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Blood components

Definitions and terminologies Blood components Preparation Leukocyte reduction . Storage lesions Individual components indications , storage , shelf life , dosage calculation , contraindications , side effects .

Separation of blood components are desirable because

1. Separation of blood components allows optimal survival for each component. 2. Allows transfusing specific blood components according to the need of the patient. 3. Allows use of unnecessary component which may be contraindicated in a patient. 4. 5. Several patients can be treated from one unit of donated blood. Use of blood components supplements blood supply and adds to the blood inventory.

6. Reduced the risk of transfusion reactions .

Definitions and terminologies

Blood product - Any therapeutic substance prepared from human blood. Whole blood- Unseparated blood collected into an approved container containing an anticoagulant-preservative solution. Blood component- A constituent of blood, separated from whole blood, such as: _ Red cell concentrate _ Red cell suspension _ Plasma _ Platelet concentrates 2 Plasma or platelets collected by apheresis 1 3 Cryoprecipitate, prepared from fresh frozen plasma: rich in Factor VIII and fibrinogen Plasma derivative - Human plasma proteins prepared under pharmaceutical manufacturing conditions, such as: _ Albumin _ Coagulation factor concentrates _ Immunoglobulins

Apheresis: a method of collecting plasma or platelets directly from the donor, usually by a mechanical method. Classification of blood constituents into Blood components Rbc concentrate, platelet concentrate , platelet rich plasma , fresh frozen plasma , cryoprecipitate , granulocyte concentrate. Plasma derivatives albumin, plasma protein fraction (PPF), Factor 8 conc. , fibrinogen,immunoglobulins, other coagulation factors .

C : centrifugal; CF : continuous flow; DF: discontinuous flow; SM: spinning membrane; PLAP: platelet by apheresis; AFFP: apheresis fresh frozen plasma; RBC: red blood cell; 2RBC : 2-unit red blood cells; TPE : therapeutic plasma exchange; SP: source plasma; HPC : hematopoietic progenitor cells PCWBC : photochemically modified white blood cells.

Blood component preparation

Blood components -------------------- 1) whole blood collected and separation 2) collection of components directly from donor. whole blood collected and separated
One unit of WB contains approximately 450 mL of blood collected from a healthy adult donor into a sterile plastic bag containing 63 mL of anticoagulant/ preservative (AP) solution. Because RBCs, platelets, and plasma have different specific gravities, they can be separated from each other via centrifugation most commonly initially by performing a soft spin, which separates the heavier RBCs from plateletrich plasma. The RBCs then are collected into a sterile satellite bag containing an anticoagulant solution. For separation of platelets from plasma, a hard spin then is performed. One unit of platelet concentrate (PC), which contains a minimum of 5.5X 1010 platelets in approximately 50 mL of remaining plasma, is the result. The typical volume of a unit of plasma collected from WB is approximately 250 mL. In order for the plasma to be labeled as fresh frozen plasma (FFP), the unit must be separated from the other blood components and stored at -18C within 8 hours of collection.

Blood anticoagulants Note: When using acid-citratedextrose (ACD), citrate-phosphate-dextrose (CPD) or citrate-phosphatedouble dextrose (CP2D), the storage is limited to 21 days, but with citrate-phosphate-dextrose-adenine (CPDA1) this can be extended to 35 days.

Apheresis, a word of Greek derivation, means removal in its broadest sense. it refers to any procedure during which blood is withdrawn from the donor or patient and separated ex vivo into some or all of its components. Some of these components are retained for donation or therapeutic purposes. The others are returned, usually on line, to the person. The word pheresis once was used synonymously with the word apheresis; however, apheresis is the preferred word. Hemapheresis is frequently used synonymously with apheresis.

History The fi rst experimental apheresis procedure was performed in 1660 by Richard Lower of Oxford, England, who performed a manual procedure on dogs. Plasmapheresis (removal of plasma with return of red cells was fi rst performed in France in 1902 and in Russia in 1914.1 In 1914 at Johns Hopkins University, Roundtree and Turner used plasmapheresis in artifi cial kidney research.1 In 1960, Soloman and Fahey used manual plasmapheresi therapeutically to reduce elevated globulin levels in a patient with a hyperviscosity syndrome, and thus began the era of therapeutic apheresis.

