Bleeding, Hemostasis, and Transfusion Medicine

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Chapter 30 Bleeding, Hemostasis, and Transfusion Medicine

The major components of the hemostatic system are the vasculature, platelets, and coagulation proteins. Deficiencies or abnormalities in any of these components can lead to coagulopathy and pathologic bleeding. Almost every imaginable quantitative and qualitative abnormality of the hemostatic system has been described following cardiac surgery, and managing postoperative bleeding remains one of the greatest challenges in caring for patients after cardiac surgery.

In this chapter, issues relating to bleeding and hemostasis in cardiac surgery patients are reviewed. Routine management of postoperative bleeding, including a protocol for blood component therapy, is outlined in Chapter 17.


Normal Hemostasis

The vascular endothelium is a nonthrombogenic surface that secretes prostacyclin, tissue plasminogen activator, heparin sulfate, antithrombin III, protein C, and nitric oxide to inhibit platelet activation, and preserve vascular patency. However, if a blood vessel is cut or otherwise damaged, the subendothelial vascular basement membrane is exposed, and tissue factor and other molecular promoters are released, leading to platelet activation and thrombin generation which, in turn, leads to the formation of fibrin from fibrinogen and the creation of a stable fibrin-platelet clot.1,2

Coagulation is classically represented as two separate pathways that converge and form a final common pathway that leads to thrombin generation (Fig. 30-1). However, this model is derived from in vitro tests of coagulation and does not represent the in vivo state. It does not explain how deficiencies of some “intrinsic” pathway factors (factor XII, high molecular weight kininogen, prekallikrein) do not cause clinical bleeding, whereas deficiencies of other intrinsic factors (factors VIII and IX) do. Further, under normal circumstances hemostasis is initiated by the release of tissue factor by damaged endothelium (i.e., the “extrinsic” pathway), not by contact activation of factor XII (i.e., the intrinsic pathway). Although hemostasis is initiated by tissue factor, the regulation of thrombin generation at the site of endothelial injury is determined almost entirely by platelets. Platelet adhesion is initiated when receptors on platelet membranes bind to the subendothelial collagen by forming a bridge with von Willebrand factor (vWF). Once platelets adhere, they expose factors on their surface that provide a template for initiation of the coagulation cascade and the formation of the hemostatic plug. The cell-based model of coagulation shown in Figure 30-2 describes this central role for platelets in the generation of thrombin. Thrombin cleaves fibrinogen to fibrin monomer, which automatically polymerizes to long-chain fibrin fibers in a few seconds. Over the next few minutes, cross-linking between fibrin strands occurs, forming a stable fibrin mesh that traps platelets and forms a hemostatic plug.


Figure 30.2 Cell-based model of coagulation. Coagulation occurs in three overlapping phases: initiation, priming, and propagation. In the initiation phase, factor VII binds to tissue factor (TF) on the surface of injured cells and is rapidly activated. The factor VIIa/TF complex activates factor IX and factor X. Factor Xa then activates factor V on tissue factor bearing cells. Xa combines with Va to convert small amounts of prothrombin (factor II) to thrombin (factor IIa). Factor VIIa/TF complex is inhibited by tissue factor pathway inhibitor (TFPI) in complex with factor Xa. In the priming phase, thrombin binds to platelets, which have adhered to the injury site, in part due to the binding of platelets to exposed collagen through the mediation of the von Willebrand factor (vWF). Collagen and thrombin activate platelets, causing the release of their α-granules, which contain factor V in a partially active form. Factor V is fully activated by thrombin. Thrombin also activates factor VIII (by cleaving it from vWF) and factor XI. This results in a primed, activated platelet that rapidly binds factors Va, VIIIa, and XIa. In the propagation phase, factor IXa (generated by factor VIIa/TF complex in the initiation phase) forms a complex with VIIIa on the platelet surface. This factor IXa/VIIIa complex activates factor X. Factor Xa then forms a complex with factor Va on the platelet surface. Platelet surface factor Xa/Va complexes generate a burst of thrombin (IIa), which is sufficient to activate fibrinogen (I) to become fibrin (Ia) and form a stable clot.

