MM/DD/2020

10:00-12:00 W Transfusion Biology and Therapy

7:30-9:30 F Medicine II
LDT Hehehe, M.D.

OUTLINE ABO ANTIGENS AND ANTIBODIES

I. Blood Group Antigens and Antibodies ABO Antigen

II. ABO Antigens and Antibodies
III. RH System  First blood group antigen system recognized in 1900 and is the
IV. Other Blood Group Systems and Alloantibodies most important in transfusion medicine
V. Pretransfusion Testing  Major blood groups of ABO: A, B, AB, & O
VI. Blood Components  Type O RBCs
VII Adverse Reaction to Transfusion o Lack A or B antigens
VIII. Immune-Mediated Reactions o These are carbohydrates attached to a precursor backbone,
IX. Nonimmunologic Reactions found on cell membrane either as glycosphingolipids or
X. Alternatives to Transfusion glycoproteins, and secreted into plasma and body fluids as
XI. Source glycoproteins
XII. Appendix  H substance
o Immediate precursor on which A and B antigens are added
BLOOD GROUP ANTIGENS AND ANTIBODIES o Formed by the addition of fucose to the glycolipid or
glycoprotein backbone
Antigens o Addition of N-acetylgalactosamine creates A antigen
o Addition of galactose creates B antigen
 Antigen systems important in transfusion medicine:  Rare individuals lack the H gene, thus, cannot form H substance.
o Red blood cells These individuals are homozygous for the silent h allele (hh) and
Along with its antibodies, form the foundation of have Bombay phenotype (O h )
transfusion medicine  Genes that determine A and B phenotypes are found on
Antigens are assigned to a blood group system based on chromosome 9p and are expressed in a Mendelian codominant
the structure and similarity of the determinant epitopes manner. Gene products are glycosyl transferases
o Platelets
Along with plasma proteins, are also antigenic and result Blood type
in alloimmunization ( production of)
o Neutrophil O
o Human Leukocyte Antigens
AB
Antibodies

 Antibodies ABO Antibodies

o Alloantibodies: antibodies directed against antigenic
determinants of another individuals  This blood group is important because all individuals produce
Anti-RBC antibodies antibodies to the ABH carbohydrate antigen that they lack
are usually produced by T cell-independent response and  Isoagglutinins: naturally occurring anti-A and anti-B antibodies
are mainly IgM isotype
Anti-human platelet antigens (HPA) antibodies Blood type Antibody produced
Anti-human leukocytes antigen (HLA) antibodies
o Recipient alloimmunization to leukocytes, platelets, and O Anti-A & Anti-B
plasma proteins may result in transfusion complications
such as fevers, urticaria, and platelet transfusion A Anti-B
refractoriness but does not cause hemolysis
o Autoantibodies: antibodies against autologous blood group B Anti-A
antigens. Arise spontaneously or as the result of infectious
AB
sequelae and are also often IgM
IgM IgG
 Persons with type AB are considered
Low affinity for antigen Autoimmune; commonly bind antigen at with regards to RBC transfusion because they do not have
at body temperature warmer temperature antibodies against any ABO phenotype
 Persons with type O can donate essentially to all recipients
Cannot cross placenta; Cross the placenta and bind to fetal because their cells are not recognized by any ABO
Activate complement erythrocytes resulting in hemolytic isoagglutinins
cascade and results in disease of the newborn or hydrops  The rare individuals with Bombay phenotype produce antibodies to
hemolysis fetalis; when directed against HPA H substance ( which is present on all red cells except those of hh
antigens on platelets can lead to fetal or phenotype) as well as to both A and B antigens and are therefore
neonatal immunization and result in compatible only with other hh donors
intracranial hemorrhage

