The role of blood transfusion in the management of upper and lower intestinal tract bleeding

Patients with gastrointestinal (GI) haemorrhage use 13.8% of all red blood cell transfusions in England. This review addresses the evidence for red blood cell, fresh frozen plasma and platelet transfusions in acute and chronic blood loss, from both the upper and lower intestinal tract. It reviews the indications for transfusion in GI bleeding, the haematological consequences of massive blood loss and massive transfusion, and the importance of managing coagulopathy in bleeding patients. It also looks at the safety and risks of blood transfusion, and provides clinicians with evidence to reduce unnecessary transfusion. Large controlled clinical trials of blood transfusion specifically in GI bleeding are required, along with further research into the use of adjuvant therapies such as recombinant activated factor VIIa. Changing clinician behaviour to reduce inappropriate blood transfusion remains a key target for future transfusion research.     

Scientific aspects of supplying blood to distant military theaters

PURPOSE OF REVIEW: Reduction in combat zone morbidity and mortality requires rapid delivery of safe blood products as an integral element of advanced trauma surgical care. This review of the current literature presents scientific aspects of supplying blood for rapid delivery to enhance survival and patient outcome in the combat zone. RECENT FINDINGS: Most deaths due to hemorrhage can be averted by transfusion during the first hour from injury; therefore, maintaining a dependable inventory of blood products in combat support hospitals is essential. Current casualty care in distant geographic locations involves rapid air evacuation to combat support hospitals or fleet hospitals, where massive transfusions may be required. Resuscitation by forward surgical teams utilizing red blood cells before air evacuation or in-flight has also been reported. To improve survival, these massive transfusions should be composed of not only red blood cells but also other blood components and plasma factors. SUMMARY: Rapid on-site combat casualty transfusion support requires specialized blood transport containers and transfusion practices not observed in noncombat settings, such as the mobile walking blood bank and a frozen blood program. Additionally, technology for improved transport containers, cell-free hemoglobin-based oxygen carriers, freeze-dried blood, and recombinant activated coagulation factor has attracted focused interest.     

Non-infectious complications of transfusion therapy.

Blood transfusion is considered safe when the infused blood is tested using state of the art viral assays developed over the past several decades. Only rarely are known viruses like HIV and hepatitis C transmitted by transfusion when blood donors are screened using these sensitive laboratory tests. However, there are a variety of transfusion risks which still remain that cannot be entirely eliminated, many of which are non-infectious in nature. Predominantly immune-mediated complications include the rapid intravascular or slow extravascular destruction (hemolysis) of transfused red cells or extravascular removal of platelets by pre-formed antibodies carried by the transfusion recipient. Alternatively, red cells can be damaged when exposed to excessive heat or incompatible intravenous fluids before or during the transfusion. Common complications of blood transfusion that at least partly involve the immune system include febrile non-hemolytic and allergic reactions. While these are usually not life-threatening, they can hamper efforts to transfuse a patient. Other complications include circulatory overload, hypothermia and metabolic disturbances. Profound hypotensive episodes have been described in patients on angiotensin-converting enzyme (ACE) inhibitors who receive platelet transfusions through bedside leukoreduction filters. These curious reactions appear to involve dysmetabolism of the vasoactive substance bradykinin. Products contaminated by bacteria during blood collection and transfused can cause life-threatening septic reactions. A long-term complication of blood transfusion therapy unique to chronically transfused patients is iron overload. Less common - but serious - reactions more specific to blood transfusion include transfusion-associated graft-versus-host disease and transfusion-associated acute lung injury. Many of these complications of transfusion therapy can be prevented by adhering to well-established practice guidelines. In addition, individuals who administer blood transfusions should recognize these complications in order to be able to quickly provide appropriate treatment.     