Apheresis became a practical reality with technologic advances, which included development of plastic bags, integrally connected tubing, and ex-vivo centrifugation. Initially, apheresis involved blood separation as an off-line disconnected process in laboratories with freestanding component separation centrifuges. Now, apheresis is routinely performed as an on-line procedure with fully automated blood cell separators at the donors or patients bedside. In the 1980s, automated on-line cell separation devices were developed by Haemonetics (Braintree, MA), Baxter Fenwal (Deerfi eld, IL), and Organon Teknika (Boxtel, The Netherlands) for collection of Source Plasma in the United States and Europe. Granulocytes, platelets, and Fresh Frozen Plasma (FFP) were the original components collected by means of apheresis technology. Today, numerous blood components are collected from a single donor by means of automated apheresis technology, including the following: 1. Platelets. 2. Plasma. 3. Red Blood Cells (RBCs). 4. RBCs plus plasma (RBCP). 5. 2-unit RBCs (2RBCs). 6. Platelets and RBCs. 7. Platelets and plasma. 8. Granulocytes stimulated with steroids or colony-stimulating factors. 9. Hematopoietic progenitor cells (HPCs) stimulated with granulocyte colony-stimulating factor (G-CSF) or granulocytemacrophage colony-stimulating factor (GM-CSF). One reason for the increase is the use of hemapheresis technology to remove red cells provides a new approach for patients with hemochromatosis. Another reason is the expanding role of photopheresis in managing conditions such as graft vs- host disease (GVHD) and graft rejection.

Edwin J. Cohn, originator of plasma fractionation processes to produce plasma derivatives such as albumin and - globulin, developed a prototype machine for centrifugal separation of the cellular elements of blood from plasma. Allen Jack Latham, cofounder of Haemonetics, working with Cohns prototype, developed a disposable polycarbonate plastic bowl with a rotary seal, which was fi rst used to collect platelets in 1971




Purpose and uses

Fenwal technology

Cs3000 blood cell separator

Fully automated Computer controlled

Platelet collection .

Platelet collection with leucocyte collection . TNX -6 chamber Cs3000 plus Amicus, one-arm venous access device for platelet collection In build in cs3000 used to collect granulocyteplatelet concentrates high extraction coeffi cient for platelets allows frequent collection of double products, such as two apheresis platelet products each containing at least 3.0 X 1011 platelets and less than 1.0 X 106 residual leukocytes without the use of a leukocyte reduction fi lter. new and compact mobile automated blood collection system that was initially developed as a 2RBC apheresis collection device. It has been approved for collection of concurrent plasma. Following collection in the rigid, cylindrical centrifuge chamber, red cells are pumped through an on-line leukocyte reduction fi lter into the fi nal storage bag(s). a spinning membrane, thus incorporating both membrane and centrifugation technology to collect plasma. In the United States, this device is commonly used to collect Source Plasma as well as apheresis FFP. This is a discontinuous system in which only a single venipuncture is performed.. it is a continuous-fl ow, doublevenipuncture system. Fresenius AS104 is currently licensed in the United States for the collection of apheresis platelets and is licensed for TPE and collection of HPCs.



Fersinius technolgy


Latest is

CaridianBCT (formerly Gambro and COBE) acquired the IBM biomedical services technology (the

COBE Spectra

COBE Spectra as a sealless system based on the original IBM-2997 rotating-channel belt. The Spectra is a continuousfl ow system in which one- or

The Spectra uses a leukocyte reduction system to collect leukocyte-reduced platelet units. The Spectra device indicates when units contain excessive numbers of leukocytes and thus when counting is needed to document leukocyte reduction status. The Spectra device also is used to collect HPCs and to perform therapeutic apheresis procedures.