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  In most people (80%), A, B, and H antigens are secreted by the o The branching process affects all the ABH antigens, which
cells and are present in the circulation as well as in various become progressively more branched in the first 2 years of
secretions such as saliva (Se phenotype) life
 o Most adults lack i expression
antigens (se phenotype) o Even though most adults express I antigen, binding is
 ABO and Se/se systems influence the susceptibility to a variety generally low at body temperature
of diseases
P System
RH SYSTEM
 P system is another group of carbohydrate antigens controlled
 The second most important blood group system in. by specific glycosyltransferases
pretransfusion testing o P antigen is also the target of autoantibodies in diseases
 Rh antigens are found on a 30- to 32-kDa RBC membrane such as syphilis and viral diseases in children, and can
protein that has no defined function result in paroxysmal cold hemoglobinuria ( an autoantibody
 Five determinants account for the vast majority of phenotypes: to P binds to RBCs in the cold and fixes complement upon
o The two RH genes are located on chromosome 1: RHD that warming)
codes for RhD protein expressing D antigen & RHCE that o P antigen is the cellular receptor of parvovirus B19 and also
codes for RhCE proteins expressing C and/or c, and E may be a receptor for Escherichia coli binding to urothelial
and/or e antigens cells
Presence of D antigen confers and o Antibodies with these biphasic properties are called
persons who lack of D Donath-Landsteiner antibodies
Determine eight main haplotypes (DCe, DcE, Dce, DCE,
dce, dCe, dcE, and dCE) whose frequencies differ MNS System
among different populations
D antigen is a potent alloantigen  MNS system is regulated by genes on chromosome 4
 Exposure of these Rh-negative people to even small amounts of o M and N are determinants on glycophorin A
Rh-positive cells, by either transfusion or pregnancy, can result o S and s are determinants on glycophorin B
in the production of anti-D alloantibody  Anti-S and anti-s IgG antibodies may develop after
pregnancy or transfusion and lead to hemolysis.
OTHER BLOOD GROUP SYSTEMS AND ALLOANTIBODIES o Glycophorin B expresses a public antigen named U
 Anti-U antibodies can occur in the rare individuals lacking
 The presence or absence of certain antigens has been the U antigen
associated with various diseases and anomalies; antigens also
act as receptors for infectious agents Kell System
 Alloantibodies of importance in routine clinical practice
 See appendix  Kell protein is very large (720 amino acids), and its secondary
structure contains many different antigenic epitopes.
Lewis System o The immunogenicity of Kell is third behind the ABO and Rh
systems
 Antibodies to Lewis system carbohydrate antigens are the o Linked to another blood group protein termed Kx
most common cause of incompatibility during pretransfusion The rare absence of this protein ( controlled by a gene on
screening X) is associated with weak KEL antigen, acanthocytosis,
o Lewis gene product is a fucosyl transferase and maps to shortened RBC survival, and a progressive form of
chromosome 19 muscular dystrophy that includes cardiac defects
McLeod phenotype
Lewis Antigen Lewis Antibody Kx gene is linked to the 91-kDa component of the
NADPH-oxidase on the X chromosome, deletion or
Not an integral membrane IgM and cannot cross mutation of which accounts for about 60% of cases of
structure but is adsorbed to the placenta chronic granulomatous disease
the RBC membrane from the
plasma Duffy System

Adsorbed onto tumor cells  Duffy antigens are codominant alleles, Fy a and Fy b, that also
and may be targets of serve as receptors for Plasmodium vivax
therapy o More than 70% of persons in sub-Saharan Africa lack these
antigens probably from selective influences of malaria
infection on the population
I System o Lack of the Duffy antigen receptor for cytokines (DARC) is
associated with mild neutropenia
 I system antigens are also oligosaccharides related to H, A, B,
and Le Kidd System
 I and i are not allelic pairs but are carbohydrate antigens that
differ only in the extent of branching  Kidd antigens, Jk a and Jk b, may elicit antibodies transiently.
o The i antigen is an unbranched chain that is converted by  A delayed hemolytic transfusion reaction (DHTR) that occurs
the I gene product, a glycosyltransferase, into a branched with blood tested as compatible is often related to delayed
chain appearance of anti-Jk a