(From Monroe DM, Hoffman M, Roberts HR: Platelets and thrombin generation. Arterioscler Thromb Vasc Biol 22:1381-1389, 2002, with permission.)

Fibrinolysis is the process by which thrombi are continuously remodeled. Circulating plasminogen has an affinity for fibrin and is incorporated into clot as it forms. Fibrinolysis is triggered when fibrin, tissue plasminogen activator, and plasminogen are in close association. Once this occurs, plasminogen is converted into plasmin, and proteolysis of fibrin begins. Plasmin is a serine protease that cleaves specific peptide bonds at multiple sites on fibrin, leading to clot dissolution and the release of fibrin degradation products, including D-dimer.

Abnormal Bleeding Following Cardiac Surgery

Excess bleeding following cardiac surgery may reflect inadequate surgical hemostasis. Commonly, however, abnormal blood clotting due to coagulopathy, platelet dysfunction, and excess fibrinolysis contribute to or are the primary causes of postoperative bleeding. The factors that contribute to postoperative bleeding may be categorized as patient-related, intraoperative, and postoperative (Table 30-1).

Table 30-1 Risk Factors for Excessive Postoperative Bleeding in Patients Undergoing Cardiac Surgery

Patient Variables
Advanced age (>70 years)
Preoperative anemia
Female gender
Increased body size
Cardiogenic shock, congestive heart failure, or poor left ventricular function
Renal insufficiency
Peripheral vascular disease
Insulin-dependent diabetes mellitus
Liver failure or hypoalbuminemia
Preoperative sepsis
Preoperative antithrombotic therapy
High intensity: abciximab, clopidogrel, direct thrombin inhibitors, low molecular weight heparin, fibrinolytic therapy
Low intensity: aspirin, dipyridamole, eptifibatide, tirofiban
Preoperative coagulopathy
Hereditary coagulopathy or platelet defect (e.g., von Willebrand disease, hemophilia A or B)
Acquired coagulopathy or platelet defect (e.g., nonspecific prolongation of bleeding time, chronic lymphocytic leukemia, lupus anticoagulant, polycythemia, myelodysplastic syndrome, idiopathic thrombocytopenic purpura, β-thalassemia)
Intraoperative and Postoperative Variables
Prolonged CPB time
Type of operation: aortic/complex >valve + CABG >valve >CABG
Use of internal mammary artery (either one or two) for CABG surgery
Reduced heparin dose
Increased protamine dose after CPB
Increased cell saver volume
Intraoperative autologous donation
Need for transfusion while on CPB
Low body temperature in ICU
Use of hydroxyethyl starch for volume expansion
Lack of transfusion algorithm with point-of-care testing

CABG, coronary artery bypass graft; CPB, cardiopulmonary bypass; ICU, intensive care unit.

Modified from Ferrasis VA, Spiess BD: Perioperative blood transfusion and blood conservation in cardiac surgery: The Society of Thoracic Surgeons and The Society of Cardiovascular Anesthesiologists Practice Guidelines Series. Ann Thorac Surg [in press].

Patient Factors

Patients may have acquired or inherited disorders of hemostasis. Of these, antithrombotic (anticoagulant and antiplatelet) drugs are the most important.

Platelet Dysfunction and Thrombocytopenia.

Treatment with antiplatelet drugs (aspirin, nonsteroidal antiinflammatory drugs, clopidogrel, and glycoprotein IIb/IIIa inhibitors) is common in patients undergoing cardiac surgery (see Chapter 3). Acquired platelet dysfunction occurs with chronic liver disease and renal failure. A blood urea nitrogen concentration greater than 35 mmol/l (> 100 mg/dl) contributes to postoperative bleeding. Treatment of uremic coagulopathy involves dialysis, desmopressin, and platelets.

