Coagulopathy in Cardiac Surgery1

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    CARDIAC SURGERYBY:Dr Hatem Mohd Altaher

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    Coagulation and bleeding assume particular importance whenoperations are performed on the heart using extracorporeal


    The interaction of the platelets, endothelial cells, andproteins to either activate or deactivate coagulation is ahighly buffered and controlled process.

    Coagulation itself the injury/controlleading to hemostasis isa four-part event




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    Platelet activation by CPB


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    CPB negativelychargedplastic surface

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    The central role of Thrombin (Thr) inhemostatic activation

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    Modulating effects of coagulation.



    Thrombin + ATIII

    II ,XIIa,XIa, and Xa;kallikrein;plasmin.



    VIIa & Xa



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    The fibrinolytic system

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    Following cardiac surgery, some patients bleed excessively.Prompt diagnostic and therapeutic action will avoidimpaired hemodynamics, decreased oxygen-carryingcapacity, and impaired hemostasis from depletion ofendogenous hemostatic resources.

    creates the potential for hemorrhage, sometimes aided bypreoperative attempts to lyse intracoronary thromboses.Beyond that, however, many factors govern whether aparticular patient will experience excessive bleeding aftercardiac surgery.

    Excessive bleeding,a chest tube drainage > 10 mLlkg in the first hour post op

    or a total of > 20 mLlkg over the first 3 hourspost opany sudden increase of >300 mLlhr or greater following

    minimal initial drainage

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    I- Patient Factorspatient with a personal or family history of abnormal bleedingfollowing surgery should be investigated.

    Concurrent systemic disease affects hemostasis duringsurgery.

    Uremia from RF results in platelet dysfunction.

    Severe hepatic compromise impairs every aspect of hemostasis:prekallikrein and most coagulation factors

    splenomegaly induces thrombocytopenia; maldistribution ofvWF lead to impairs platelet adhesiveness and aggregation;

    impaired clearance of endogenous plasminogen activatorsaccentuates fibrinolysis; and decreased levels of coagulationinhibitors induce a consumptive coagulopathy.

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    II- Medications

    warfarin hold 2 to 5 days.urgent surgery parenteral vitamin K or FFP

    thrombolytic therapy as streptokinase should respond toantifibrinolytic therapy with (EACA) or tranexamic acid.

    ASA or other platelet-inhibiting drugs regularly cannot haltthat therapy within 7 days of surgery. No antidote can correct

    the platelet defect.

    B-Lactam antibiotics coat the platelet membrane, while thecephalosporins are rather profound but short-term plateletinhibitors. Many cardiac surgeons may not realize that theirstandard drug regimen for antibiotics may be far more of ableeding risk than aspirin

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    RouteIndicationsMechanismCompositionDrug Type



    OralCAD, AMI,


    Irreversible COX






    OralPainReversible COXinhibition


    12 hrOralVHD, PVDReversible COX


    MultipleAdhesion inhibitors

    (e.g., dipyridamole)5days


    Irreversibleinhibition of ADPbinding

    ThienopyridinesADP receptorantagonists

    (e.g., clopidogrel)

    GPllb/llla receptorinhibitors

    12 to18 hr

    IVPCI, ACSNonspecific-bindsto other receptors


    Abciximab (ReoPro)

    2 to 4hr

    IVPCI, ACSReversible-specific toGPllb/llla

    PeptideEptifibatide (Integrilin)

    2 to 4hr

    IVPCI, ACSReversible -specific to

    Nonpeptide-t rosine

    TIrofiban (Aggrastat)

    II- Anti-platelet

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    III- Insult of CPB

    A-FibrinolysisNumerous investigations support the notion that CPB activates thefibrinolytic pathway.

    Why might this occur?Despite clinically adequate doses and blood concentrations of heparin,coagulation pathway activity persists. Formation of prothrombin and

    fibrinopeptide fragments and thrombin-antithrombin complexescontinued.

    The site of thrombin activity probably resides in the ECC , whichcontains a large surface of thrombogenic material. Thrombinactivation results in fibrinolytic activity. Activation of fibrinolysis

    Plasminogen activator concentrations rise during CPB, while levels ofits inhibitor PAl-I remain unchanged.

    Does fibrin formation during CPB constitute a consumptivecoagulopathy?