Current practice and future directions for optimization of platelet transfusions in patients with severe therapy-induced cytopenia

Platelet transfusions are mainly used for patients with thrombocytopenia due to bone marrow failure, especially cancer patients developing severe chemotherapy-induced thrombocytopenia (e.g. patients with acute leukemia or other hematologic malignancies). A prophylactic transfusion strategy is now generally accepted in developed countries. Some clinical data, however, support the use of a therapeutic transfusion strategy at least for certain subsets of these patients. Several methodological approaches can then be used to evaluate the outcome of platelet transfusions, including peripheral blood platelet increments and bleeding assessments. Several factors will influence the efficiency of platelet transfusions; fever and ongoing hemorrhage are among the most important patient-dependent factors, but the number and quality of the transfused platelets are also important. The quality of transfused platelets can be evaluated by analyzing platelet activation, metabolism or senescence/apoptosis. Only evaluation of metabolism is included in international guidelines, but high-throughput methods for evaluation of activation and senescence/apoptosis are available and should be incorporated into routine clinical practice if future studies demonstrate that they reflect clinically relevant platelet characteristics. Finally, platelet transfusions have additional biological effects that may cause immunomodulation or altered angioregulation; at present it is not known whether these effects will influence the long-time prognosis of cancer patients. Thus, several questions with regard to the optimal use of platelet transfusions in cancer patients still need to be answered.     

Clinical aspects of platelet transfusions

Refractoriness is the most important complication of platelet transfusion therapy, occurring in about 50% of patients receiving repeated transfusions. The major causes are HLA alloimmunization and non-immune platelet consumption associated with clinical factors such as septicaemia. DIC and splenomegaly. Initial management of alloimmunized patients who are refractory to platelet transfusions from random donors is the use of HLA-matched platelet transfusions, which improve responses to transfusions in about 65% of patients. It may be difficult to provide effective platelet transfusion support for alloimmunized patients not responding to HLA-matched transfusions. There has been much interest in methods for the prevention of HLA alloimmunization. Primary HLA alloimmunization is dependent on the presence of HLA class II antigen-bearing cells in transfusions; pure platelet transfusions are non-immunogenic as platelets only express HLA class I antigens. The use of leucocyte-depleted blood components in multitransfused patients has resulted in a reduction in HLA alloimmunization and platelet refractioness. Improvements in the techniques for leucocyte-depletion of red cell and platelet concentrates and the possibility of inactivation of HLA class II antigen-bearing cells by UV irradiation makes prevention of alloimmunization an attainable goal.     

Decreased transfusion requirements in patients given stem cell allografts using a non-myeloablative conditioning regimen: a single institution experience

We report our experience of allogeneic peripheral blood stem cell transplantation using non-myeloablative conditioning regimens delivered and supported on an outpatient basis. A group of 44 patients underwent 47 allograft procedures using peripheral blood stem cells. Approximately one third of the individuals did not require red blood cells transfusions: the median of transfused red blood cells units was 1 (range 0-10). In addition one out of three did not require platelet transfusions either, the median of platelet transfusions being 1 (range 0-6). In fourteen allografts (30%) neither red blood cells nor platelet transfusions were used. An inverse correlation was found between the number of CD34 cells infused and the PRBC and PLT transfusion requirements, those patients receiving high numbers of CD34 cells needing fewer transfusions of both PRBC and platelets. The possibility of conducting allografts without transfusion of blood products in some patients may result in a decrease in both cost and the risks stemming from exposure to human blood derivatives.     

Replacement of Massive Blood Loss

Treatment of massive blood loss has experienced major changes during the recent decade. The transition towards pure component therapy has been the most significant issue, which has compelled the clinician to revise some of their basic strategics in treatment of massively bleeding patients. The importance of adequate volume resuscitation with crystalloids and colloids is still unrefutable, but the therapy of hemorrhagic derangements has changed. Plasma-poor red cells (RC) are now commonly used instead of whole blood (WB) or packed red blood cells (PRBC) to correct oxygen carrying capacity during massive blood loss. As the plasma content of RC is minimal, deficit of plasma and coagulation factors develops earlier than during transfusion of WB and PRBC. Hypofibri- nogenemia develops first followed by other coagulation factor deficits and later by thrombocytopenia. Therefore the use of fresh frozen plasma (FFP) is the primary intervention to treat abnormal bleeding encountered in the replacement of massive blood loss with RC. As the development of thrombocytopenia is a highly individual phenomenon, the transfusion of platelets should be guided by repeatedly determined platelet counts.     

