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Achieving hemostasis after cardiac surgery with cardiopulmonary bypass

Achieving hemostasis after cardiac surgery with cardiopulmonary bypass
Authors:
Kamrouz Ghadimi, MD, MHSc, FAHA
Ian J Welsby, BSc, MBBS, FRCA
Section Editor:
Jonathan B Mark, MD
Deputy Editors:
Nancy A Nussmeier, MD, FAHA
Jennifer S Tirnauer, MD
Literature review current through: May 2025. | This topic last updated: Jun 23, 2025.

INTRODUCTION — 

Blood and coagulation management are key components of anesthetic care for cardiac surgical procedures requiring cardiopulmonary bypass (CPB).

This topic discusses the management and prevention of bleeding after weaning from CPB.

Separate topics discussed:

Use of protamine to reverse systemic anticoagulation after CPB. (See "Protamine reversal of heparin anticoagulation after cardiopulmonary bypass", section on 'Protamine administration after cardiopulmonary bypass'.)

Transfusions and strategies to minimize blood loss with CPB. (See "Anticoagulation and blood management strategies during cardiac surgery with cardiopulmonary bypass".)

General principles of perioperative blood management. (See "Perioperative blood management: Strategies to minimize transfusions" and "Intraoperative transfusion and administration of clotting factors".)

REVERSAL OF ANTICOAGULATION

Reversal of heparin anticoagulation — Systemic anticoagulation with heparin is reversed with protamine after weaning from CPB. Techniques for protamine administration, dosing considerations, and recognition, treatment, and prevention of adverse reactions to protamine are discussed separately. (See "Protamine reversal of heparin anticoagulation after cardiopulmonary bypass", section on 'Protamine administration after cardiopulmonary bypass'.)

Management of bivalirudin anticoagulation — In rare cases, bivalirudin is used as an alternative to heparin (eg, in patients with known severe protamine allergy or heparin-induced thrombocytopenia [HIT] when HIT antibodies are present). (See "Management of heparin-induced thrombocytopenia (HIT) during cardiac or vascular surgery".)

Bivalirudin has a half-life of approximately 45 minutes in normothermic patients with normal kidney function; thus, its anticoagulant effects typically resolve within approximately two hours of administration of the last dose. However, kidney dysfunction or residual hypothermia can result in prolongation of the anticoagulant effect.

There is no reversal agent for bivalirudin. If bleeding is excessive in the postbypass period, more rapid offset of action may be achieved with combinations of therapies that reduce circulating bivalirudin blood levels, such as [1]:

Dilution with blood component replacement (if needed)

Plasmapheresis with plasma exchange

Hemodialysis

ACHIEVING HEMOSTASIS AND MANAGEMENT OF BLEEDING

Overview of risk factors for bleeding — After weaning from CPB and reversing anticoagulation, excessive bleeding may occur due to surgical and/or nonsurgical factors that affect hemostasis [2-5].

The ability to achieve hemostasis may be affected by:

Preoperative risk factors [6-10] (see "Perioperative blood management: Strategies to minimize transfusions", section on 'Preoperative strategies'):

Advanced age

Decreased preoperative red blood cell (RBC) mass (eg, preoperative anemia)

Preexisting coagulopathy

Failure to discontinue anticoagulants and antiplatelet drugs in a timely fashion [11]

Intraoperative risk factors

Significant blood loss, which may occur during any surgical procedure involving the heart and great vessels, particularly complex, redo, or emergency cardiac surgical operations – (See "Intraoperative transfusion and administration of clotting factors", section on 'When to transfuse'.)

Inadequate surgical hemostasis – (See 'Fastidious surgical hemostasis' below.)

Coagulopathy that occurs during CPB and is due to hyperfibrinolysis, coagulation factor consumption, and/or platelet dysfunction (due to platelet activation and consumption) – (See "Anticoagulation and blood management strategies during cardiac surgery with cardiopulmonary bypass", section on 'Effects of cardiopulmonary bypass on hemostasis'.)

Hemodilution due to fluid priming of the extracorporeal circuit, which may be exacerbated in smaller patients – (See "Anticoagulation and blood management strategies during cardiac surgery with cardiopulmonary bypass", section on 'Minimize further hemodilution during CPB'.)

Effects of heparin due to:

-Inadequate reversal with protamine – (See "Protamine reversal of heparin anticoagulation after cardiopulmonary bypass", section on 'Dosing for continued bleeding after initial protamine administration'.)

-Heparin rebound – (See "Protamine reversal of heparin anticoagulation after cardiopulmonary bypass", section on 'Avoiding heparin rebound'.)

Residual hypothermia after CPB – (See 'Fastidious surgical hemostasis' below.)

Loss of platelets and coagulation factors due to high volume cell saver use – (See "Surgical blood conservation: Intraoperative blood salvage", section on 'Potential complications'.)

Fastidious surgical hemostasis — The primary means to achieve hemostasis after CPB is meticulous surgical technique that includes systematic intraoperative checking of potential surgical sites of bleeding, apparent or hidden.

In a meta-analysis involving 18 studies and over 5000 patients requiring mediastinal re-exploration for bleeding or cardiac tamponade after cardiac surgery, a surgical site of bleeding was identified in two-thirds of cases [12].

Maintenance of normothermia — Mild-to-moderate hypothermia is induced in most patients undergoing CPB to provide neurologic and cardiac protection, while deep hypothermia to temperatures as low as 16 to 18°C may be employed for selected patients undergoing elective circulatory arrest. (See "Management of cardiopulmonary bypass", section on 'Management during cooling and hypothermia' and "Anesthesia for aortic surgery with hypothermia and elective circulatory arrest in adult patients", section on 'Considerations for anesthetic management'.)

Rewarming during CPB and subsequent maintenance of normothermia in the postbypass period are necessary; this is because hypothermia is associated with coagulopathy due to impairment of platelet aggregation and reduced activity of clotting enzymes [13-15]. The combination of platelet and coagulation factor impairment reduces clot formation and increases perioperative blood loss and the need for blood transfusion [16-18].

Active warming techniques must be employed to achieve normothermia during the rewarming phase of CPB and subsequently, to maintain normothermia during the postbypass and postoperative periods. Details regarding warming strategies are discussed separately:

(See "Management of cardiopulmonary bypass", section on 'Management during rewarming and weaning'.)

(See "Perioperative temperature management", section on 'Prevention and management of hypothermia'.)

Use of transfusion algorithms — We use goal-directed protocols or algorithms to guide transfusion decisions based on measurement of hemoglobin or hematocrit (HCT), as well as assessment of specific abnormalities of hemostasis using standard laboratory tests (algorithm 1), and/or point-of-care (POC) tests of hemostasis [2]; details are discussed in separate topics:

(See "Intraoperative transfusion and administration of clotting factors", section on 'Use of a transfusion algorithm or protocol'.)

(See "Intraoperative transfusion and administration of clotting factors", section on 'Intraoperative diagnostic testing'.)

(See "Point-of-care hemostasis testing (viscoelastic tests)".)

This practice is consistent with guidelines from several professional societies for both cardiac and noncardiac surgical cases [6,7,19-23].

Use of such transfusion protocols and algorithms to guide decision-making can avoid or reduce unnecessary transfusions of blood components, including RBCs, plasma, platelets, or Cryoprecipitate (table 1) [2,6,19,21,24-35].