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    Thrombocytopenia occurs during CPB as a result of

    Hemodilution. Heparin.

    hypothermia-induced. splenic sequestration of platelets.

    platelet destruction from the blood-gas and blood-tissueinterfaces created by cardiotomy suction, filters, and bubbleoxygenators.

    Platelet count rarely drops below 50,000/mm3.

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    C- platelet dysfunction

    Not only does the number of platelets decrease during CPB, but

    remaining platelets become impaired by partial activation.

    Fibrinogen and fibrin, which adhere to artificial surfaces of the ECC,form a nidus for platelet adhesion and aggregation. reducedcontent of platelet granules constitutes the evidence for partialactivation.

    Nearly one-third of circulating platelets undergo a-granular releaseduring CPB.

    also depletes platelet glycoprotein receptors Ib and IIb/I1Ia.Use of frequent cardiotomy suction and bubble oxygenators

    aggravates the extent of platelet activation.

    Activation of the fibrinolytic system may contribute to plateletdysfunction.

    Antifibrinolytic medications preserve platelet function and preventsome platelet abnormalities that occur during bypass

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    D-Clotting Factors

    Denaturation of plasma proteins, including the coagulationfactors, occurs at blood-air interfaces. Liberal use ofcardiotomy suction and prolonged use of bubbleoxygenators potentially impair coagulation by decreasingcoagulation.

    Hemodilution also decreases factor concentrations.

    However, rarely do coagulation factor levels fall below thethresholds for adequate formation of fibrin in adult surgery.

    In infants, however, the smallest achievable pump primingvolumes can dilute factors to below 30% of normal levels.

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    First, the splanchnic circulation responds to hypothermia withsequestration of platelets.

    Second, transient platelet dysfunction occurs, evidenced by aplatelet shape change, increased adhesiveness, inhibition ofADP-induced aggregation, and decreased synthesis of boththromboxane and prostacyclin.

    Third, hypothermia slows the enzymatic cleavage upon whichactivation of coagulation factors depends.

    Many biologic phenomena display a 7% attenuation of activity

    for each decrease of 1C in temperature. While coagulationfactor structure remains unaltered, formation of fibrin may besluggish when the patient is cold.

    Fourth, hypothermia accentuates fibrinolysis.

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    Prevention of BleedingA-Preoperative Factors

    Identified and treated existing disorders of hemostasis.

    The bleeding diathesis of uremia responds to hemodialysis, redblood cell transfusion, and administration of desmopressin.

    Impaired hemostasis from hepatic failure may respond tointravenous desmopressin.

    Correction of hematologic disordersAdministration of platelet-inhibiting drugs should cease pre OR

    Aspirin 10 days NSAIDs 2 days ADP receptor antagonists (e.g., c1opidogrel)5 days GPllbllla receptor inhibitors Tirofiban (Aggrastat) 2 to 4hr

    P ti f Bl di

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    Prevention of Bleeding

    B-Physical Factors

    Correction of Hypothermia

    Incomplete surgical hemostasis

    Limiting the intensity and frequency of use of thecardiotomy suction Selection.

    membrane Vs bubble-type oxygenator

    Centrifuge Vs Roller pump

    A small priming volum.ANH

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    B-Physical Factorscont.- Speed of surgery Shorter CPB duration

    Preserves platelet function and limits the coagulant stimulus for subsequent fibrinolysis. limits tissue exposure to the hypothermia

    positive END-EXPIRATORY PRESSURE(5 to 10cm H20).

    A tamponade effect in the mediastinum may explain thissalutary effect.

    Unfortunately, controlled studies have not confirmed thisbenefit. Also, excessive pressure impedes venous return,

    worsening hemodynamics in the hypoovolemic patient.

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    B-Physical Factorscont

    - maiaintenance of systemic blood pressure inthe low-normal range promotes tissue perfusionwhile limiting leakage around suture lines.

    Adequate depth of anesthesia during surgery andsufficient postoperative analgesia and sedationshould be verified prior to initiating vasodilatortherapy.

    Topical haemostatic agents Fibrin sealants arecomposed of human fibrinogen, human or bovinethrombin or human factor VIII and bovineaprotinin.