Platelet transfusion reaction associated with interdonor HLA incompatibility

An HLA-compatible platelet transfusion was followed by chills, fever, and severe respiratory distress in a multitransfused patient with chronic lymphocytic leukemia. During the previous 7 days the patient had received blood products without incident, including 8 units of red blood cells (RBC), 24 units of pooled random donor platelet concentrates, and five HLA-compatible platelet pheresis products. The patient had no demonstrable RBC, HLA lymphocytotoxic, platelet or granulocyte antibodies. The platelet donor, a multiparous female, had no granulocyte or RBC antibodies but had lymphocytotoxic antibodies against HLA-A2 CREG (cross-reacting group A2, A28, A23, A24) which reacted not with lymphocytes of the patient but with lymphocytes of the donor whose RBC were transfused 24 h prior to the platelet transfusion reaction and whose HLA type is A23, A24; B44, B57. No RBC donors had HLA lymphocytotoxic, granulocyte, or platelet antibodies against the platelet donor. The patient received three subsequent platelet transfusions from the same donor after removal of the antibody-laden plasma with no adverse reaction. These data suggest an interdonor reaction caused by the presence of cells from the RBC donor received by the patient 24 h prior to the transfusion of donor lymphocytotoxic antibody to HLA-A2 CREG antigens.     

Hypercoagulability in non-transfusion-dependent thalassemia

Beta (β)-thalassemia is characterized by a hypercoagulable state and an increased risk of thrombosis, which can result in significant morbidity and mortality. The molecular and cellular mechanisms contributing to hypercoagulability are diverse and include chronic platelet activation, alteration of red blood cell membranes, abnormal expression of adhesion molecules on vascular endothelial cells, and dysregulation of hemostasis. Regular transfusions decrease the risk of thrombosis, whereas splenectomy significantly increases the risk. Splenectomized adults with non-transfusion-dependent thalassemia are also at high risk for ischemic brain damage. Strategies to lower the risk of thrombosis should be considered, including transfusion therapy to raise hemoglobin levels and avoidance or delay of splenectomy.     

Massive platelet transfusion after splenectomy in a case of myelofibrosis

A patient with myelofibrosis complicated by massive splenomegaly underwent splenectomy to alleviate the increasing transfusion requirements and iron overload. The platelets exhibited qualitative defects pre-operatively. Following splenectomy the patient bled profusely and required massive blood and platelet transfusions. The postoperative haemorrhage was controlled by giving sufficient platelets to normalize the platelet aggregation.     

Blood group genotyping: from patient to high-throughput donor screening

Blood group antigens, present on the cell membrane of red blood cells and platelets, can be defined either serologically or predicted based on the genotypes of genes encoding for blood group antigens. At present, the molecular basis of many antigens of the 30 blood group systems and 17 human platelet antigens is known. In many laboratories, blood group genotyping assays are routinely used for diagnostics in cases where patient red cells cannot be used for serological typing due to the presence of auto-antibodies or after recent transfusions. In addition, DNA genotyping is used to support (un)-expected serological findings. Fetal genotyping is routinely performed when there is a risk of alloimmune-mediated red cell or platelet destruction. In case of patient blood group antigen typing, it is important that a genotyping result is quickly available to support the selection of donor blood, and high-throughput of the genotyping method is not a prerequisite. In addition, genotyping of blood donors will be extremely useful to obtain donor blood with rare phenotypes, for example lacking a high-frequency antigen, and to obtain a fully typed donor database to be used for a better matching between recipient and donor to prevent adverse transfusion reactions. Serological typing of large cohorts of donors is a labour-intensive and expensive exercise and hampered by the lack of sufficient amounts of approved typing reagents for all blood group systems of interest. Currently, high-throughput genotyping based on DNA micro-arrays is a very feasible method to obtain a large pool of well-typed blood donors. Several systems for high-throughput blood group genotyping are developed and will be discussed in this review.     