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 PRETRANSFUSION TESTING o Plasma as well as RBCs and granulocytes may also be
collected
 Pretransfusion testing of a potential recipient consists of the  Plasma-derived products such as albumin, intravenous
type and screen immunoglobulin, antithrombin, and coagulation factor
 determines the ABO and Rh phenotype of the concentrates are prepared from pooled plasma from many
donors
D antigens
 Whole Blood
should correlate with the ABO phenotype, or forward type
 Provides both oxygen-carrying capacity and volume expansion
Alloantibody Screen  The ideal component for patients who have sustained acute
hemorrhage of ≥25% total blood volume loss
 Identifies antibodies directed against other RBC antigens  Stored at 4°C to maintain erythrocyte viability, but platelet
 Performed by mixing patient serum with type O RBCs that dysfunction and degradation of some coagulation factors occur
contain the major antigens of most blood group systems and o Storage problem: fall of 2,3-biphosphoglycerate overtime
whose extended phenotype is known leading to increase in oxygen affinity of hemoglobin and
 The specificity of the alloantibody is identified by correlating the decreased delivery capacity of oxygen to tissues
presence or absence of antigen with the results of the  It is not readily available
agglutination
Packed RBCs
Cross Matching
 This product increases oxygen-carrying capacity in the anemic
 Ordered when there is a high probability that the patient will patient
require a packed RBC (PRBC) transfusion  PRBC are stored in additive solution up to 35 42 days at 4°C
 Blood selected for cross-matching must be ABO compatible and  Adequate oxygenation can be maintained with a hemoglobin
lack antigens for which the patient has alloantibodies content of 70 g/L in the normovolemic patient without cardiac
 Nonreactive cross-matching confirms the absence of any major disease
incompatibility and reserves that unit for the patient  The decision to transfuse should be guided by the clinical
 In the case of Rh (D) -negative patients, every attempt must be situation and not by an arbitrary laboratory value
made to provide Rh-negative blood components to prevent  In most patients requiring transfusion, levels of hemoglobin of
alloimmunization to the D antigen 80 g/L are sufficient to keep oxygen supply from being critically
 In an emergency, Rh-positive blood can be safely transfused to low
an Rh-negative patient who lacks anti-D  Majority of cellular blood products are now leukocyte-reduced
 Rh-negative women of childbearing age who are transfused and universal pre-storage leukocyte reduction has been
with products containing Rh-positive RBCs should receive recommended
passive immunization with anti-D ( RhoGam or WinRho) to o PRBC units contain <1 to 5.106 donor leukocytes, and their use
reduce or prevent sensitization lowers the incidence of posttransfusion fever and chills,
cytomegalovirus (CMV) infections, and alloimmunization
BLOOD COMPONENTS  Patients with hemoglobinopathies such as sickle cell disease
may undergo RBC exchange, an apheresis procedure by which
 Blood products intended for transfusion are routinely collected sickled RBCs are replaced by donor RBCs
as whole blood (450 mL) in various anticoagulants
 Most donated blood is processed into components: Platelets
o PRBCs
o Platelets  Thrombocytopenia is a risk factor for hemorrhage, and platelet
o Fresh-frozen plasma (FFP) or cryoprecipitate trans- fusion reduces the incidence of bleeding
 Whole blood can be first separated into PRBCs and platelet-rich  Platelets are stored in plasma or in additive solution up to 5 7
plasma by slow centrifugation days at 20 24°C and under permanent motion
o Platelet-rich plasma is then centrifuged at high speed to  Threshold for prophylactic platelet transfusion is 10,000/μL. In
yield one unit of random donor (RD) platelets patients without fever or infections, a threshold of 5000/μL may
( subsequently pooled ) and one unit of FFP be sufficient to prevent spontaneous hemorrhage. For invasive
 Alternatively, whole blood can undergo high speed procedures, 50,000/μL platelets is the usual target level
centrifugation to separate a P -  Platelets are given either as pools of 4 to 6 prepared RDs or as
containing leukocytes and platelets SDAPs from a single donor
o The buffy coat then undergoes pooling and is centrifuged at  In an unsensitized patient without increased platelet
low speed to produce pooled platelets consumption two units of transfused RD per square-meter body
o Leukocyte level of blood products can be lowered by an surface area (BSA) is anticipated to increase the platelet count
additional filtration step after which they are referred to as by ~10,000/uL
leukoreduced (or leukodepleted) (<1 to 5 × 106 leukocytes  Patients who have received multiple transfusions may be
per product) alloimmunized to many HLA- and platelet-specific antigens and
 Apheresis technology is used for the collection of multiple units have little or no increase in their posttransfusion platelet
of platelets from a single donor counts
o Contain the equivalent of at least five units of RD platelets o Best served by receiving leukocyte-reduced components
and before eventual leukoreduced, have fewer to lower the risk of alloimmunization
contaminating leukocytes than pooled RD platelets  Refractoriness to platelet transfusion may be evaluated using the
corrected count increment (CCI):