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    C-blood ProductsThe bleeding patient becomes subject to additional hemostatic

    derangements. The need to maintain intravascular blood volume

    arises in nearly all cases prior to identification of the cause ofbleeding.

    However, red blood cells,platelets, and coagulation factorsbecome diluted when continued bleeding is treated with suchreplacement. Also, PRBCs and banked whole blood do not

    provide platelets or sufficient factor V & VIII to maintainhemostasis.

    Although routine prophylactic administration of FFP or plateletsplays no role in modern cardiac surgical care.

    A platelet counr below 100,000/mm3 or prolongation of the PTor aPTT despite adequate heparin neutralization in a patientactively bleeding is an indication for platelet or plasmareplacement in the absence of coagulation tests toguide therapy

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    D-Pharmacological Intervention


    Too little heparin invites active fibrin formation during CPB withconsumption of clotting factors and platelets and excessiveactivation of the fibrinolytic system.

    Too much heparin risks postoperative heparin rebound.

    With too little protamine, the remaining unneutralized heparinimpairs hemostasis by its anticoagulant action.

    Doses of protamine excessive enough to overwhelm theendogenous proteases may exert an anticoagulant effect, aswell as induced lung injury and pulmonary vasoconstriction.

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    ACT nearly doubling following a protamine dosefour times

    that needed to neutralize heparin.

    At a lO-fold dose, the ACT prolonged andthrombocytopenia developed

    The optimal approach utilizes coagulation testingto estimate the appropriate heparin and

    protamine doses, and confirm both adequateanticoagulation and its neutralization.

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    D-Pharmacological Interventioncont.


    This analog of vasopressin desmopressin releases coagulationsystem mediators from vascular endothelium.

    Factor VIII increases 2- to 20-fold.

    Factor XII levels Endothelium : releases of vWF.

    Specific applications of desmopressin's hemostatic benefitinclude :

    uremia, Correction of prolonged bleeding times

    Liver cirrhosis patientsshortens prolonged bleeding times.

    corrected the aspirin-induced prolongation in bleeding time

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    D-Pharmacological Interventioncont.SYNTHETIC ANTIFIBRINOlYTICS

    For decades, antifibrinolytics have been proposed as potentialhemostatic agents during cardiac surgery.

    Prophylactic antifibrinolytics may spare platelet function byinhibiting the deleterious effects of plasmin.

    These simple molecules analogs of the amino acid lysine, bindto plasminogen and plasmin, thus inhibiting binding ofplasminogen at the lysine residues of fibrinogen.

    Antifibrinolytics undergo renal concentration and excretion witha plasma half-life of about 80 minutes.

    The loading dose of 10mg/kgfor TA followed by 1mg/kg/hror 50 mg/kg of EACAthen 25 mg/kg/hr

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    Pharmacokinetic studies demonstrate a need to readministera bolus of EACA upon institution of CPB.

    Several investigations, using prophylactic antifibrinolytics;document a savings in blood loss, as well as in bloodtransfused in a general population of cardiac surgery

    chest tube drainage in the first 12 hours following operationdecreased by 30%,

    The likelihood of receiving banked blood within 5 days ofoperation decreased from 41% to 22%:48

    Administration of very largedoses of antifibrinolytics appearsto offer no greater savings.

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    Recombinant Factor Seven

    Factor VII is synthesized in the liver has the shortest half-life ofall procoagulant factors (3-6 h).

    Novel indications for rFVIIa (based on case reports & clinicaltrials)

    Patients with liver disease,

    Thrombocytopenia, or Qualitative platelet dysfunction

    Patients with no coagulation disorders who are bleeding as aresult of extensive surgery or major trauma

    D-Pharmacological Interventioncont.

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    Activated recombinant factor VII aftercardiopulmonary bypass

    reduces allogeneic transfusion in complexnon-coronary

    cardiac surgery: randomized double-blindplacebo-controlled pilot study

    British Journal of Anaesthesia

    95 (5): 596602 (2005)

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    2006Effective Management of Refractory Postcardiotomy

    Bleeding With the Use of Recombinant ActivatedFactor VII

    Farzan Filsoufi, MD, Javier G. Castillo, MD, Parwis B.Rahmanian, MD,Corey Scurlock, MD, Gregory Fischer, MD,

    and David H. Adams, MDDepartments of Cardiothoracic Surgery and Anesthesiology,

    Mount Sinai Hospital, New York, New York

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    Crit. Care Med. 2005;

    33(10)Von HeymannC ;et al, Department of

    Anesthesiology and Intensive Care

    Medicine, St. Mary's Medical Center,San Francisco, CA, USA

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    STUDIESBlood loss and transfusion requirementswere significantly reduced in the periodafter the administration of rFVIIa.