Von Willebrand disease is the most common inherited bleeding disorder, affecting about 1% of the population. It is characterized by low levels of vWF, which results in impaired platelet adhesion. Most patients with von Willebrand disease have a mildly increased bleeding tendency (easy bruising, menorrhagia, recurrent epistaxis). The platelet count and prothrombin time are usually normal, whereas the activated partial thromboplastin time (aPTT) and bleeding time may be elevated. Rarely, von Willebrand disease is associated with a severe, life-threatening bleeding tendency. Treatment of bleeding involves desmopressin, transfusion of plasma-derived concentrates containing vWF, and platelets.

Causes of low platelet counts include: (1) heparin-induced thrombocytopenia (see subsequent material); (2) drugs (Table 30-2); (3) splenic sequestration, commonly due to splenomegaly secondary to portal hypertension or tumor infiltration; (4) reduced bone marrow activity (e.g., cytotoxic drugs, fibrosis, or tumor infiltration); (5) HIV/AIDS; and (6) idiopathic thrombocytopenic purpura, which is a condition characterized by immunologic destruction of platelets; it may be acute or chronic, mild or severe. The treatment of severe thrombocytopenia due to idiopathic thrombocytopenic purpura is usually corticosteroids. Patients with chronic cyanosis due to right-to-left intracardiac shunting have increased bleeding tendencies due to thrombocytopenia, platelet dysfunction, and reduced levels of some coagulation factors.

Table 30-2 Drugs Associated With Thrombocytopenia That May Be Used in Patients in the ICU

Antimicrobials Analgesics
Trimethoprim/sulfamethoxazole Acetaminophen
Rifampin H2-receptor antagonists
Amphotericin Ranitidine
Vancomycin Cimetidine
Piperacillin CNS drugs
Ampicillin Haloperidol
Cardiovascular drugs Chlorpromazine
Thiazide diuretics Diazepam
Amiodarone Lithium
Quinidine Carbamazapine
Amrinone Glycoprotein IIb/IIIa antagonists
Digoxin Abciximab
Nitroglycerine Eptifibatide
Alprenolol Tirofiban

Modified from Rizvi MA, Shah SR, Raskob GE, et al: Drug-induced thrombocytopenia. Curr Opin Hematol 6:349-353, 1999. CNS, central nervous system; ICU, intensive care unit; NSAIDs, nonsteroidal antiinflammatory drugs.


Acquired coagulopathy may occur as the result of treatment with heparins, warfarin or, less commonly, thrombin inhibitors (e.g., bivalirudin). Herbal supplements, notably garlic, gingko, and ginseng,3 can also cause coagulopathy. The most important nonpharmacologically acquired coagulopathy is that associated with chronic liver disease, which can lead to deficiency of all coagulation proteins (especially factors I, II, V, VII, IX, and X). Chronic liver disease also causes portal hypertension, which is associated with esophageal varices and splenomegaly (with platelet sequestration). Esophageal varices can rupture, either spontaneously or during instrumentation of the esophagus, causing catastrophic bleeding.

Vitamin K is a fat-soluble vitamin that is required for the hepatic synthesis of factors II, VII, IX, and X. Vitamin K deficiency is caused by poor dietary intake and malabsorption; it often coexists with chronic liver disease, particularly biliary cirrhosis. Coagulopathy may also occur due to sepsis (see subsequent material), most commonly in patients with acute endocarditis. Congenital defects of coagulation, such as hemophilia A (factor VIII deficiency) and hemophilia B (factor IX deficiency), are uncommon.

Intraoperative Factors

Intraoperative factors that contribute to postoperative bleeding include the effects of cardiopulmonary bypass (CPB), the type and duration of the surgical procedure, and the management of anticoagulation. The effects of CPB and surgery on hemostasis are complex.4 CPB and surgical trauma elicit a marked systemic inflammatory response characterized by leukocyte activation, release of inflammatory mediators, and activation of platelets and the coagulation and complement cascades (see Chapter 2). Activation of platelets and coagulation occurs through blood contact with the CPB circuit, through surgical trauma, and through the reinfusion of pericardial blood. Platelets are also activated by heparin and hypothermia. Hemodilution of platelets and coagulation proteins occurs because of the CPB prime solution and other intravenous fluids. Platelets are sequestered onto Dacron grafts. Fibrinolysis is stimulated by hypothermia, contact activation of thrombin and factor XII, and the release of tissue plasminogen activator from the vascular walls. These adverse effects are more pronounced when CPB is prolonged and deep hypothermia is utilized.