Hemoglobin or hematocrit – We check the hemoglobin or hematocrit following weaning from CPB, then approximately every 30 minutes, or more frequently in a profusely bleeding patient. Indications for RBC transfusion are listed below. (See 'RBC transfusions for anemia' below.)

Standard coagulation tests – Standard laboratory tests of hemostasis include prothrombin time (PT) and international normalized ratio (INR), activated partial thromboplastin time (aPTT), fibrinogen level, and platelet count. Clinically significant bleeding at any time during the postbypass period should trigger repeat evaluation of standard laboratory tests (algorithm 1), and/or POC tests as noted below, to aid decision-making regarding which therapies will likely reverse coagulation abnormalities.

Although platelet transfusions are typically guided by platelet count, platelet function testing can be performed. Detecting a residual effect of P2Y12 inhibitors may be helpful in patients with mild-to-moderate microvascular bleeding. Preoperative platelet function testing for P2Y12 inhibition may be valuable and accurate, as any abnormality that was present preoperatively will persist during the postbypass period. In contrast, most platelet function testing performed following CPB is inaccurate due to dilutional changes and platelet activation [36]. In an actively bleeding patient, additional inaccuracy may result because test accuracy depends on a relatively normal platelet count. (See "Platelet function testing".)

POC tests of hemostatic function – In addition to standard laboratory coagulation tests, we employ POC viscoelastic coagulation tests such as thromboelastography (TEG), rotational thromboelastometry (ROTEM), or sonorheometry to guide transfusion therapy, if available, as recommended in professional society guidelines [6,19,37]. Use of viscoelastic testing is discussed in a separate topic. (See "Point-of-care hemostasis testing (viscoelastic tests)".)

RBC transfusions for anemia — We generally transfuse RBCs if hemoglobin is <7 to 8 g/dL (or HCT <21 to 24 percent) [7,8], similar to professional society practice guidelines for blood conservation during cardiac surgery (algorithm 1) [5-8,19,38,39].

However, we may target a higher hemoglobin in a patient with poorly controlled hemorrhage or signs of worsening myocardial or other organ ischemia. (See "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Cardiac surgery' and "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells' and "Massive blood transfusion" and "Overview of the acute management of non-ST-elevation acute coronary syndromes", section on 'Anemia'.)

When transfusion is necessary, available recovered blood is returned first, followed by reinfusion of blood harvested via normovolemic hemodilution, then transfusion of allogeneic RBCs [6,19]. (See "Surgical blood conservation: Intraoperative blood salvage" and "Anticoagulation and blood management strategies during cardiac surgery with cardiopulmonary bypass", section on 'Acute normovolemic hemodilution'.)

Bleeding necessitating transfusion occurs commonly after cardiac surgery with CPB, although transfusion rates vary widely among institutions, ranging from 10 to 90 percent [6,19,40]. In general, studies have noted that patients who received transfusions have worse outcomes than those who did not; however, this association does not necessarily reflect cause and effect [41,42]. (See "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Impact of anemia on morbidity and mortality'.)

Treatments to improve hemostasis

Platelet transfusions for bleeding with thrombocytopenia — Thrombocytopenia is common in the immediate postbypass period due to a combination of:

Hemodilution

Platelet loss (eg, due to persistent surgical bleeding, adherence to the CPB circuit surface, or consumption as coagulation occurs)

Accelerated clearance caused by thrombin-mediated platelet activation

Platelet transfusions are generally not used if there is thrombocytopenia without bleeding or bleeding without thrombocytopenia. Rather, transfusion is reserved for patients with clinically significant or ongoing microvascular bleeding who have a platelet count <100,000/microL (algorithm 1) or platelet dysfunction (eg, due to residual antiplatelet drug effect after administration of antiplatelet medication, particularly P2Y12 receptor inhibitors such as clopidogrel, prasugrel, or ticagrelor) [6,19].

In a large retrospective analysis of 119,132 cardiac surgical patients, of whom 93,759 received platelet transfusions, platelet transfusions were associated with improvements in some key outcomes (including survival) and worsening in others [43]:

Reduced operative mortality (odds ratio [OR] 0.63, 99% CI 0.47-0.84)

Reduced 90-day mortality (OR 0.66, 95% CI 0.51-0.85)

Reduced risk of sternal wound infection

Reduced risk of acute kidney injury (AKI)

Increased risk for:

Bleeding

Pneumonia

Intubation for >24 hours

Inotrope use for >4 hours

Readmission to the hospital within 30 days

Some of these outcomes may indicate an association between thrombocytopenia and other complications rather than an effect of platelet transfusion [43]. (See "Intraoperative transfusion and administration of clotting factors", section on 'Platelets' and "Early noncardiac complications of coronary artery bypass graft surgery", section on 'Antiplatelet agents'.)

Platelet transfusion is also included in massive transfusion protocols. (See "Massive blood transfusion", section on 'Component ratio (1:1:1)'.)

Rarely, thrombocytopenia occurs as a manifestation of other conditions requiring distinct interventions that are discussed in separate topic reviews. (See "Diagnostic approach to thrombocytopenia in adults", section on 'Postoperative or hospitalized'.)

These include:

Acute disseminated intravascular coagulation (DIC) – (See "Evaluation and management of disseminated intravascular coagulation (DIC) in adults", section on 'Acute DIC'.)

Heparin-induced thrombocytopenia (HIT) – (See "Management of heparin-induced thrombocytopenia (HIT) during cardiac or vascular surgery".)

Other drug-induced thrombocytopenias – (See "Drug-induced immune thrombocytopenia".)

Fibrinogen concentrate or Cryoprecipitate to treat hypofibrinogenemia — Fibrinogen is critical for normal hemostasis and can be depleted during CPB, with resulting hypofibrinogenemia. (See "Disorders of fibrinogen", section on 'Acquired abnormalities'.)

While administration of fibrinogen concentrate or Cryoprecipitate will not always resolve coagulopathic bleeding after CPB, we treat hypofibrinogenemia if fibrinogen concentration is <150 mg/dL in patients with clinically significant bleeding. This is usually done as a component of a multifactorial transfusion algorithm [24]. (See 'Use of transfusion algorithms' above.)

Indications – Congenital and acquired hypofibrinogenemias with bleeding are clear indications for administering a fibrinogen product. Other indications are discussed separately. (See "Disorders of fibrinogen".)

The European Association for Cardio-Thoracic Surgery and the European Association of Cardiothoracic Anaesthesiology recommend fibrinogen administration for patients with low fibrinogen levels and persistent microvascular bleeding [5]. However, these groups do not recommend prophylactic fibrinogen administration since available data do not support beneficial effects such as reduction of postoperative bleeding or transfusion risks. In non-bleeding patients, the efficacy of prophylactic fibrinogen concentrate has not been demonstrated, and administration is not recommended [44-47].

Choice of product – If available, we prefer fibrinogen concentrate over Cryoprecipitate or plasma to treat hypofibrinogenemia; this is because fibrinogen concentrate is not an allogeneic blood product and therefore has less risk of infection, alloimmunization, and transfusion reactions compared with Cryoprecipitate or plasma [5,6,19,44,48-54].

However, the choice of product depends on which product is stocked at the institution. (See "Intraoperative transfusion and administration of clotting factors", section on 'Cryoprecipitate or fibrinogen concentrate'.)

Fibrinogen concentrate is typically selected to treat hypofibrinogenemia in continental Europe and Canada due to its lower risk of infection and transfusion reactions. Cryoprecipitate is not typically available in these regions [44,45,49,55].