    Early Mortality and 6-month survival rates

    were not different between the groups.

    No thromboembolic complications wereobserved in the rFVIIa group

    CONCLUSIONS: When used as a lastresort, rFVIIa was safe , efficacious overconventional hemostatic therapy


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    Recombinant Activated Factor VII inCardiacSurgery: A Systematic Review

    Oliver Warren, MRCS, et al, Department of

    BioSurgery and Surgical Technology, St.Marys Hospital, London, UK

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    Journal ofCardiothoracic and

    Vascular Anesthesia,Recombinant Activated Factor VII in Cardiac Surgery: A Meta-


    2009performed a meta-analysis of 5 clinical trials

    hemostatic properties of rFVIIa could reduce the rate of surgicalreexploration after cardiac surgery even if an increase of hazardous side

    effects (eg, perioperative stroke) could not be excluded.

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    Pediat. Crit Care Med. 2005

    WittensteinB ;NgC ;RavnH;GoldmanA

    Great Ormond Street Hospital forChildren, London, UK

    Th b b li d f d f

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    Thromboembolic adverse events after used offactor VIIa

    OConnell K JAMA 2006: 295:293

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    Retrospective review of factor VII use in 18Canadian centres, 2003 2006

    Data collected on 503 patients

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    Blood Coag Fibrinolysis 2006;17:389

    Factor VIIa in cardiac surgery: a systematic

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    Factor VIIa in cardiac surgery: a systematicreview

    Warren O Ann Thorac Surg 2007; 83:707

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    Thromboembolic adverse events after used of

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    Thromboembolic adverse events after used offactor VIIa

    OConnell K JAMA 2006: 295:293

    431 AE reports

    168 patients had thrombotic events

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    Coagulation monitoring


    PlateletsPlatelet count 150,000-400,0001IlLBleeding time

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    Coagulation monitoring

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    Coagulation monitoring

    ADP Test

    No oozing at puncture sites;

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    Desmopressin O.3uglkgIV

    Aminocaproic acid or

    Tranexamic acid

    Fibrinogen 1.5 timescontrol

    Platelet count 150 sec or aPTT >1.5

    times control

    Core" temperature

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    There have been fewer randomized trials of tranexamicacid or aminocaproic acid. One trial [15] of 210 cardiacsurgery patients randomized to receive tranexamic acid orplacebo resulted in a significant reduction in the proportionof patients requiring any blood product in thetranexamic group (12.5%) compared with the placebogroup (31.1%).A Cochrane review [8] of over 200 clinical trials (notlimited to cardiac surgery) found that antifibrinolyticdrugs used at the time of major surgery reduced bleeding,the need for transfusion and the need for repeat surgerybecause of bleeding. The authors [8] found that lysineanalogues were probably as effective as aprotinin and

    were cheaper; the evidence for tranexamic acid is strongerthan for aminocaproic acid. Large variations indosages used between the published studies make itimpossible to evaluate the relationship between dosageand efficacy.In the paediatric population, antifibrinolytics have beenused for scoliosis surgery. A Cochrane review [16] showed

    that antifibrinolytics reduce blood loss, but their effect on

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    rFVIIa binds to tissue factor at the site of tissue injury andvascular wall disruption, generating thrombin and activatingplatelets. The activated platelet surface thenforms a template, on which rFVIIa mediates furtheractivation of coagulation. This in turn generates a thrombin

    burst, which leads to the conversion of fibrinogen tofibrin. Furthermore, rFVIIa-mediated activation ofthrombin-activatable fibrinolysis inhibitor results in clotstabilization by inhibition of fibrinolysis [1].

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    Recombinant FVIIa is an expensive therapy; a singleadult dose of 90mgkg1 costs approximately 6000 Euros.Its use is difficult to justify on economic grounds alone,given the cost of one unit of red blood cells (175 Euros).There is evidence that the clinical efficacy varies at

    different doses; in a meta-analysis, a subgroup analysisdetermined that at least 50mgkg1 was required for asignificant benefit [18]. Therefore, the role of this drughas yet to be established, and further research is required.