IBM-2997 cell separator)

two-arm venous access is used for platelet collection.


Trima device is fully automated; the technology is similar to that of the Spectra device. The Trima is a one-arm venous access device, has no rotating seal, and has a smaller footprint than does the Spectra. The Trima is capable of collecting double units (_6.0 _ 1011 platelets) that are leukocyte reduced to 1.0 _ 106 or fewer residual white cells. The Trima has been designed and is FDA approved to collect a single or double RBC unit along with the apheresis platelet product. it can collect the same number of platelets as the standard Trima but in a shorter time, 2) it can collect more platelets in the same time as the standard Trima, or 3) it can collect the same number of platelets in the same time as the standard Trima, but do it by processing less of the donors blood, which means delivering less citrate to the donor and reducing citrate-induced donor reactions. discontinuous technology is amenable to a one- or two-arm protocol, although the one-arm venous access technique is used more often because of donor preference for a single needlestick.8 the MCS+cell separators are fairly lightweight [60 to 70 lb (27 to 31.5 kg)], extremely portable and mobile, fully automated, and fl exible in terms of blood components collected. The MCS+ LN9000 is used strictly to collect platelets with or without concurrent plasma. the initial platelet product is not leukocyte reduced to an acceptable level (_1.0 X 106 residual white cells) and must undergo leukocyte reduction via fi ltration, which is now accomplished with an on-line process that produces a fi nal transfusable product that contains _1.0X_ 106 residual white cells in 3.0 X 1011 or more platelets. The MCS_ LN8150 has been developed for collection of either RBCP or 2RBC.9-11 Each RBC unit contains approximately 180 to 200 mL of absolute red cell mass with the machine preprogrammed for the desired amount of red cell mass. Both MCS_ devices

Trima Accel

Haemonetics Technology MCS+ LN9000; MCS+ LN8150; PCS-2)

(LN9000 and LN8150) have a functionally closed rotating seal to maximize product shelf life. a small, lightweight, portable, discontinuous fl ow device intended for the collection of 2 RBC units. Cymbal Automated Blood Collection System

Therakos (Johnson & Johnson) Technology The newest photopheresis device (UVAR-XTS system) is a discontinuous-fl ow cell separator that collects buffy coat containing mononuclear cells from patients with a variety of conditions such as cutaneous T-cell lymphoma, GVHD resulting from marrow transplantation, or solid-organ rejection. Methoxsalen (Uvadex) is injected into the buffy coat product, the cells are incubated and irradiated with ultraviolet light, and the component is transfused back to the patient. Amelioration of the pathologic process through immunologic effects on clones of mononuclear cells is the desired outcome. The older Therakos UVAR photopheresis system used oral administration of methoxypsoralen and is no longer supported. Table 41-2. Advantages of Apheresis-Derived Blood Components Reduced donor exposure: full transfusion dose Frequent repeat donor: pedigreed donors Higher quality products: more quality control per component collected Consistent and standardized products (yields) Matching donors to patients Reduced donor reactions High donor acceptance Double yield or multiple full-dose blood component collections Safety enhancement: for the patient.

Leukocyte depletion White blood cells or leukocytes are present in all cellular blood components that are prepared by standard techniques. Studies have increasingly shown that leukocyte contamination of erythrocyte or platelet preparations can cause a wide variety of side effects after their transfusion. A leukodepleted blood component is most commonly defined as containing fewer than 5 x 106 white blood cells per unit of component. Blood filtration by using leukocyte filters is a commonly used method of leukodepleting blood components. The filtration can be performed either at the bedside during transfusion or in the component-processing laboratory. The latter mode of filtration (prestorage filtration) is superior to bedside filtration because leukocytes are removed before storage, thus preventing further biological changes associated with the storage of these cells, and because quality assurance can be guaranteed. Performing leukodepletion within a relatively short timeusually within 48 hours after blood collectionalso eliminates leukocytes before they release cytokines, fragments of cell membrane, and possibly intracellular viruses. These factors may not be removable by bedside filtration. The cytokines and cell membrane fragments may lead to FNHTRs and primary HLA alloimmunisation,36 respectively, even if the blood is transfused through a bedside leukocyte filter.