Cryoprecipitate is often used to treat hypofibrinogenemia in the United States and the United Kingdom because of its wider availability and lower cost in these regions compared with fibrinogen concentrate [48]. Dosing considerations for Cryoprecipitate are discussed separately. (See "Intraoperative transfusion and administration of clotting factors", section on 'Cryoprecipitate'.)

Of the two products, fibrinogen concentrate preparations are generally more expensive in the United States and the United Kingdom [56,57]. However, the overall cost of fibrinogen concentrate may be lower, as demonstrated in a cost-effectiveness analysis from the Canadian health care system in cardiac surgical patients with active bleeding and acquired hypofibrinogenemia [58]. The increasing use of fibrinogen concentrates as a source of fibrinogen in surgical patients is discussed in more detail separately. (See "Intraoperative transfusion and administration of clotting factors", section on 'Fibrinogen concentrate'.)

Fibrinogen concentrate does not contain von Willebrand factor (VWF), factor VIII, or factor XIII. Thus, it may not be ideal for all cardiac surgical patients with hypofibrinogenemia and coagulopathy due to acquired VWF or factor XIII deficiency, particularly after a prolonged duration of CPB [44,48]. (See "Anticoagulation and blood management strategies during cardiac surgery with cardiopulmonary bypass", section on 'Effects of cardiopulmonary bypass on hemostasis'.)

Dosing and administration

Fibrinogen concentrate The initial dose of fibrinogen concentrate is calculated to target a fibrinogen level to be >200 mg/dL. A dose of 70 mg/kg will typically increase the plasma fibrinogen concentration by approximately 100 mg/dL [59]. Details are explained in a separate topic. (See "Cryoprecipitate and fibrinogen concentrate", section on 'Fibrinogen concentrate (dosing and administration)' and "Cryoprecipitate and fibrinogen concentrate", section on 'Cryoprecipitate (dosing and administration)'.)

Cryoprecipitate The typical Cryoprecipitate dose, as received from the blood bank, is a pooled product that has been prepared by combining individual units derived from 5 to 10 blood donors in a volume of 50 to 200 mL (table 1). Ten units (or two 5-unit pools) will raise the fibrinogen by approximately 60 to 100 mg/dL in a 70 kg recipient. (See "Cryoprecipitate and fibrinogen concentrate", section on 'Fibrinogen concentrate (dosing and administration)' and "Cryoprecipitate and fibrinogen concentrate", section on 'Cryoprecipitate (dosing and administration)'.)

Supporting evidence – Randomized trials suggest that hemostatic efficacy is similar in adults or children undergoing cardiac surgery receiving fibrinogen concentrates or Cryoprecipitate [49,52,60].

The largest trial was the 2019 FIBRES (FIBrinogen REplenishment in Surgery) trial, which randomly assigned 735 individuals experiencing clinically significant bleeding and hypofibrinogenemia after CPB to receive fibrinogen concentrate (4 grams) or Cryoprecipitate (10 units) [49]. The need for transfusion of additional blood components (RBCs, platelets, and plasma) was similar in patients who received fibrinogen concentrate versus Cryoprecipitate. Serious adverse events were also similar between groups (32 percent for fibrinogen concentrate versus 35 percent for Cryoprecipitate). Rates of thromboembolism were 7 percent with fibrinogen concentrate and 9.6 percent with Cryoprecipitate (not statistically different).

Previous smaller trials comparing fibrinogen concentrate and Cryoprecipitate in cardiac surgical patients have noted similar results.

Prothrombin complex concentrate (PCC) or plasma for other clotting factor deficiencies

Indications – Clotting factor replacement is generally indicated in individuals who have active bleeding and increased clotting times (typically, with INR at least 1.5 times normal) that are not due to another cause such as an anticoagulant (algorithm 1) [7,61].

Before administering a clotting factor product, common causes of microvascular bleeding after CPB should be sought and treated (eg, surgical sources, thrombocytopenia, low fibrinogen, platelet dysfunction, DIC) [62,63]. (See "Intraoperative transfusion and administration of clotting factors", section on 'Use of a transfusion algorithm or protocol'.)

Clotting factor products are not used in the absence of significant bleeding and laboratory evidence of coagulopathy [19,38,61]. An exception is an individual with significant blood loss. Plasma is a component of massive transfusion protocols, usually in a 1:1:1 ratio with RBCs and platelets; together, these components replace massive blood loss [64]. (See "Intraoperative transfusion and administration of clotting factors", section on 'Plasma'.)

Choice of product – Clotting factors can be supplied using a PCC, which contains vitamin K-dependent clotting factors in concentrated form (factors II, IX, and X in 3-factor PCC and factors II, VII, IX, and X in 4-factor PCC) (table 2), or a plasma product.

Plasma products contain all clotting factors in unconcentrated form. Plasma products are an allogeneic blood product with associated risks. These products require ABO matching and thawing, which delays administration. The volume is 200 to 250 mL/unit. Several plasma products are available, including Fresh Frozen Plasma (FFP), PF24, and thawed plasma. These are generally considered interchangeable for hemostasis; differences among them are discussed separately (see "Clinical use of plasma components", section on 'Plasma products').

If available, we prefer an unactivated PCC product over plasma to treat coagulopathic bleeding after CPB. PCC products are not an allogeneic blood product and therefore have less risk of infection, alloimmunization, and transfusion reactions compared with plasma products. Furthermore, PCC products do not require thawing or ABO matching and contain minimal volume, thereby avoiding volume overload. However, PCC products are generally more expensive than plasma products.

4-factor unactivated PCC is approved for use in emergency surgery in patients receiving warfarin or another vitamin K antagonist. CPB is considered an off-label indication for PCC. (See "Management of warfarin-associated bleeding or supratherapeutic INR", section on 'Urgent surgery/procedure'.)

In contrast to unactivated PCC, the activated PCC product factor eight inhibitor bypassing activity (FEIBA) contains activated factor VII [62]; it may carry a greater thrombotic risk and is only used for life-threatening bleeding or other rare indications (table 2) [63,65]. (See "Intravenous plasma derivatives and recombinant DNA-produced coagulation factors", section on 'PCCs'.)

Supporting evidence – Intraoperative administration of unactivated 4-factor or 3-factor PCC products is effective for hemostasis for patients with intractable coagulopathy, diffuse bleeding, and elevated PT/INR after CPB [5,6,19,66,67].

PCC versus plasma – A 2025 trial that randomly assigned 538 patients with bleeding after CPB to receive an intraoperative 4-factor PCC (1500 units if ≤60 kg; 2000 units if >60 kg) or FFP (3 units if ≤60 kg; 4 units if >60 kg) reported better outcomes in the PCC group [66]. A modified intent-to-treat analysis was performed after 213 patients received PCC as randomized and 207 patients received FFP as randomized (N = 420). Effective hemostasis (defined as not needing any hemostatic intervention from 60 minutes to 24 hours after treatment) was achieved in 77.9 percent of patients receiving PCC compared with 60.4 percent of patients receiving FFP (difference, 17.6 percent; 95% CI 8.7-26.4 percent). Also, the PCC group received fewer transfusions (mean difference in the combined number of units of RBCs, platelets, and additional non-trial units of FFP within 24 hours was 7.2 units; 95% CI 5.4-9.0). Also, there were fewer serious adverse events overall (relative risk [RR] 0.76, 95% CI 0.61-0.96), and a lower risk of AKI (RR 0.55, 95% CI 0.34-0.89) in patients receiving PCC.