Successful thyroidectomy in a patient with Hermansky-Pudlak syndrome treated with recombinant activated factor VII and platelet concentrates.

Hermansky-Pudlak syndrome is a rare autosomal recessive disorder characterized by the absence of platelet dense bodies in association with albinism. We present the use of recombinant activated factor VII (rFVIIa) in a patient with Hermansky-Pudlak syndrome who underwent total thyroidectomy because of a large richly vascularized nodule (10 cm) compressing the trachea. The patient had a prolonged bleeding time (> 20 min) that remained unchanged after platelet transfusions. However, after infusion of platelets plus rFVIIa, it diminished to 5 min. The platelet aggregation response to adenosine diphosphate and collagen was diminished. Since an early age, the patient had repeated nose bleeding and an episode of melena requiring several tampons, cauterization and transfusions of packed red cells. In this case, we used rFVIIa in bolus for 1 day (four doses of 120 microg/kg every 2 h and six doses of 100 microg/kg every 3 h) and transfusion of platelet concentrates beginning just prior to surgery. No evidence of local bleeding complication could be detected during the entire post-operative period. The hemoglobin level remained normal and no transfusions of packed red cells were necessary. No adverse events occurred.     

Transfusion strategies in patients undergoing stem-cell transplantation

Hemopoietic stem-cell transplant patients may require intensive blood component support. Complications of transfusions include transmission of viral and bacterial infections, transfusion-associated graft-versus-host disease and transfusion-related acute lung injury. Alloimmunization to red cell antigens may cause difficulties in selecting compatible blood, while alloimmunization to HLA expressed on platelets may cause subsequent platelet transfusion refractoriness. It is essential to define robust transfusion policies and procedures and these should be regularly audited. This article reviews blood component transfusion in the setting of hemopoietic stem-cell transplant and specifically discusses the management of ABO-mismatched transplants, the prevention of cytomegalovirus transmission, the prevention of transfusion-associated graft-versus-host disease and the use of granulocyte transfusions.     

Splenic platelet-sequestration following routine blood transfusion is reduced by filtered/washed blood products

The mean fall in the platelet count following 23 routine transfusions of 3-5 units packed cells for anaemia was 32.5%. This was significantly reduced to 12.5% in 15 similar transfusions through a 40 microns microaggregate filter (P less than 0.01) and to 4.6% following five transfusions through a polyester fibre filter (P less than 0.005). In 10 transfusions with frozen or polyester fibre filtered, washed red cells, the decrease in platelet count was 4.2% (P less than 0.001). A study of 111In-oxine labelled autologous platelets in nine patients indicated that the fall in platelet count was due to increased splenic sequestration. Since thrombocytopenia following routine transfusion is reduced by procedures which filter the packed cells, the decrease in platelets is probably caused by their adherence to infused microaggregate debris causing their premature removal from the circulation. Patients with preexisting thrombocytopenia who receive red cell transfusions for anaemia, should therefore receive blood products depleted of microaggregate debris in order to avoid exacerbation of thrombocytopenia and haemorrhagic complications.     