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  anti-A or anti-B antibodies: responsible for the majority of these
reactions
 Alloantibodies directed against other RBC antigens, i.e., Rh, Kell,
and Duffy, are responsible for fatal hemolytic transfusion
o Refractoriness can be investigated by detecting anti-HLA reactions as well
anti-  Clinical Presentation: hypotension, tachypnea, tachycardia,
fever, chills, hemoglobinemia, hemoglobinuria, chest and/ or
Fresh Frozen Plasma flank pain, and discomfort at the infusion site
 Monitoring the
 Contains stable coagulation factors and plasma proteins: transfusion is important to identify reactions promptly
o Fibrinogen  When acute hemolysis is suspected
o Antithrombin
o Transfusion must be stopped immediately
o Albumin
o Intravenous access maintained
o Proteins C and S
 Indications for FFP include correction of coagulopathies, o Reaction reported to the blood bank
including:  Laboratory evaluation for hemolysis
o Rapid reversal of warfarin o measurement of serum haptoglobin
o Supplying deficient plasma proteins o lactate dehydrogenase (LDH)
o IgA-deficient o Indirect bilirubin levels
o Treatment of auto-antibody-mediated thrombotic  The immune complexes that result in RBC lysis can cause renal
thrombocytopenic purpura (TTP) dysfunction and failure
Therapeutic plasma exchange allows both the removal of  Diuresis: induced with intravenous fluids and furosemide or
the autoantibody and the supplementation of the depleted mannitol
enzyme (ADAMTS13)  Tissue factor released from the lysed erythrocytes may initiate
 Should not be routinely used to expand blood volume
DIC
 FFP is an acellular component and does not transmit intracellular
 Coagulation studies should be monitored
infections, e.g., CMV.
 Pre-thawed or never frozen plasma as well as freeze-dried o Prothrombin time (PT)
plasma are increasingly used to insure immediate availability o Activated partial thromboplastin time (aPTT)
when required o Fibrinogen
o Platelet count
Cryoprecipitate  Errors such as mislabeling the sample or transfusing the wrong
patient, are responsible for the majority of these reactions
 A source of fibrinogen, factor VIII, and von Wille- brand factor  Blood bank investigation
(vWF) o Examination of the pre- and posttransfusion samples for
 It is ideal for supplying fibrinogen to the volume- sensitive patient hemolysis
 Each unit contains ~80 units of factor VIII o Repeat typing of the patient samples
 May also supply vWF to patients with dysfunctional (type II) or o Direct antiglobulin test (DAT) aka direct Coombs test:
absent (type III) von Willebrand disease detects the presence of antibody or complement bound to
RBCs in vivo
Plasma Derivatives
o Repeating the cross-matching of the blood component
o Checking all clerical records for errors
 Plasma from thousands of donors may be pooled to derive
specific protein concentrates, including albumin, intravenous
Delayed Hemolytic and Serologic Transfusion Reactions
immunoglobulin, antithrombin, and coagulation factors
 Donors who have high-titer antibodies to specific agents or
antigens provide hyperimmune globulins, such as anti-D  Not completely preventable
(RhoGam, WinRho), and antisera to hepatitis B virus (HBV),  Occur in patients previously sensitized to RBC alloantigens who
varicella-zoster virus, CMV, and other infectious agents have a negative alloantibody screen due to low antibody levels
 Anamnestic response: results in the early production of
ADVERSE REACTION TO BLOOD TRANSFUSION alloantibody that binds donor RBCs when the patient is
 transfused with antigen-positive blood, an
 The most common reactions are not life threatening, although  The alloantibody is detectable 1 2 weeks following the
serious reactions can present with mild symptoms and signs transfusion
 Blood product pathogen reduction is an option for platelets and  Posttransfusion DAT may become positive due to circulating
plasma, and underway for whole blood and PRBC donor RBCs coated with antibody or complement
 When an adverse reaction is suspected, the transfusion should  The transfused, alloantibody-coated erythrocytes are cleared by
be stopped and reported to the blood bank for investigation
the reticuloendothelial system
 No specific therapy is usually required, although additional RBC
IMMUNE MEDIATED REACTIONS
transfusions may be necessary
 Delayed serologic transfusion reactions are similar to DHTR, as
Acute Hemolytic Transfusion Reactions
the DAT is positive and alloantibody is detected; however, RBC
clearance is not increased
 Recipient has preformed antibodies that lyse donor erythrocytes