Previous smaller randomized trials and observational studies comparing PCC and plasma in cardiac surgical patients have noted a similar safety profile for PCC products compared with FFP groups, without a clear demonstration of hemostatic efficacy [67-72].

Dosing and administration – We use a goal-directed protocol or algorithm to assess specific abnormalities of coagulation, with data obtained from standard laboratory tests or POC viscoelastic tests such as TEG or ROTEM. PCCs are avoided in patients with an increased risk of thrombosis.

Dosing is titrated to reduce bleeding and improve coagulation studies.

PCCs – A typical starting dose of PCC is 1000 to 2000 units, or 12 to 28 units/kg, titrated to reduce bleeding. A 2025 randomized trial comparing PCC versus FFP used an initial PCC dose of approximately 25 units/kg [66]. The authors suggested that failure to show efficacy in previous trials may have been due to use of a lower initial PCC dose of 15 units/kg.

Repeat doses may be administered. However, risk for thromboembolic events may be more likely with repeat or excessive dosing of PCCs, and this risk may extend well into the postoperative period [73,74]. A study of thrombin generation in patients who received 4-factor PCC (15 units/kg) or plasma (10 to 15 mL/kg) to treat coagulopathy after CPB noted that restoration of thrombin generation was better and faster in the PCC group, without overshooting into a prothrombotic range [75]. This suggests that 15 units/kg might be sufficient for the hemostatic efficacy of 4-factor PCC, with redosing if necessary, although clinical endpoints are needed for confirmation. (See "Intraoperative transfusion and administration of clotting factors".)

Plasma – A typical starting dose of plasma is 2 units, titrated to reduce bleeding. (See "Intraoperative transfusion and administration of clotting factors", section on 'Plasma'.)

Typically, the INR is monitored, and an INR <1.5 is targeted. The goal is not to lower the INR to 1.0, because the INR of normal plasma can be as high as 1.2 to 1.3. Plasma administration is also limited by the volume load and the patient's cardiovascular status. (See "Clinical use of plasma components", section on 'Settings in which plasma is not appropriate'.)

Other hemostatic agents for bleeding post-bypass — Other products may be used to treat excessive bleeding in selected patients during the post-bypass period.

Antifibrinolytic agents — A prophylactic antifibrinolytic agent (eg, epsilon-aminocaproic acid [EACA] or tranexamic acid [TXA]) is usually initiated in the prebypass period.

The timing to discontinue EACA or TXA varies among institutions.

If active bleeding necessitating transfusion persists, we typically continue administering the antifibrinolytic agent throughout the post-bypass period for several hours or until bleeding ceases. (See "Intraoperative use of antifibrinolytic agents", section on 'Timing of administration'.)

In the absence of bleeding, continuing postoperative prophylactic infusion of an antifibrinolytic agent is not indicated and may cause adverse effects such as seizures. (See "Intraoperative use of antifibrinolytic agents", section on 'Seizures'.)

TXA may accumulate in patients with reduced kidney function.

Desmopressin

Indications – Routine use of desmopressin (DDAVP) in cardiac surgical patients is not warranted [5,19,23].

In selected patients with acquired platelet dysfunction due to uremia or acquired von Willebrand syndrome (AVWS; eg, due to chronic aortic stenosis or a left ventricular assist device), we administer DDAVP in the postbypass period, but only if persistent microvascular bleeding is evident [5,6,19,76-79]. Additional information about treating uremic platelet dysfunction and AVWS is presented separately. (See "Uremic platelet dysfunction", section on 'Treatment of bleeding'.)

Some clinicians administer DDAVP to reduce blood loss in cardiac surgical patients with intractable microvascular bleeding due to platelet dysfunction suspected to be caused by hypothermia, acidosis, aspirin use, and/or the effects of CPB.

Dosing – A typical dose is 0.3 mcg/kg administered intravenously. DDAVP should be infused slowly over 15 to 30 minutes to avoid vasodilation. Tachyphylaxis occurs after the initial dose and during the initial three to five days of administration. (See "Uremic platelet dysfunction", section on 'Details of DDAVP administration'.)

Adverse effects – Possible adverse side effects of DDAVP include hypertension, hypotension, flushing, fluid overload (unlikely to be relevant in patients undergoing CPB), hyponatremia (which may cause seizures if close attention to free water restriction is not used), and rare thrombotic events (table 3).

Supporting evidence – Data suggesting the benefit of DDAVP in cardiac surgical patients with intractable microvascular bleeding are very limited [19,80-83] and inconsistent [84,85].

Two 2017 meta-analyses of the efficacy of DDAVP in patients undergoing cardiac or noncardiac surgery noted only small reductions in perioperative blood loss and volume of RBC transfusions compared with placebo, with quality of evidence rated as low [82,83].

Recombinant activated factor VII — Recombinant activated factor VII (rFVIIa) is licensed for selected indications and is occasionally used off-label to treat intractable bleeding.

Indications – In rare instances of severe, intractable, life-threatening coagulopathic bleeding after CPB, off-label administration of rFVIIa has been used in attempts to stop bleeding and reduce transfusion requirements [6,19,86-89]. However, high thromboembolism rates >20 percent (including myocardial infarction) with mortality >30 percent have been described in retrospective evaluations of registries for refractory bleeding in cardiac surgery [90,91]. (See "Recombinant factor VIIa: Administration and adverse effects", section on 'Off-label uses' and "Intraoperative transfusion and administration of clotting factors", section on 'Recombinant activated factor VII (rFVIIa)'.)

Failure to treat the primary reason for bleeding increases the likelihood of an inadequate response to the initial dose of rFVIIa [90-92]; this may also result in the use of higher doses that are more likely to cause thrombosis [93,94]. (See "Recombinant factor VIIa: Administration and adverse effects", section on 'General approach to administration'.)

Dosing – Optimal dosing and timing of rFVIIa are unknown for intractable bleeding after CPB. We employ a cautious dosing strategy in the rare instances that rFVIIa is administered, such as giving small incremental doses of 10 mcg/kg or 1 mg vials, approximately every 15 minutes, targeting hemostatic efficacy. This dose is far less than the 90 to 120 mcg/kg used in hemophilia.

One study in cardiac surgical patients reported cessation of bleeding after administration of incremental aliquots of rFVIIa at a median dose of 13.3 mcg/kg [86].

A randomized trial reported that smaller total doses were necessary if rFVIIa was administered earlier in the postbypass period when no more than one RBC unit had been transfused (required dose, 12.2 mcg/kg [range, 9.7 to 16.4 mcg/kg]), while higher doses were necessary if five or more RBC units had been transfused (required dose, 18.0 mcg/kg [range, 11.8 to 29.0 mcg/kg]) [87].

Adverse effects – Thromboembolic complications are more likely with dose escalation, or in the presence of stagnant flow, or the presence of devices such as extracorporeal membrane oxygenation (ECMO) [19].

EARLY POSTOPERATIVE MANAGEMENT

Management of bleeding and coagulopathy — Close monitoring for bleeding continues in the postoperative period. Return to the operating room for mediastinal re-exploration and intervention may be necessary based on the rate and presumed location of bleeding, as well as the surgeon's assessment of the potential for a surgical cause [95,96].