Various intraoperative strategies may be employed to reduce bleeding and allogenic (i.e., donor) blood transfusion. They include: (1) antifibrinolytics; (2) heparin-coated CPB circuits; (3) avoidance of deep hypothermia; (4) autologous (i.e., the patient’s) blood donation; (5) normovolemic hemodilution; (6) intraoperative blood recovery and reinfusion through a cell saver. Surgical strategies to reduce postoperative blood loss include meticulous surgical hemostasis and the use of topical agents such as surgical adhesives (e.g., BioGlue) and thrombin preparations (e.g., Thrombostat).

Postoperative Factors

In the early postoperative period, the major contributors to postoperative bleeding are inadequate surgical hemostasis, hypothermia, residual heparin effect (sometimes referred to as heparin rebound), platelet dysfunction, thrombocytopenia, and dilutional coagulopathy. In particular, platelet dysfunction—usually in association with thrombocytopenia, but not always—is a major cause of postoperative bleeding. Less commonly, excessive fibrinolysis is present, although the widespread preemptive use of antifibrinoltyics minimizes this as a cause. Assuming there are no specific concerns regarding neurologic function, patients who are bleeding excessively should be actively warmed to 36°C. Massive transfusion causes coagulopathy by several different mechanisms; it is discussed later in this chapter.

Beyond the early postoperative period, pathologic bleeding is usually related to antithrombotic drugs. Acute gastrointestinal stress ulceration and hemorrhage is the most common nonsurgical cause of bleeding. Stress ulcer prophylaxis is discussed in Chapter 34. Thrombocytopenia is common in patients with critical illness. The causes include: (1) heparin-induced thrombocytopenia (see subsequent material); (2) drugs (see Table 30-2); (3) platelet destruction due to intraaortic balloon counterpulsation, renal replacement therapy, or mechanical cardiac support; (4) sepsis and disseminated intravascular coagulation (see subsequent material); (5) posttransfusion purpura (see subsequent material). Usually, platelet transfusion is required only to treat bleeding or before invasive procedures.

Disseminated Intravascular Coagulation

Disseminated intravascular coagulation (DIC) is a generalized disorder of the coagulation system involving the inappropriate activation of platelets, coagulation, and fibrinolysis, resulting in a consumptive coagulopathy and pathologic thrombosis. It is characterized by pathologic bleeding from surgical sites, intravenous cannula sites, and mucosal surfaces and, rarely, by clinically significant thrombosis. Following an initiating event, there are normally two stages of DIC. Stage 1 (early) involves excessive activation of platelets and coagulation proteins, resulting in generalized microvascular thrombosis and obstruction. This obstruction leads to red cell fragmentation and coagulation factor and platelet consumption, resulting in bleeding due to hemostatic factor and platelet depletion (stage 2, late). DIC has multiple causes, including trauma, hemolytic transfusion reaction, obstetric complications and, most important, sepsis. In addition, the consumptive coagulopathy that accompanies prolonged CPB or extracorporeal membrane oxygenation (ECMO) shares many of the hemostatic features of late DIC, namely, low platelet numbers, low fibrinogen, prolonged prothrombin time, prolonged aPTT, elevated D-dimer, and characteristic changes on the thromboelastogram (see Fig. 30-4).5 Management of DIC involves treating the underlying causes and controlling bleeding by means of blood component therapy. In the relatively rare circumstance of clinically important thrombosis, systemic heparinization is indicated.

Prothrombotic States

Several inherited and acquired conditions are associated with hypercoagulability. These conditions should always be considered in patients who develop thromboembolism without recognizable risk factors.