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 Febrile Nonhemolytic Transfusion Reaction o Fever
o Characteristicc cutaneous eruption
 Most frequent reaction associated with the transfusion of cellular o Diarrhea
blood components o Liver function abnormalities
 Characterized by chills and rigors and a ≥1°C rise in  Can also occur when blood components that contain viable T
temperature lymphocytes are transfused to immunodeficient recipients or to
 Diagnosed when other causes of fever in the transfused patient immunocompetent recipients who share HLA antigens with the
are ruled out donor (e.g., a family donor)
 Mediators:  Transfusion-associated GVHD (TA-GVHD) is characterized by
o Antibodies directed against donor leukocyte and HLA marrow aplasia and pancytopenia
antigens  TA-GVHD is highly resistant to treatment with immunosuppres-
 Multiply transfused patients and multiparous women are sive therapies, including glucocorticoids, cyclosporine,
felt to be at increased risk antithymocyte globulin, and ablative therapy followed by
o Cytokines released from leukocytes within stored blood allogeneic bone marrow transplantation
components  Clinical manifestations appear at 8 10 days, and death occurs at
 leukoreduction before storage may prevent these 3 4 weeks posttransfusion.
reactions  TA-GVHD can be prevented by irradiation of cellular
o Cytokines and chemokines released from platelets components (minimum of 2500 cGy) before transfusion to
components, released during storage may also mediate patients at risk
FNHTR  Pathogen inactivation technologies have shown to prevent TA-
 Investigation is not routinely done because of the mild nature of GVHD as well
most FNHTRs  Patients at risk for TA-GVHD:
 Leukocyte-reduced blood products may prevent or delay o Fetuses receiving intrauterine transfusions
sensitization to leukocyte antigens and thereby reduce the o Selected immunocompetent (e.g., lymphoma patients) or
incidence of these febrile episodes immunocompromised recipients
o Recipients of donor units known to be from a blood relative
Anaphylactic Reaction o Recipients who have undergone marrow transplantation
 Directed donations by family members should be discouraged
 Severe allergic reaction presents after transfusion of only a few (they are not less likely to transmit infection); lacking other
milliliters of the blood component options, the blood products from family members should
 Symptoms and signs: always be irradiated
o Difficulty breathing
o Coughing Transfusion-Related Lung Injury (TRALI)
o Nausea and vomiting
o Hypotension  Among the most common cause of transfusion related fatalities
o Bronchospasm  Recipient develops symptoms of hypoxia (PaO2/FiO2 < 300
o Loss of consciousness mmHg) and signs of noncardiogenic pulmonary edema,
o Respiratory arrest including bilateral interstitial infiltrates on chest x-ray, either
o Shock during or within 6 h of transfusion
 Treatment includes:  Treatment is supportive, and patients usually recover without
o Stopping the transfusion sequelae
o Maintaining vascular access  TRALI usually results from the transfusion of donor plasma that
o Administering epinephrine (0.5 1 mL of 1:1000 dilution contains high-titer anti-HLA class II antibodies that bind
subcutaneously) recipient leukocytes
o Glucocorticoids may be required in severe cases  Anti-HLA class I and anti-human neutrophil antigen (HNA)
 IgA-deficient patients antibodies can be involved as well
o <1% of the population  Leukocytes aggregate in the pulmonary vasculature and release
o May be sensitized to this Ig class and are at risk for mediators that increase capillary permeability
anaphylactic reactions associated with plasma transfusion  -HLA antibodies can support
o Severe IgA-deficient patients should receive only IgA- this diagnosis
deficient plasma and washed cellular blood components  Implicated donors are frequently multiparous women
 Patients who have anaphylactic or repeated allergic reactions to  Transfusion of plasma and platelets from male and nulliparous
women donors reduces the risk of TRALI
blood components should be tested for IgA deficiency
 Recipient factors that are associated with increased risk of
TRALI include
Graft-Versus-Host Disease
o Smoking
o Chronic alcohol use
 A frequent complication of allogeneic stem cell transplantation o Shock
 Lymphocytes from the donor attack and cannot be eliminated by o Liver surgery (transplantation)
an immunodeficient host. o Mechanical ventilation with >30 cm H 20 pressure support
 Mediated by donor T lymphocytes that recognize host HLA o Positive fluid balance.
antigens as foreign and mount an immune response
 Clinical manifestations:

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 Posttransfusion Purpura  Use of fresh or washed RBCs, are preventive measures warranted
for neonatal transfusions because this complication can be fatal
 Presents as thrombocytopenia 7 10 days after platelet  Citrate: commonly used to anticoagulate blood components,
transfusion chelates calcium and thereby inhibits the coagulation cascade
 Occurs predominantly in women  Hypocalcemia, manifested by circumoral numbness and/or
 Platelet-specific antibodies are found in the recipient tingling sensation of the fingers and toes, may result from
 HPA-1a: the most frequently recognized antigen, found on the multiple rapid transfusions
platelet glycoprotein IIIa receptor  Calcium infusion is seldom required in this setting because
 The delayed thrombocytopenia is due to the production of citrate is quickly metabolized to bicarbonate
antibodies that react to both donor and recipient platelets  If calcium or any other intravenous infusion is necessary, it must
 Additional platelet transfusions can worsen the be given through a separate line
thrombocytopenia and should be avoided
 Treatment with intravenous immunoglobulin may neutralize the Iron Overload
effector antibodies, or plasmapheresis can be used to remove
the antibodies.  Signs of iron overload affecting endocrine, hepatic, and cardiac
function are common after 100 units of RBCs have been
Alloimmunization transfused (total-body iron load of 20 g)
 Preventing this complication by using alternative therapies (e.g.,
 Alloantibodies to RBC antigens are detected during pretrans- erythropoietin) and judicious transfusion is preferable and cost
fusion testing, and their presence may delay finding antigen- effective
 Chelating agents, such as deferoxamine and deferasirox, are
negative cross-match-compatible products for transfusion
 Women of childbearing age who are sensitized to certain RBC available, but the response though is often suboptimal
antigens (i.e., D, c, E, Kell, or Duffy) are at risk for bearing a fetus
with hemolytic disease of the newborn Hypotensive Reactions
 Matching for RBC antigen is the only pretransfusion selection
test to prevent RBC alloimmunization.  Transient hypotension may be noted among transfused patients
 Alloimmunization to antigens on leukocytes and platelets can who take angiotensin-conv erti ng enzyme (ACE) inhibitors
result in refractoriness to platelet transfusions  Since blood products contain bradykinin that is normally
 Once alloimmunization has developed, HLA-compatible platelets degraded by ACE, patients on ACE inhibitors may have
increased bradykinin levels that cause hypotension in the
from donors who share similar antigens with the recipient may be
recipient
difficult to find
 Blood pressure typically returns to normal without intervention
 Prudent transfusion practice directed at preventing sensitization
o Leukocyte-reduced cellular components
Immunomodulation
o Limiting antigenic exposure by the judicious use of
transfusions and use of SDAPs
 Transfusion-related immunomodulation is thought to be
mediated by transfused leukocytes
NONIMMUNOLOGIC REACTIONS  Leukocyte-depleted cellular products may cause less
immunosuppression, though controlled data are unlikely to be
Fluid Overload obtained as the blood supply becomes universally leukocyte-
depleted
INFECTIOUS COMPLICATIONS
 Dyspnea with O 2% <90 on room air, bilateral infiltrates on CXR
with systolic hypertension are found with transfusion-associated Viral Infections
circulatory overload (TACO)
 Brain natriuretic peptide (BNP) is often elevated (>1.5) that of  Hepatitis C Virus
pre-transfusion levels o Blood donations are tested for antibodies to HCV and HCV
 Monitoring the rate and volume of the transfusion and using a RNA
diuretic can minimize this problem o Risk of acquiring HCV through transfusion is now calculated
to be 0,1 to 1 in 1,000,000 units
Hypothermia o Infection with HCV may be asymptomatic or lead to chronic
active hepatitis, cirrhosis, and liver failure
 Refrigerated (4°C) or f  Human Immunodefici ency Virus Type 1
can result in hypothermia when rapidly infused o Donated blood is tested for antibodies to HIV-1, HIV-1 p24
 Cardiac dysrhythmias can result from exposing the sinoatrial antigen, and HIV RNA using NAT
node to cold fluid o Risk of HIV-1 infection per transfusion episode is 0,1 to 1 in
 In-line warmer will prevent this complication 1 million
 Hepatitis B Virus
Electrolyte Toxicity
o Donated blood is screened for HBV using assays for
 RBC leakage during storage increases the concentration of hepatitis B surface antigen (HbsAg) most combined with
potassium in the unit NAT testing
 At risk for hyperkalemia: Neonates and patients in renal failure