Excessive bleeding requiring mediastinal re-exploration has been associated with adverse outcomes that include death, need for mechanical circulatory support, stroke, acute kidney injury, sternal wound infection, and prolonged mechanical ventilation [97,98].

Fastidious surgical hemostasis is the most important measure to prevent postoperative blood transfusions and surgical re-exploration. (See 'Fastidious surgical hemostasis' above.)

We repeat standard laboratory tests of coagulation and viscoelastic testing, as well as hemoglobin measurements, to guide transfusion decisions until bleeding slows [5,25,35,39,73,99]. (See "Postoperative care after cardiac surgery", section on 'Hemostasis'.)

Management of anemia — Postoperative anemia is common due to exacerbation of preexisting anemia, blood loss during surgery, and excessive postoperative phlebotomies [61,100]. (See "Diagnostic approach to anemia in adults", section on 'Iatrogenic (hospitalized patients)'.)

Similar to the intraoperative period, we use a hemoglobin threshold of <7 to 8 g/dL to transfuse red blood cells (RBCs) but may target a higher hemoglobin in a patient with poorly controlled hemorrhage or signs of worsening myocardial or other organ ischemia. As an alternative, one randomized trial reported the use of central venous oxygen saturation (SvO2) measurements ≤65 percent as the trigger for RBC administration [101]. Transfusion of fewer RBC units was reported with this target, compared with use of a fixed hemoglobin target of 9 g/dL (odds ratio [OR] 0.03, 95% CI 0-0.15). (See 'RBC transfusions for anemia' above.)

Iron deficiency is very common after cardiac surgery with CPB. Management is summarized in the algorithm and discussed separately (algorithm 2). (See "Perioperative blood management: Strategies to minimize transfusions", section on 'Management of postoperative anemia'.)

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Transfusion and patient blood management" and "Society guideline links: Management of cardiopulmonary bypass".)

SUMMARY AND RECOMMENDATIONS

Stopping anticoagulation

Reversal of heparin with protamine Systemic heparin anticoagulation is reversed with protamine, as discussed separately. (See "Protamine reversal of heparin anticoagulation after cardiopulmonary bypass", section on 'Protamine administration after cardiopulmonary bypass'.)

Discontinuation of bivalirudin Bivalirudin is rarely used; its anticoagulant effects typically resolve within two hours following discontinuation in individuals with normal kidney function. More rapid offset of action may be achieved with therapies that reduce circulating blood levels (hemodilution, plasmapheresis with plasma exchange, dialysis). (See 'Management of bivalirudin anticoagulation' above.)

Management of intraoperative bleeding

Surgical hemostasis The primary means to achieve hemostasis is meticulous surgical technique. (See 'Fastidious surgical hemostasis' above.)

Normothermia Active warming techniques to achieve and maintain normothermia are employed as necessary. (See 'Maintenance of normothermia' above.)

Transfusion algorithm We use a goal-directed protocol or algorithm to guide transfusion decisions, based on measurement of hemoglobin or hematocrit (HCT), assessment of specific abnormalities of hemostasis using standard laboratory tests of hemostatic function (algorithm 1), and point-of-care viscoelastic tests of coagulation if available (eg, thromboelastography [TEG], rotational thromboelastometry [ROTEM], sonorheometry). (See 'Use of transfusion algorithms' above.)

Transfusion decisions for individual blood components include (table 1):

-Red blood cells (RBCs) for anemia – We typically transfuse RBCs for hemoglobin <7 to 8 g/dL (or HCT <21 to 24 percent), as discussed separately. (See "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Cardiac surgery' and "Intraoperative transfusion and administration of clotting factors", section on 'Red blood cells' and 'RBC transfusions for anemia' above.)

Available recovered blood is returned first, followed by reinfusion of blood harvested via normovolemic hemodilution, followed by transfusion of allogeneic RBCs.

-Platelets for thrombocytopenia – Platelet transfusions are reserved for patients with clinically significant and ongoing bleeding and platelet count <100,000/microL or those with platelet dysfunction (eg, due to residual anti-platelet drug effects). (See 'Platelet transfusions for bleeding with thrombocytopenia' above.)

-Fibrinogen concentrate or Cryoprecipitate for hypofibrinogenemia – For patients with hypofibrinogenemia (fibrinogen <150 mg/dL) and intractable diffuse bleeding, we suggest fibrinogen concentrate, if available, rather than Cryoprecipitate (Grade 2C). (See 'Fibrinogen concentrate or Cryoprecipitate to treat hypofibrinogenemia' above.)

Fibrinogen concentrate is not a blood product and has lower risks of infection and transfusion reactions compared with Cryoprecipitate; it is used in continental Europe and Canada. In the United States and the United Kingdom, Cryoprecipitate is often used because of its wider availability and lower cost.

-Prothrombin complex concentrate (PCC) or plasma for other clotting factor deficiencies – For most patients with intractable diffuse bleeding associated with a prolonged prothrombin time/international normalized ratio (PT/INR; eg, >1.5), we suggest an unactivated PCC product (table 2), if available, rather than plasma (Grade 2B). (See 'Prothrombin complex concentrate (PCC) or plasma for other clotting factor deficiencies' above.)

PCC is a plasma derivative and has lower risks of infection and transfusion reactions than plasma products. However, plasma may be preferred for patients who require significant volume replacement or for those with increased risk for thrombosis.

Other hemostatic agents

-Antifibrinolytic agents If active bleeding necessitating transfusion persists, we typically continue the antifibrinolytic agent throughout the post-bypass period and into the postoperative period. (See 'Antifibrinolytic agents' above.)

-Desmopressin (DDAVP) – DDAVP can be administered to selected patients with persistent microvascular bleeding and acquired platelet dysfunction due to uremia or acquired von Willebrand disease; the table summarizes dosing (table 3). (See 'Desmopressin' above.)

-Recombinant activated factor VII (rFVIIa) – In rare instances of severe intractable life-threatening coagulopathic bleeding after CPB, off-label administration of rFVIIa has been used. (See 'Recombinant activated factor VII' above.)

Postoperative management

Management of postoperative bleeding – Close monitoring for bleeding continues in the postoperative period. Return to the operating room for surgical re-exploration is occasionally necessary based on the rate and presumed location of bleeding, as well as the surgeon's assessment of the potential for a surgical cause of bleeding. (See 'Management of bleeding and coagulopathy' above.)

Management of postoperative anemia Transfusions are given if needed (algorithm 2). Iron deficiency is common, and iron replacement is provided. (See 'Management of anemia' above and "Perioperative blood management: Strategies to minimize transfusions", section on 'Management of postoperative anemia'.)