Important inherited prothrombotic conditions include factor V Leiden (the product of a specific mutation in the factor V gene that confers resistance to factor V cleavage by activated protein C); deficiencies of protein C and protein S (a cofactor for activated protein C); antithrombin III deficiency; and a mutant gene for prothrombin that causes increased levels of the normal protein. Antiphospholipid syndrome and elevated plasma homocysteine are two important acquired prothrombotic conditions. Antiphospholipid syndrome is caused by antibodies (including lupus anticoagulant and anticardiolipin antibodies) directed against cell membrane phospholipids. The term lupus anticoagulant is misleading because patients typically do not have systemic lupus erythematosus and, although the aPTT is elevated, patients have a prothrombotic tendency. Severe systemic illnesses are also associated with an increased risk for pathologic thrombosis. Cancer, major surgery (including cardiac and thoracic surgery), congestive heart failure, myocardial infarction, and stroke all provoke a hypercoagulable state and are risk factors for thromboembolism. High platelet counts and fibrinogen levels, as part of systemic inflammation, also contribute.

Patients with known or suspected hypercoagulability should receive prophylaxis against deep vein thrombosis (DVT) and pulmonary embolism (see Chapter 17) as soon as postoperative bleeding has settled. If an inherited or acquired hypercoagulable state (excluding pregnancy or systemic illness) is suspected, a thrombophilia screen should be obtained.


Laboratory Versus Point-of-Care Testing

Traditionally, tests of hemostatic function (other than activated clotting time) have been performed in the hematology/coagulation laboratory. However, in an actively bleeding patient, the time required to label, transport, and report on the test causes a significant delay in obtaining the results. This has led to efforts to develop hemostatic tests that can be performed at or near the bedside (i.e., the point of care). Most of the hemostatic tests described here can be performed as point-of-care tests. By incorporating point-of-care testing into management algorithms, bleeding and transfusion requirements can be reduced.7,8

Activated Partial Thromboplastin Time

The aPTT monitors primarily the competency of the intrinsic coagulation pathway (i.e., high molecular weight kininogen, prekallikrein, and factors VIII, IX, X, XI, XII) and, to a lesser extent, the common pathway. The test involves adding a phospholipid tissue extract—which activates factor XII and calcium ions—to citrated plasma. The aPTT is used to monitor the effectiveness of anticoagulation with unfractionated heparin and direct thrombin inhibitors (see subsequent material). The normal range is 20 to 35 seconds but values vary slightly among laboratories. The therapeutic range for systemic heparinization is 50 to 80 seconds. Causes of prolonged aPTT include (1) deficiency of intrinsic pathway factors (e.g., due to consumptive coagulopathy or hemophilia); (2) unfractionated heparin; (3) the presence of acquired inhibitors (i.e., antibodies) of factors VIII and IX; and (4) the presence of lupus anticoagulant. Although typically associated with an elevated prothrombin time (PT), a mildly elevated aPTT may also be seen with warfarin overdose, liver disease, and vitamin K deficiency.

If the aPTT is prolonged preoperatively, correction studies in which the patient’s plasma is mixed with pooled normal plasma may be performed. Normalization of the aPTT suggests that there is a coagulation factor deficiency; partial or no correction suggests a heparin effect or the presence of an inhibitor or lupus anticoagulant. A heparin effect can be excluded by adding protamine to the sample. Although the aPTT is often measured after cardiac surgery, abnormalities may not always correlate with bleeding.

Prothrombin Time, Prothrombin Ratio, and International Normalized Ratio

The PT monitors the competency of the extrinsic (tissue factor, factor VII) and common (factors V, X, II, and I) pathways. The test involves adding tissue factor and calcium ions to citrated plasma. The prothrombin ratio (PR) is the patient’s PT divided by the mean PT obtained from healthy individuals using the laboratory’s reagents. The normal value for PT is 10 to 14 seconds; the normal PR is 0.8 to 1.2, but values vary among laboratories. Causes of a prolonged PT include: (1) consumptive coagulopathy, (2) warfarin anticoagulation, (3) vitamin K deficiency, (4) liver disease, and (5) hypofibrinogenemia. Large amounts of heparin also elevate the PT but not to the same extent as the aPTT is raised. Inhibitors of extrinsic pathway factors can occur but are much less common than those of factors VIII and IX, which affect the aPTT. Although the PT is commonly measured after cardiac surgery, abnormalities may not always correlate with bleeding.