Critical issues in hematology: anemia, thrombocytopenia, coagulopathy, and blood product transfusions in critically ill patients

Systematic evaluations of anemia, thrombocytopenia, and coagulopathy are essential to identifying and managing their causes successfully. In all cases, clinicians should evaluate RBC measurements alongside WBC and platelet counts and WBC differentials. Multiple competing factors may coexist; certain factors affect RBCs independent of those that affect WBCs or platelets. Ideally, clinicians should examine the peripheral blood smear for morphologic features of RBCs, WBCs, and platelets that provide important clues to the cause of the patient's hematologic disorder. Thrombocytopenia arises from decreased platelet production, increased platelet destruction, or dilutional or distributional causes. Drug-induced thrombocytopenias present diagnostic challenges, because many medicines can cause thrombocytopenia and critically ill patients often receive multiple medications. If they suspect type II HIT, clinicians must promptly discontinue all heparin sources, including LMWHs, without awaiting laboratory confirmation, to avoid thrombotic sequelae. Because warfarin anticoagulation induces acquired protein C deficiency, thereby exacerbating the prothrombotic state of type II HIT, warfarin should be withheld until platelet counts increase to more than 100,000/microL and type II HIT is clearly resolving. The presence of a consumptive coagulopathy in the setting of thrombocytopenia supports a diagnosis of DIC, not TTP-HUS, and is demonstrated by decreasing serum fibrinogen levels, and increasing TTs, PTs, aPTTs, and fibrin degradation products. Increasing D-dimer, levels are the most specific DIC parameter and reflect fibrinolysis of cross-linked fibrin. Elevated PTs or a PTTs can result from the absence of factors or the presence of inhibitors. Clinicians should suspect factor inhibitors when the prolonged PT or aPTT does not correct or only partially corrects following an immediate assay of a 1:1 mix of patient and normal plasma. In addition to factor inhibitors, antiphospholipid antibodies (e.g., lupus anticoagulant) can produce a prolonged aPTT that does not correct with normal plasma but is overcome by adding excess phospholipid or platelets. Paradoxically, a tendency to thrombosis, not bleeding, accompanies lupus anticoagulants and the antiphospholipid antibody syndrome. Transfusion of red blood cells, platelets, or plasma products is sometimes warranted, but clinicians must carefully weigh potential benefits against known risks. In critically ill patients, administering RBCs can enhance oxygen delivery to tissues. Among euvolemic patients who do not have ischemic heart disease, guidelines recommend a transfusion threshold of HGB levels in the range of 6.0 to 8.0 g/dL; patients who have HGB that is at least 10.0 g/dL are unlikely to benefit from blood transfusion. The use of rHuEPO to increase erythropoiesis offers an alternative to RBC transfusion, assuming normal, responsive progenitor cells and adequate iron, folate, and cobalamin stores. Future research should examine whether clinical outcomes from rHuEPO use in critically ill patients are important and cost-effective. Because platelets play an instrumental role in primary hemostasis, platelet transfusions are often important in managing patients who are bleeding or at risk of bleeding with thrombocytopenia or impaired platelet function. Platelet transfusions carry risks, and decisions to transfuse platelets must consider clinical circumstances. Most important, platelet transfusions are generally contraindicated if the underlying disorder is TTP or type II HIT, because platelet transfusion in these settings may fuel thrombosis and worsen clinical signs and symptoms. Plasma products can correct hemostasis when bleeding arises from malfunction, consumption, or underproduction of plasma coagulation proteins. Choice of plasma product for transfusion depends on clinical circumstances. FFP is the most commonly used plasma product to correct clotting factor deficiencies, particularly coagulopathies that are attributable to multiple clotting factor deficiency states as in liver disease, DIC, or warfarin anticoagulation. PCC or rFVIIa that is administered in small volumes may provide advantages over FFP when coagulopathies require quick reversal without risk of volume overload. Factor concentrates can replace specific factor deficiencies. Recombinant FVIIa bypasses inhibitors to factors VIII and IX and vWF. Use of rFVIIa in managing hemostatic abnormalities from severe liver dysfunction; extensive surgery, trauma, or bleeding; excessive warfarin anticoagulation; and certain platelet disorders requires further study to determine optimal and cost-effective dosing regimens. Recombinant activated protein C reduces mortality from severe sepsis that is associated with organ dysfunction in adults who are at high risk for death (APACHE scores of at least 25). In severe sepsis, levels of protein C decrease, as do fibrinogen and platelet levels. Because of its anticoagulant effect, however, drotrecogin alfa may induce bleeding. Guidelines for drotrecogin alfa use must take into account bleeding risks.     