  1. Shore-Lesserson L, Baker RA, Ferraris VA, et al. The Society of Thoracic Surgeons, The Society of Cardiovascular Anesthesiologists, and The American Society of ExtraCorporeal Technology: Clinical Practice Guidelines-Anticoagulation During Cardiopulmonary Bypass. Ann Thorac Surg 2018; 105:650.
  2. Erdoes G, Faraoni D, Koster A, et al. Perioperative Considerations in Management of the Severely Bleeding Coagulopathic Patient. Anesthesiology 2023; 138:535.
  3. Sniecinski RM, Chandler WL. Activation of the hemostatic system during cardiopulmonary bypass. Anesth Analg 2011; 113:1319.
  4. Despotis GJ, Avidan MS, Hogue CW Jr. Mechanisms and attenuation of hemostatic activation during extracorporeal circulation. Ann Thorac Surg 2001; 72:S1821.
  5. Casselman FPA, Lance MD, Ahmed A, et al. 2024 EACTS/EACTAIC Guidelines on patient blood management in adult cardiac surgery in collaboration with EBCP. Eur J Cardiothorac Surg 2025; 67.
  6. Tibi P, McClure RS, Huang J, et al. STS/SCA/AmSECT/SABM Update to the Clinical Practice Guidelines on Patient Blood Management. Ann Thorac Surg 2021; 112:981.
  7. Society of Thoracic Surgeons Blood Conservation Guideline Task Force, Ferraris VA, Brown JR, et al. 2011 update to the Society of Thoracic Surgeons and the Society of Cardiovascular Anesthesiologists blood conservation clinical practice guidelines. Ann Thorac Surg 2011; 91:944.
  8. Society of Thoracic Surgeons Blood Conservation Guideline Task Force, Ferraris VA, Ferraris SP, et al. Perioperative blood transfusion and blood conservation in cardiac surgery: the Society of Thoracic Surgeons and The Society of Cardiovascular Anesthesiologists clinical practice guideline. Ann Thorac Surg 2007; 83:S27.
  9. Dhir A, Tempe DK. Anemia and Patient Blood Management in Cardiac Surgery-Literature Review and Current Evidence. J Cardiothorac Vasc Anesth 2018; 32:2726.
  10. Pleym H, Wahba A, Videm V, et al. Increased fibrinolysis and platelet activation in elderly patients undergoing coronary bypass surgery. Anesth Analg 2006; 102:660.
  11. Douketis JD, Spyropoulos AC, Murad MH, et al. Executive Summary: Perioperative Management of Antithrombotic Therapy: An American College of Chest Physicians Clinical Practice Guideline. Chest 2022; 162:1127.
  12. Biancari F, Kinnunen EM, Kiviniemi T, et al. Meta-analysis of the Sources of Bleeding after Adult Cardiac Surgery. J Cardiothorac Vasc Anesth 2018; 32:1618.
  13. Martini WZ. Coagulopathy by hypothermia and acidosis: mechanisms of thrombin generation and fibrinogen availability. J Trauma 2009; 67:202.
  14. Wolberg AS, Meng ZH, Monroe DM 3rd, Hoffman M. A systematic evaluation of the effect of temperature on coagulation enzyme activity and platelet function. J Trauma 2004; 56:1221.
  15. Valeri CR, Khabbaz K, Khuri SF, et al. Effect of skin temperature on platelet function in patients undergoing extracorporeal bypass. J Thorac Cardiovasc Surg 1992; 104:108.
  16. Rajagopalan S, Mascha E, Na J, Sessler DI. The effects of mild perioperative hypothermia on blood loss and transfusion requirement. Anesthesiology 2008; 108:71.
  17. Reed RL 2nd, Johnson TD, Hudson JD, Fischer RP. The disparity between hypothermic coagulopathy and clotting studies. J Trauma 1992; 33:465.
  18. Lester ELW, Fox EE, Holcomb JB, et al. The impact of hypothermia on outcomes in massively transfused patients. J Trauma Acute Care Surg 2019; 86:458.
  19. Raphael J, Mazer CD, Subramani S, et al. Society of Cardiovascular Anesthesiologists Clinical Practice Improvement Advisory for Management of Perioperative Bleeding and Hemostasis in Cardiac Surgery Patients. Anesth Analg 2019; 129:1209.
  20. Mueller MM, Van Remoortel H, Meybohm P, et al. Patient Blood Management: Recommendations From the 2018 Frankfurt Consensus Conference. JAMA 2019; 321:983.
  21. Curry NS, Davenport R, Pavord S, et al. The use of viscoelastic haemostatic assays in the management of major bleeding: A British Society for Haematology Guideline. Br J Haematol 2018; 182:789.
  22. Kozek-Langenecker SA, Ahmed AB, Afshari A, et al. Management of severe perioperative bleeding: guidelines from the European Society of Anaesthesiology: First update 2016. Eur J Anaesthesiol 2017; 34:332.
  23. American Society of Anesthesiologists Task Force on Perioperative Blood Management. Practice guidelines for perioperative blood management: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Blood Management*. Anesthesiology 2015; 122:241.
  24. Ghadimi K, Levy JH, Welsby IJ. Perioperative management of the bleeding patient. Br J Anaesth 2016; 117:iii18.
  25. Karkouti K, Callum J, Wijeysundera DN, et al. Point-of-Care Hemostatic Testing in Cardiac Surgery: A Stepped-Wedge Clustered Randomized Controlled Trial. Circulation 2016; 134:1152.
  26. Weber CF, Görlinger K, Meininger D, et al. Point-of-care testing: a prospective, randomized clinical trial of efficacy in coagulopathic cardiac surgery patients. Anesthesiology 2012; 117:531.
  27. Avidan MS, Alcock EL, Da Fonseca J, et al. Comparison of structured use of routine laboratory tests or near-patient assessment with clinical judgement in the management of bleeding after cardiac surgery. Br J Anaesth 2004; 92:178.
  28. Spalding GJ, Hartrumpf M, Sierig T, et al. Cost reduction of perioperative coagulation management in cardiac surgery: value of "bedside" thrombelastography (ROTEM). Eur J Cardiothorac Surg 2007; 31:1052.
  29. Girdauskas E, Kempfert J, Kuntze T, et al. Thromboelastometrically guided transfusion protocol during aortic surgery with circulatory arrest: a prospective, randomized trial. J Thorac Cardiovasc Surg 2010; 140:1117.
  30. Hanke AA, Herold U, Dirkmann D, et al. Thromboelastometry Based Early Goal-Directed Coagulation Management Reduces Blood Transfusion Requirements, Adverse Events, and Costs in Acute Type A Aortic Dissection: A Pilot Study. Transfus Med Hemother 2012; 39:121.
  31. Karkouti K, McCluskey SA, Callum J, et al. Evaluation of a novel transfusion algorithm employing point-of-care coagulation assays in cardiac surgery: a retrospective cohort study with interrupted time-series analysis. Anesthesiology 2015; 122:560.
  32. Görlinger K, Fries D, Dirkmann D, et al. Reduction of Fresh Frozen Plasma Requirements by Perioperative Point-of-Care Coagulation Management with Early Calculated Goal-Directed Therapy. Transfus Med Hemother 2012; 39:104.
  33. Fabbro M 2nd, Winkler AM, Levy JH. Technology: Is There Sufficient Evidence to Change Practice in Point-of-Care Management of Coagulopathy? J Cardiothorac Vasc Anesth 2017; 31:1849.