The international normalized ratio (INR) pertains to monitoring warfarin anticoagulation; it is the patient’s PT divided by the result that would have been obtained if the PT were measured using standardized reagents (the international reference preparation). An individual laboratory’s reagents have a specific sensitivity relative to the international reference preparation. Thus, the INR avoids differences in PR due to differences in the reagents used by various laboratories.


D-dimer is a degradation product of cross-linked fibrin. Levels are normally low (<500 μg/l). Higher levels occur in any situation in which there is excess clotting followed by fibrinolysis; in particular, higher levels occur with venous thromboembolism (see Chapter 23), major hemorrhage, therapy, and DIC. Moderate elevations in the D-dimer are also seen in patients with severe systemic illness. Following cardiac surgery, the fibrinolytic D-dimer concentration is commonly greater than 1000 μg/l and remains elevated for as long as 60 days.9

Activated Clotting Time

The activated clotting time (ACT) is a bedside test that is used to assess the effectiveness of heparin anticoagulation. Whole blood is added to a tube or cartridge containing an activator (celite, kaolin, glass beads, or phospholipid tissue extract), which stimulates contact activation of the intrinsic coagulation pathway. The activated blood sample is then placed in a device that warms the blood and records the time it takes for clot to form. Devices from different manufacturers use different activators and different methodologies of assessing clot formation; thus, ACT values from different machines cannot be used interchangeably. The normal range for ACT depends on the device being used, but it is usually within the range of 70 to 150 seconds. Values above 400 seconds are generally used for CPB; values of 160 to 180 seconds are used for continuous renal replacement therapy (CRRT; see Chapter 33) and ECMO (see Chapter 22).

The ACT has the advantage of being able to be rapidly performed at the bedside. Most ACT devices have two channels, one of which can be used with a heparinase-containing cartridge. Heparinase is an enzyme that neutralizes heparin. An elevated ACT with a normal heparinase ACT indicates a heparin effect; if both ACTs are elevated, coagulopathy is suggested. The ACT has several limitations. First, as outlined earlier, values vary among devices and may not reliably correlate with plasma heparin concentrations.10 Second, values for ACT (more so than values for aPTT) are influenced by factor depletion, thrombocytopenia, platelet dysfunction, and antifibrinolytic therapy. Finally, as a point-of-care test, a quality assurance program must be maintained, but most ACT machines do not allow patient and user identification to be recorded.


Thromboelastography is a hemostatic test that measures the shear elasticity and the dynamics of clot formation and the strength and stability of formed clot. In one method (TEG 5000 Thromboelastograph Hemostasis Analyzer, Hemoscope, Niles, IL), whole blood is placed in a heated oscillating cup into which a pin, suspended from a torsion wire, is lowered. Initially, the pin is undisturbed by the oscillating cup, but as fibrin strands develop, the pin becomes progressively constrained by the developing clot, creating tension in the wire, which is transduced and displayed on a computer screen. This is represented as an increasing deflection from the midline. In another device (ROTEM Whole Blood Haemostasis Analyser, Pentapharm, Basel Switzerland), the sensor shaft, rather than the cup, rotates; otherwise the principles are similar.

Various activators (celite, tissue factor) can be added to the cups to accelerate initial coagulation, and heparinase cups are commonly paired with plain cups to identify a heparin effect. Thromboelastography provides information about all components of hemostasis (coagulation, platelet function, fibrinolysis) but offers a particular advantage in diagnosing fibrinolysis. Also, the diagnosis of platelet dysfunction can be inferred by the findings of an abnormal thromboelastogram (in particular, a maximum amplitude <45 mm) in combination with a normal platelet count and normal tests of coagulation.

Standard thromboelastogram parameters are shown in Figure 30-3; typical abnormal patterns are shown in Figure 30-4. Point-of-care thromboelastogram-guided blood transfusion algorithms, either alone7,14 or in conjunction with other tests,8 have been shown to reduce transfusion requirements. As with ACT, point-of-care thromboelastogram analysis requires a quality assurance program.