Use of platelets and other transfusion products in patients with malignancy.

The need for blood components for oncology patients is small compared with the need for patients with hematologic malignancies. Appropriate use of blood components is necessary, not only medically, but also because of limited supply and availability. Agreement on when to use components is extremely important. In fact, at the time of this writing, the Transfusion Practices Committee of the AABB is conducting an extensive survey on the use of platelets in the oncology and hematology cancer patients (Questionnaire on Institutional Policy on Platelet Transfusion Practice for Hematology/Oncology Patients). The results will, it is hoped, provide a consensus on the proper times and counts that require prophylactic use of components for these patients. Since these patients use the vast majority of components (see Table 15), their proper use is imperative to maintaining an adequate platelet and frozen plasma supply. Transfusion support in cancer patients is vital for their survival. Platelets, in particular, are necessary to prevent serious bleeding. However, refractoriness to platelet transfusions can develop. It must be appreciated that refractoriness is not a general problem and need not require the expensiveness of a universal decision for handling all platelet transfusions in the same manner. Total refractoriness probably occurs in 15 to 20% of patients frequently transfused. In patients in whom frequent platelet transfusion is anticipated, that is, bone marrow transplantation, the development of platelet refractoriness may be reduced by using SDPC and administering them through leukocyte filters. Patients who become refractory to either random or SDPC can either be cross-matched for single-donor platelets that are compatible or can be given HLA-A,B matched platelets. Certainly, the success of platelet transfusion in leukemic patients cannot be denied, since only a small number of these patients now die because of bleeding due to platelet refractoriness. Most of the serious bleeding still seen is associated with sepsis. The risks from transfusion must always be considered. Fortunately, with increased monitoring of the blood supply, they have been reduced. As with any therapeutic regimen, these risks must be weighed against the benefit the patient may gain. Transfusion should always be used prudently.     

Prevention and Management of Platelet Transfusion Refractoriness

Platelet transfusion refractoriness is a major complication of long-term platelet supportive care. Refractoriness may lead to fatal bleeding complications in thrombocytopenic patients. Major factors involved are factors related to the clinical condition of the patient as well as HLA alloimmunisation. Non-alloimmune factors may occur in up to 80% of the patients. However, platelet transfusion outcome is impaired in only 50% of the patients having these conditions. HLA alloimmunisation has been convincingly reduced by the use of leucocytedepleted transfusions. UV-B irradiation of platelet transfusions may be alternatively used to reduce HLA alloimmunisation. Despite these measures, patients with a history of pregnancy or non-leucocyte-depleted transfusions form HLA antibodies in a high proportion (up to 50%). HPA antibodies play a minor but relatively important role in patients with HLA antibodies. ABO antibodies may play a role in refractoriness, which can be abolished by transfusion of ABO-identical platelets. Screening for the presence of HLA and/or HPA antibodies is indicated in case of transfusion failure after ABO-identical or HLA-matched platelets. If no alloantibodies are detected, further analysis to define a role of drugrelated or autoantibodies is required. In case of HLA and/or HPA alloimmunisation associated with refractoriness, matched platelet transfusions are indicated. In case of non-alloimmune factors associated with increased platelet consumption, increasing the transfusion frequency can be considered. Additional investigations are still necessary to define risk factors for secondary HLA alloimmunisation and refractoriness due to non-immune factors to further decrease the incidence of refractoriness.     