  34. Kuiper GJAJM, van Egmond LT, Henskens YMC, et al. Shifts of Transfusion Demand in Cardiac Surgery After Implementation of Rotational Thromboelastometry-Guided Transfusion Protocols: Analysis of the HEROES-CS (HEmostasis Registry of patiEntS in Cardiac Surgery) Observational, Prospective Open Cohort Database. J Cardiothorac Vasc Anesth 2019; 33:307.
  35. Irving AH, Harris A, Petrie D, et al. Impact of patient blood management guidelines on blood transfusions and patient outcomes during cardiac surgery. J Thorac Cardiovasc Surg 2020; 160:437.
  36. Le Quellec S, Bordet JC, Negrier C, Dargaud Y. Comparison of current platelet functional tests for the assessment of aspirin and clopidogrel response. A review of the literature. Thromb Haemost 2016; 116:638.
  37. Demailly Z, Wurtz V, Barbay V, et al. Point-of-Care Viscoelastic Hemostatic Assays in Cardiac Surgery Patients: Comparison of Thromboelastography 6S, Thromboelastometry Sigma, and Quantra. J Cardiothorac Vasc Anesth 2023; 37:948.
  38. Wahba A, Milojevic M, Boer C, et al. 2019 EACTS/EACTA/EBCP guidelines on cardiopulmonary bypass in adult cardiac surgery. Eur J Cardiothorac Surg 2020; 57:210.
  39. Raphael J, Mazer CD, Subramani S, et al. Society of Cardiovascular Anesthesiologists Clinical Practice Improvement Advisory for Management of Perioperative Bleeding and Hemostasis in Cardiac Surgery Patients. J Cardiothorac Vasc Anesth 2019; 33:2887.
  40. Bennett-Guerrero E, Zhao Y, O'Brien SM, et al. Variation in use of blood transfusion in coronary artery bypass graft surgery. JAMA 2010; 304:1568.
  41. Hajjar LA, Vincent JL, Galas FR, et al. Transfusion requirements after cardiac surgery: The TRACS randomized controlled trial. JAMA 2010; 304:1559.
  42. Transfusion of Red Blood Cells, Fresh Frozen Plasma, or Platelets Is Associated With Mortality and Infection After Cardiac Surgery in a Dose-Dependent Manner. Anesth Analg 2020; 130:e32.
  43. Fletcher CM, Hinton JV, Xing Z, et al. Platelet Transfusion in Cardiac Surgery: An Entropy-Balanced, Weighted, Multicenter Analysis. Anesth Analg 2024; 138:542.
  44. Erdoes G, Koster A, Meesters MI, et al. The role of fibrinogen and fibrinogen concentrate in cardiac surgery: an international consensus statement from the Haemostasis and Transfusion Scientific Subcommittee of the European Association of Cardiothoracic Anaesthesiology. Anaesthesia 2019; 74:1589.
  45. Kozek-Langenecker SA, Afshari A, Albaladejo P, et al. Management of severe perioperative bleeding: guidelines from the European Society of Anaesthesiology. Eur J Anaesthesiol 2013; 30:270.
  46. Bilecen S, de Groot JA, Kalkman CJ, et al. Effect of Fibrinogen Concentrate on Intraoperative Blood Loss Among Patients With Intraoperative Bleeding During High-Risk Cardiac Surgery: A Randomized Clinical Trial. JAMA 2017; 317:738.
  47. Rahe-Meyer N, Levy JH, Mazer CD, et al. Randomized evaluation of fibrinogen vs placebo in complex cardiovascular surgery (REPLACE): a double-blind phase III study of haemostatic therapy. Br J Anaesth 2016; 117:41.
  48. Hensley NB, Mazzeffi MA. Pro-Con Debate: Fibrinogen Concentrate or Cryoprecipitate for Treatment of Acquired Hypofibrinogenemia in Cardiac Surgical Patients. Anesth Analg 2021; 133:19.
  49. Callum J, Farkouh ME, Scales DC, et al. Effect of Fibrinogen Concentrate vs Cryoprecipitate on Blood Component Transfusion After Cardiac Surgery: The FIBRES Randomized Clinical Trial. JAMA 2019; 322:1966.
  50. Ranucci M, Baryshnikova E, Crapelli GB, et al. Randomized, double-blinded, placebo-controlled trial of fibrinogen concentrate supplementation after complex cardiac surgery. J Am Heart Assoc 2015; 4:e002066.
  51. Ghadimi K, Welsby IJ. Pro: Factor Concentrates are Essential for Hemostasis in Complex Cardiac Surgery. J Cardiothorac Vasc Anesth 2018; 32:558.
  52. Rahe-Meyer N, Solomon C, Hanke A, et al. Effects of fibrinogen concentrate as first-line therapy during major aortic replacement surgery: a randomized, placebo-controlled trial. Anesthesiology 2013; 118:40.
  53. Maeda T, Miyata S, Usui A, et al. Safety of Fibrinogen Concentrate and Cryoprecipitate in Cardiovascular Surgery: Multicenter Database Study. J Cardiothorac Vasc Anesth 2019; 33:321.
  54. Li JY, Gong J, Zhu F, et al. Fibrinogen Concentrate in Cardiovascular Surgery: A Meta-analysis of Randomized Controlled Trials. Anesth Analg 2018; 127:612.
  55. Levy JH, Goodnough LT. How I use fibrinogen replacement therapy in acquired bleeding. Blood 2015; 125:1387.
  56. Novak A, Stanworth SJ, Curry N. Do we still need cryoprecipitate? Cryoprecipitate and fibrinogen concentrate as treatments for major hemorrhage - how do they compare? Expert Rev Hematol 2018; 11:351.
  57. Cushing MM, Haas T, Karkouti K, Callum J. Which is the preferred blood product for fibrinogen replacement in the bleeding patient with acquired hypofibrinogenemia-cryoprecipitate or fibrinogen concentrate? Transfusion 2020; 60 Suppl 3:S17.
  58. Abrahamyan L, Tomlinson G, Callum J, et al. Cost-effectiveness of Fibrinogen Concentrate vs Cryoprecipitate for Treating Acquired Hypofibrinogenemia in Bleeding Adult Cardiac Surgical Patients. JAMA Surg 2023; 158:245.
  59. Hanna JM, Keenan JE, Wang H, et al. Use of human fibrinogen concentrate during proximal aortic reconstruction with deep hypothermic circulatory arrest. J Thorac Cardiovasc Surg 2016; 151:376.
  60. Galas FR, de Almeida JP, Fukushima JT, et al. Hemostatic effects of fibrinogen concentrate compared with cryoprecipitate in children after cardiac surgery: a randomized pilot trial. J Thorac Cardiovasc Surg 2014; 148:1647.
  61. Burns CD, Brown JP, Corwin HL, et al. Special Report From the Society for the Advancement of Blood Management: The Choosing Wisely Campaign. Anesth Analg 2019; 129:1381.
  62. Ghadimi K, Levy JH, Welsby IJ. Prothrombin Complex Concentrates for Bleeding in the Perioperative Setting. Anesth Analg 2016; 122:1287.
  63. Song HK, Tibayan FA, Kahl EA, et al. Safety and efficacy of prothrombin complex concentrates for the treatment of coagulopathy after cardiac surgery. J Thorac Cardiovasc Surg 2014; 147:1036.
  64. Delaney M, Stark PC, Suh M, et al. Massive Transfusion in Cardiac Surgery: The Impact of Blood Component Ratios on Clinical Outcomes and Survival. Anesth Analg 2017; 124:1777.
  65. Rota M, Cortesi PA, Crea R, et al. Thromboembolic event rate in patients exposed to anti-inhibitor coagulant complex: a meta-analysis of 40-year published data. Blood Adv 2017; 1:2637.
  66. Karkouti K, Callum JL, Bartoszko J, et al. Prothrombin Complex Concentrate vs Frozen Plasma for Coagulopathic Bleeding in Cardiac Surgery: The FARES-II Multicenter Randomized Clinical Trial. JAMA 2025; 333:1781.