Blood Products

Red Blood Cells

Red blood cells are usually administered as packed cells from which much of the non-red-cell component has been removed and the blood has been resuspended in an anticoagulant storage solution, usually citrate-phosphate-dextrose-adenine. A unit of packed red cells has a volume of about 300 ml and a hematocrit of about 60%. Without continuing blood loss, transfusion of 4 to 5 ml/kg of packed red cells increases hemoglobin concentration by about 1 g/dl. Packed red cells are stored at 4°C and have a shelf life of 35 to 42 days. During storage, red cells metabolize dextrose into lactate, resulting in a fall in pH and an increase in lactate. Red cell fragility increases progressively, and temperature-sensitive failure of the red cells’ sodium-potassium pump occurs, resulting in an increase in the concentrations of free hemoglobin and extracellular potassium. There is also progressive loss of cellular 2,3-diphosphoglycerate (2,3-DPG), which is probably responsible for the short-lived (12 to 24 hours) leftward shift in patients’ oxygen-hemoglobin curves (and therefore the reduced tissue unloading of oxygen) that occurs with the transfusion of old blood. Despite these effects, no convincing data indicate an association between length of storage of red blood cells and adverse outcomes in cardiac surgery patients.15

Blood Groups and Compatibility Testing.

Red blood cell membranes contain many blood group antigens, the most important of which are those of the ABO and rhesus (Rh) blood groups. The ABO blood group is composed of two antigens, A and B, and their respective antibodies, anti-A and anti-B (Table 30-4). Antibodies naturally develop to nonself antigens during early childhood. Administration of red cells containing A or B antigen to a patient with a corresponding antibody results in a life-threatening hemolytic transfusion reaction. The compatibility of ABO groups with red cell and plasma products are shown in Table 30-5.

Table 30-4 ABO Blood Group Antigens and Antibodies

Blood Group Red Cells Plasma
A A antigen Anti-B antibody
B B antigen Anti-A antibody
O Neither A nor B antigens Both anti-A and anti-B antibodies
AB Both A and B antigens Neither anti-A nor anti-B antibodies

Table 30-5 Compatibility of ABO Groups for Red Cells and Plasma oxygen-hemoglobin

Recipient ABO Blood Group Compatible Donor ABO Groups
Red Cells  
Unknown O
O O only
A A or O
B B or O
AB AB or B or O
Plasma Components  
Unknown AB
O O or A or B or AB
A A or AB
B B or AB
AB AB (or A if AB is unavailable)

There are many Rh antigens but the most important ones are D, C, c, E, and e, of which D is the most antigenic. The notations Rh (+) and Rh (−) refer to the presence or absence of the D antigen. About 85% of Caucasians and more than 99% of Asians are Rh (+). In contrast to anti-A and anti-B, anti-D does not form unless an individual is exposed to D antigen, usually following transfusion of Rh (+) blood into an Rh (−) recipient or when an Rh (−) mother is exposed to the blood of her Rh (+) fetus. Thus ideally, Rh (+) blood should not be administered to an Rh (−) recipient. However, if blood supplies are low, Rh (+) red blood cells may be issued to males and to females who are beyond the reproductive years; in such cases, anti-D immunoglobulin should be administered as soon as possible (see subsequent material under the heading Platelets). Multiple other blood group antigens exist (e.g., Kell, Duffy, Kidd, Lewis, etc.) and can cause hemolytic transfusion reactions.

Before blood is issued for transfusion, three processes usually occur: (1) ABO and Rh typing of the recipient’s blood; (2) antibody screening, in which recipient’s plasma and commercially supplied red cells containing antigens responsible for hemolytic transfusion reactions are combined; (3) cross-matching of the donor red blood cells and the recipient’s plasma. These processes usually take about 45 minutes. Before surgical procedures that are unlikely to require a blood transfusion a “type and screen” is performed, so if blood is subsequently required, only a cross-match is necessary. Most transfusion services issue type-specific blood, that is, group A blood to a group A recipient, Rh (+) blood to an Rh (+) recipient. Alternatively, cross-matched group O blood may be issued (see Table 30-5

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