Adverse effects of leucocytes in blood transfusion

Transmission of cell-associated infectious agents Transfused erythrocytes, platelet concentrates, and granulocyte concentrates have all been implicated as the cause of infection by transfusion-transmitted CMV (TT-CMV), while fresh frozen plasma and cryoprecipitate have not been reported to cause CMV transmission.2 The cells that serve as reservoirs for CMV have not been identified, but monocytes have been considered to be the dominant cell-type that is infected in peripheral blood. The use of CMV-seronegative blood products has been the gold standard method of preventing TT-CMV infection. Even so, they are still associated with a risk of TT-CMV of approximately 4%.

Studies have found that depleting blood components of leukocytes is successful in preventing TT-CMV infection in neonates, patients with acute leukaemia, and bone marrow transplant recipients.9-11 Using leukodepleted blood components is thus an effective alternative method to using CMV-seronegative blood components to prevent TT-CMV infection to at-risk patients. Besides CMV, other herpesviruses such as Epstein-Barr virus (EBV), human herpesvirus (HHV)-6, HHV-7, and HHV-8 (or Kaposis sarcomarelated herpesvirus [KSHV]) are associated with leukocyte contamination during transfusion.

Leukocyte depletion filters can directly and indirectly remove bacteria from platelet and erythrocyte preparations. Bacteria adhere to the filter matrix, while phagocytic leukocytes, which adhere to or ingest bacteria, are retained by the filters. T gondii transmission can be minimised by transfusing leukocyte-depleted blood components. Prions cause neurodegenerative disorders in both human and animals, such as kuru, Creutzfeldt-Jakob disease (CJD), bovine spongiform encephalopathy, and the new-variant CJD (nvCJD).19 The abnormal prion-related protein can be found in the tonsils and the spleen of patients with nvCJD, but not in those with classical CJD. Hence, circulating B lymphocytes might harbour the agent responsible for the development of nvCJD. 20

Febrile non-haemolytic transfusion reactions

Febrile non-haemolytic transfusion reactions (FNHTRs) have been reported to occur with an incidence of 6.8% after erythrocyte transfusion and 37.5% after platelet transfusion.25 The major cause of severe FNHTRs to erythrocytes is human leukocyte antigen (HLA) alloimmunisation. A reduction in the number of leukocytes to 5 x 108 leukocytes per unit of blood component is sufficient to prevent FNHTRs in most cases. There is increasing evidence that the major cause of FNHTRs after platelet transfusion is due to the presence of pyrogenic cytokines, especially IL-1, that are released from leukocytes during the storage of platelets at 22C.27 Hence, FNHTRs following platelet transfusion are not reliably prevented by the bedside leukocyte filtration of platelet concentrates. In contrast, performing leukodepletion before storage not only removes the leukocytes, but can also markedly reduce the level of cytokines in platelet concentrates.2 The third mechanism of the onset of FNHTRs is relatively more common after the transfusion of platelets than after that of erythrocytes. The adverse reaction is due to the formation of immune complexes of the recipients antibodies with cells or proteins in the blood product, which triggers the recipients immune system to release cytokines. Leukocyte depletion would therefore not prevent FNHTRs that occur due to this mechanism. Refractoriness to platelet transfusion Platelet refractoriness is the repeated failure to obtain satisfactory responses to platelet transfusion and is a common problem for patients receiving multiple transfusions. Platelet refractoriness can arise due to immune or non-immune causes. Non-immune causes can include septicaemia, fever, disseminated intravascular coagulation, and splenomegaly. The main immune cause is HLA alloimmunisation. The development of an immune response to transfused platelets depends mainly on the interaction of the donors transfused antigen-presenting cells (APCs) with the recipients T cells, which then signal the recipients B cells to produce alloantibodies. It has been postulated that removing the donors leukocytes (including APCs: mainly dendritic cells, monocytes, and B lymphocytes) prior to transfusion may reduce the rates of platelet antigen alloimmunisation.