Early Immunization against Platelet Glycoprotein Ilia in a Newborn Glanzmann Type I Patient

Alloimmunization against platelet glycoprotein IIb and/or IIIa is a complication rarely observed during the evolution of type I Glanzmann's thrombasthenic patients. The occurrence of such alloantibodies is usually due to repeated blood transfusion and greatly complicates the treatment of these patients since they prevent effective platelet transfusion and might, theoretically, cause posttransfusion purpura. We describe the case of a newborn thrombasthenic patient who developed an IgG platelet allo-antibody 1 month after birth. The diagnosis of Glanzmann's thrombasthenia was complicated by the rare platelet phenotype (PLA1-negative PLA2-positive) of the healthy mother, which was probably heterozygous for the abnormal thrombasthenic gene. Immunofluorescence and immunoblotting techniques demonstrated that the patient antibody was principally directed against the platelet glycoprotein IIIa. Surprisingly, this patient had only received four blood transfusions (fresh frozen plasma on days 1 and 2, and standard red blood cell concentrates on days 5 and 6) before the discovery of the antibody, suggesting prior in utero sensitization. This study emphasizes the need for early diagnosis of the disease. Thrombasthenic patients should be transfused with deleukocyted platelet-free blood products.     

Leukocyte reduction in blood component therapy.

PURPOSE: To review methods of preventing or minimizing the adverse effects associated with the transfusion of passenger leukocytes present in cellular blood components and to define groups of patients who are at risk for adverse effects. DATA SOURCES: English-language articles on transfusion medicine. STUDY SELECTION: Original reports describing the pathogenesis of leukocyte-induced adverse effects in transfusion recipients and the influence of leukocyte-reduced blood components on these effects. DATA EXTRACTION: Evaluation of the diagnosis, transfusion history, and treatment of the study patients; the methods and results of leukocyte reduction; and specific outcomes, including development of alloimmunization to leukocytes, febrile reactions to transfusion, and platelet refractoriness. DATA SYNTHESIS: Passenger leukocytes are the chief cause of alloimmunization to human leukocyte antigen (HLA) and leukocyte-specific antigens in transfusion recipients. Alloimmunization may result in febrile transfusion reactions, platelet refractoriness, and acute lung injury. Leukocytes are also the vector for transfusion-associated cytomegalovirus infection. Technologic advances in the leukocyte reduction of cellular blood components have made it possible to reduce the number of leukocytes to fewer than 10(7) per transfusion. Findings suggest that the use of leukocyte-reduced cellular blood components may minimize or prevent recurrent febrile reactions and alloimmunization to leukocyte antigens. Cytomegalovirus may not be transmitted by blood components containing fewer than 10(7) leukocytes. CONCLUSIONS: Leukocyte reduction in red blood cell and platelet transfusions using third-generation filters is indicated for selected patients who are likely to receive long-term transfusion support, to prevent recurrent febrile reactions and to prevent or delay alloimmunization to leukocyte antigens. Leukocyte-depleted transfusions may also be indicated to delay or prevent refractoriness to platelet transfusion.     

The annual cost of blood transfusions in the United Kingdom

This study estimated the annual cost of blood transfusions in the UK during 1994/1995. The analysis was based on published data, information derived from interviews with relevant NHS personnel and a purpose-designed structured questionnaire of blood donors. The cost to the UKs blood transfusion services of providing blood and blood products for transfusion was £165.5 million in 1994/1995. During this period, 2.75 million conventional donations of whole blood and 144 000 apheresis donations of platelets and plasma were collected: 2.58 million units of red blood cells were issued, resulting in ≈ 866 000 red blood cell transfusions; 334 000 units of fresh frozen plasma and 1.16 million units of platelets were issued, resulting in ≈ 17 000 and 188 000 isolated plasma and platelet transfusions, respectively. Hospital resource use attributable to providing blood transfusions during 1994/1995 cost the NHS £52.6 million. In total, blood transfusions cost the NHS £218.2 million during 1994/1995. Of this, red blood cell transfusions accounted for 76% of the annual cost, isolated platelet transfusions 16%, isolated plasma transfusions 1% and other products 7%. Donors incurred direct costs of £3.1 million and indirect costs of £11.2 million were accrued due to lost productivity. Additionally, blood donors gave up 2.5 million hours of their leisure time donating blood.