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    Topical haemostatic agentsFibrin sealants are composed of human fibrinogen,human or bovine thrombin or human factor VIII andbovine aprotinin. They are topically applied and are usedquite commonly in cardiothoracic, vascular, liver and

    spleen surgery to aid haemostasis at sites of cannulation,laceration and along suture lines [1]. A systematic review[26] of the use of fibrin sealants to minimize perioperativeallogeneic blood transfusion suggested that they areefficacious,although large methodologically rigorous trials arestill needed. In addition, such sealants are very expensive,and costbenefit analysis has yet to be performed, despiteaggressive marketing from the manufacturers.

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    Autologous blood transfusionThere are three types of autologous blood transfusion:preoperative blood donation, acute normovolaemic haemodilution(ANH) and red blood cell salvage (intraoperativeand postoperative) [27]. A systematic review [28] ofrandomized controlled trials found that all three autologous

    transfusion techniques consistently reduced the frequencyof allogeneic transfusions; the greatest relative riskreduction occurring with preoperative blood donation

    Carless PA, Moxey A, OConnell D, Henry D. Autologoustransfusion

    techniques: a systematic review of their efficacy. Transfus Med2004;14:123144.

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    Acute normovolaemic haemodilutionANH is an autologous blood collection technique thatinvolves the removal of whole blood from the patientimmediately before surgery, along with simultaneousreplacement with an intravenous fluid (crystalloid or

    colloid) in order to maintain normovolaemia. The bloodis collected in standard blood bags containing citrateanticoagulant; it remains in the operating room and isreinfused at an appropriate time during surgery, or at theend of surgery, usually after major blood loss has ceased.

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    The efficacy of ANH in reducing allogeneic transfusion isdubious. Several prospective randomized trials [4043]have demonstrated that ANH reduces allogeneic bloodtransfusions in patients undergoing elective total kneereplacement, liver resection and cardiac surgery; however,

    others [44,45] have failed to document any benefit.A meta-analysis of 42 trials [46] comparing ANH withalternative blood conservation methods or usual caresuggested that the efficacy of ANH was likely to besmall. It appears to modestly reduce bleeding and the

    volume of allogeneic blood required, but its efficacy withregard to avoidance of allogeneic transfusion is unproven.

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    Red blood cell salvageRed blood cell salvage has become popular over the past10 years and is now used extensively in the surgicalsetting. Cell salvage is a term that covers a range oftechniques that scavenge blood from operative fields or

    wound sites and reinfuse the blood back into the patient.Cell salvage can be performed during intraoperative orpostoperative periods or during both. To remove noncellularmatter prior to reinfusion, some of the devices usecentrifugal washing of the salvaged blood [48], whereas

    others use a countercurrent system similar tohaemofiltration[49]. The processing of blood, however, necessarily

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    removes platelets and plasma proteins, which maycontributeto a dilutional coagulopathy. The washing processcan also lead to haemolysis, especially if suction pressuresare not carefully regulated or the washing process is

    accelerated. In addition, retained plateletleukocytedeposits may produce procoagulant leukotactic substances,increasing the risk of disseminated intravascularcoagulation [50]. Relative contraindications include thepotential for aspiration of malignant cells, the presence ofinfection, gross bacterial contamination of the surgical field

    and the presence of other contaminants such as amnioticfluid [51].

    The effect of acute autologous blood transfusion on

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    The effect of acute autologous blood transfusion oncoagulation dysfunction after cardiopulmonary bypassAnaesthesiol 26:868873 Q 2009 European Society of


    electivecardiac surgery with cardiopulmonary bypass. The patientsin group A underwent acute autologous blood transfusionwith acute normovolemic haemodilution and those in groupH received homologous blood, if needed, and served ascontrols.

    Autologous blood transfusion of 15%estimated blood volume did not affect postcardiopulmonarybypass coagulopathy, nor did it decrease blood loss orhomologous blood and its products transfusion in the earlypostoperative period. TEG is a valuable measure fordetecting coagulation dysfunction with a potential role in thepostoperative management of cardiac patients