  67. Smith MM, Schroeder DR, Nelson JA, et al. Prothrombin Complex Concentrate vs Plasma for Post-Cardiopulmonary Bypass Coagulopathy and Bleeding: A Randomized Clinical Trial. JAMA Surg 2022; 157:757.
  68. Karkouti K, Bartoszko J, Grewal D, et al. Comparison of 4-Factor Prothrombin Complex Concentrate With Frozen Plasma for Management of Hemorrhage During and After Cardiac Surgery: A Randomized Pilot Trial. JAMA Netw Open 2021; 4:e213936.
  69. Roman M, Biancari F, Ahmed AB, et al. Prothrombin Complex Concentrate in Cardiac Surgery: A Systematic Review and Meta-Analysis. Ann Thorac Surg 2019; 107:1275.
  70. Fitzgerald J, Lenihan M, Callum J, et al. Use of prothrombin complex concentrate for management of coagulopathy after cardiac surgery: a propensity score matched comparison to plasma. Br J Anaesth 2018; 120:928.
  71. Arnékian V, Camous J, Fattal S, et al. Use of prothrombin complex concentrate for excessive bleeding after cardiac surgery. Interact Cardiovasc Thorac Surg 2012; 15:382.
  72. Nemeth E, Varga T, Soltesz A, et al. Perioperative Factor Concentrate Use is Associated With More Beneficial Outcomes and Reduced Complication Rates Compared With a Pure Blood Product-Based Strategy in Patients Undergoing Elective Cardiac Surgery: A Propensity Score-Matched Cohort Study. J Cardiothorac Vasc Anesth 2022; 36:138.
  73. Hashmi NK, Ghadimi K, Srinivasan AJ, et al. Three-factor prothrombin complex concentrates for refractory bleeding after cardiovascular surgery within an algorithmic approach to haemostasis. Vox Sang 2019; 114:374.
  74. Franchini M, Lippi G. Prothrombin complex concentrates: an update. Blood Transfus 2010; 8:149.
  75. Welsby IJ, Schroeder DR, Ghadimi K, et al. Thrombin generation after prothrombin complex concentrate or plasma transfusion during cardiac surgery. J Thromb Thrombolysis 2025; 58:309.
  76. Tiede A, Rand JH, Budde U, et al. How I treat the acquired von Willebrand syndrome. Blood 2011; 117:6777.
  77. Sadler JE. Aortic stenosis, von Willebrand factor, and bleeding. N Engl J Med 2003; 349:323.
  78. Vincentelli A, Susen S, Le Tourneau T, et al. Acquired von Willebrand syndrome in aortic stenosis. N Engl J Med 2003; 349:343.
  79. Steinlechner B, Zeidler P, Base E, et al. Patients with severe aortic valve stenosis and impaired platelet function benefit from preoperative desmopressin infusion. Ann Thorac Surg 2011; 91:1420.
  80. Hanke AA, Dellweg C, Kienbaum P, et al. Effects of desmopressin on platelet function under conditions of hypothermia and acidosis: an in vitro study using multiple electrode aggregometry*. Anaesthesia 2010; 65:688.
  81. Ying CL, Tsang SF, Ng KF. The potential use of desmopressin to correct hypothermia-induced impairment of primary haemostasis--an in vitro study using PFA-100. Resuscitation 2008; 76:129.
  82. Desborough MJ, Oakland K, Brierley C, et al. Desmopressin use for minimising perioperative blood transfusion. Cochrane Database Syst Rev 2017; 7:CD001884.
  83. Desborough MJ, Oakland KA, Landoni G, et al. Desmopressin for treatment of platelet dysfunction and reversal of antiplatelet agents: a systematic review and meta-analysis of randomized controlled trials. J Thromb Haemost 2017; 15:263.
  84. de Prost D, Barbier-Boehm G, Hazebroucq J, et al. Desmopressin has no beneficial effect on excessive postoperative bleeding or blood product requirements associated with cardiopulmonary bypass. Thromb Haemost 1992; 68:106.
  85. Orlov D, McCluskey SA, Callum J, et al. Utilization and Effectiveness of Desmopressin Acetate After Cardiac Surgery Supplemented With Point-of-Care Hemostatic Testing: A Propensity-Score-Matched Analysis. J Cardiothorac Vasc Anesth 2017; 31:883.
  86. Baral P, Cotter E, Gao G, et al. Characteristics Associated With Mortality in 372 Patients Receiving Low-Dose Recombinant Factor VIIa (rFVIIa) for Cardiac Surgical Bleeding. J Cardiothorac Vasc Anesth 2019; 33:2133.
  87. Sutherland L, Houchin A, Wang T, et al. Impact of Early, Low-Dose Factor VIIa on Subsequent Transfusions and Length of Stay in Cardiac Surgery. J Cardiothorac Vasc Anesth 2022; 36:147.
  88. Hessel EA 2nd. What's New in Cardiopulmonary Bypass. J Cardiothorac Vasc Anesth 2019; 33:2296.
  89. Flynn BC, Steiner ME, Mazzeffi M. Off-label Use of Recombinant Activated Factor VII for Cardiac Surgical Bleeding. Anesthesiology 2023; 139:197.
  90. Karkouti K, Beattie WS, Arellano R, et al. Comprehensive Canadian review of the off-label use of recombinant activated factor VII in cardiac surgery. Circulation 2008; 118:331.
  91. Lee AI, Campigotto F, Rawn JD, et al. Clinical significance of coagulation studies in predicting response to activated recombinant Factor VII in cardiac surgery patients. Br J Haematol 2012; 157:397.
  92. Andersen ND, Bhattacharya SD, Williams JB, et al. Intraoperative use of low-dose recombinant activated factor VII during thoracic aortic operations. Ann Thorac Surg 2012; 93:1921.
  93. Levi M, Levy JH, Andersen HF, Truloff D. Safety of recombinant activated factor VII in randomized clinical trials. N Engl J Med 2010; 363:1791.
  94. Gill R, Herbertson M, Vuylsteke A, et al. Safety and efficacy of recombinant activated factor VII: a randomized placebo-controlled trial in the setting of bleeding after cardiac surgery. Circulation 2009; 120:21.
  95. Shander A, Javidroozi M, Perelman S, et al. From bloodless surgery to patient blood management. Mt Sinai J Med 2012; 79:56.
  96. Muñoz M, Acheson AG, Bisbe E, et al. An international consensus statement on the management of postoperative anaemia after major surgical procedures. Anaesthesia 2018; 73:1418.
  97. Biancari F, Mikkola R, Heikkinen J, et al. Estimating the risk of complications related to re-exploration for bleeding after adult cardiac surgery: a systematic review and meta-analysis. Eur J Cardiothorac Surg 2012; 41:50.
  98. Knapik P, Cieśla D, Saucha W, et al. Outcome Prediction After Coronary Surgery and Redo Surgery for Bleeding (From the KROK Registry). J Cardiothorac Vasc Anesth 2019; 33:2930.
  99. Ali JM, Gerrard C, Clayton J, Moorjani N. Reduced re-exploration and blood product transfusion after the introduction of the Papworth haemostasis checklist†. Eur J Cardiothorac Surg 2019; 55:729.
  100. Matzek LJ, LeMahieu AM, Madde NR, et al. A Contemporary Analysis of Phlebotomy and Iatrogenic Anemia Development Throughout Hospitalization in Critically Ill Adults. Anesth Analg 2022; 135:501.
  101. Zeroual N, Blin C, Saour M, et al. Restrictive Transfusion Strategy after Cardiac Surgery. Anesthesiology 2021; 134:370.
Topic 122792 Version 27.0

References

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