (incidence is ~30%) Antiplatelet antibodies develop in 20% of patients after transfusions Indictions in active bleeding: plt<50K or plt<100K in setting of ICH; trauma victims who have received multiple transfusion Contraindicated in HIT and TTP

35 Transfusion FFP ~250 mL collected from 1 unit whole blood by apheresis Stored between -18 and -30 degree C and is good for 1 year Dose is ~10-15mL/kg Contains all coagulation factors, protein C, protein S, and AT-III (only blood product with factor V) Indications-warfarin overdose, liver failure, dilutional coagulopathy associated with massive transfusion Highest risk of TRALIimportant to distinguish from volume overload. Tx=supportive

36 Name that movie

37 Evaluation of the Surgical Patient at Hemostatic Risk Preoperative Assessment History Bruises without apparent injury Prolonged bleeding after injury PMHxliver disease, congenital or acquired bleeding disorders Medications LabsCBC, Coagulation panel, T&S or T&C Intraoperative and Postoperative Ineffective local hemostasis Complications of blood transfusion Consumptive coagulopathy Fibrinolysis

38 Questions?


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