Transfusion-associated graft-versus-host disease

Transfusion-associated graft-versus-host disease (TA-GVHD) occurs when an immunosuppressed or immunodeficient patient receives cellular blood products that possess immunologically competent lymphocytes. The transfused donor lymphocytes are able to proliferate and engraft in the immunologically incompetent recipient because they are unable to detect and reject foreign cells. The degree of similarity between HLA antigens also increases the ability of donor lymphocytes to engraft with the recipient.

Clinical symptoms of TA-GVHD include fever, an erythematous rash that may progress to bullae and desquamation, anorexia, and diarrhea, which develop within 3 to 30 days of receiving cellular blood components Because the hematopoietic progenitor cells (HPCs) in particular are affected, severe cytopenia usually is present. Mild hepatitis to fulminant liver failure may occur.Mortality for TAGVHD is 90% in the pediatric population. Patients at high risk for TA-GVHD include [14] Patients who have congenital immunodeficiencies of cellular immunity Those receiving intrauterine transfusion followed by neonatal exchange transfusion Bone marrow transplant recipients Recipients of HLA-matched cellular components or blood components from blood-related donors Patients who have hematologic malignancies and cancer patients undergoing intense chemotherapy or immunomodulatory therapy (ie, fludarabine and other purine analogs)

A rare but usually fatal complication of transfusion is transfusion-associated graft-versus-host disease (TA-GVHD). The risk associated with an individual transfusion depends on the number and viability of contaminating lymphocytes, the susceptibility of the patients immune system to their engraftment, and the degree of the immunological (HLA) disparity between the donor and recipient. The transfused viable T lymphocytes, under certain circumstances, engraft and proliferate in the recipient. The interaction between donor T lymphocytes and recipient cells bearing either class I or class II HLA antigens results in cellular damage, which may be mediated by natural killer cells. Major target tissues include skin, thymus, gastro-intestinal tract, liver, spleen, and bone marrow. No cases of TAGVHD have been described following the transfusion of frozen deglycerolized cells, cryoprecipitate, fresh frozen plasma, or fractionated plasma products such as clotting factor concentrates, albumin, and intravenous immunoglobulin. But Lymphocyte viability is retained in stored erythrocytes for at least 3 weeks, and cases of TA-GVHD following the transfusion of whole blood, red blood cells, platelets, and granulocytes have been reported. Current filtration technology cannot consistently produce the levels of lymphocyte removal required. The current mainstay of preventing lymphocyte proliferation continues to be gamma irradiation. The recommended minimum dose to prevent TA-GVHD is 25 Gy. Generalised immunosuppression after transfusion Allogeneic blood transfusions produce a variety of effects on the recipients immunological functions, such as the decreased function of natural killer cells, macrophage migration to sites of injury, lymphocyte proliferation, and cutaneous delayed hypersensitivity. The presence of donor leukocytes in allogeneic blood may play a role in suppressing cellular immune function. Graft rejection rates after organ transplantation The sensitisation of an individual to transplantation antigens by preceding transfusions can lead to graft rejection after organ transplantation. Allogeneic blood containing leukocytes has been shown to have an adverse effect in patients with aplastic anaemia who undergo bone marrow transplantation34 and in renal transplant patients. The sensitisation to transplantation antigens can potentially be prevented by leukodepleting blood components that are to be used in pretransplantation transfusions.

Dosage calculations of various components

component Dose calculation

Rbc conc.

Dose calculation for packed red cell transfusion is: desired rise in haemoglobin (in grams per dL) x weight x 3 (usually 10-20 mls/kg).


Dose calculation for platelet transfusion is 10-20 mls/kg for children weighing less than 15 kg. Children weighing more than 15 kg should receive a single apheresis unit. Dose calculation for FFP is 10-20 mls/kg.


cryoprecipitate Dose calculation for cryoprecipitate is 5-10 mls/kg. Whole blood