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 o Risk of transfusion-associated HBV infection is several times o Onset of symptoms and signs is often sudden and
greater than for HCV fulminant, which distinguishes bacterial contamination from
 Other Hepatitis Viruses an FNHTR
o Hepatitis A virus: rarely transmitted by transfusion; infection o Reactions, particularly those related to gram-negative
is typically asymptomatic and does not lead to chronic contaminants, are the result of infused endotoxins formed
disease within the contaminated stored component
o Hepatitis E (HEV): can be transmitted by transfusion and o When these reactions are suspected, the transfusion must
may lead to chronic disease be stopped immediately
 Cytomegalovirus o Therapy is directed at reversing any signs of shock, and
o Infects ≥50% of the general population broad-spectrum antibiotics should be given
o T
transfused PRBCs or platelet components Other Infectious Agents
o Groups at risk: immunosuppressed patients, CMV-
seronegative transplant recipients, and neonates and  Various parasites that can be transmitted by blood transfusion
should receive leukocyte-depleted components or CMV include those causing
seronegative products o Malaria
 Human T Lymphotropic Virus (HTLV) Type 1 o Babesiosis
o Assays to detect HTLV-I and -II are used to screen all o Chagas disease
donated blood o Dengue
o associated with adult T cell leukemia/lymphoma and o Zika
tropical spastic paraparesis in a small percentage of o Variant Creutzfeldt-Jakob disease
infected persons Risk of transfusion-mediated HTLV-1 o Anaplasma phagocytophilum
infection is further mitigated by blood product o yellow fever vaccine virus
leukoreduction  Tests for some pathogens are available ( Trypanosoma cruzi)
o HTLV-II is not clearly associated with any disease  Others are being developed (Babesia microti)
 Parvovirus B-19
o Blood components and pooled plasma products can ALTERNATIVES TO TRANSFUSION
transmit this virus
 Autologous blood remains an option when transfusion is
o Shows tropism for erythroid precursors and inhibits both
anticipated
erythrocyte production and maturation
 Additional methods of autologous transfusion in the surgical
o Pure red cell aplasia, presenting either as acute aplastic patient include
crisis or chronic anemia with shortened RBC survival, may o Preoperative hemodilution
occur in individuals with an underlying hematologic disease, o Recovery of shed blood from sterile surgical sites
such as sickle cell disease or thalassemia o Postoperative drainage collection
o The fetus of a seronegative woman is at risk for developing  Directed or designated donation from friends and family of the
hydrops from this virus potential recipient has not been safer than volunteer donor
component transfusions
Bacterial Contamination o At higher risk for complications such as GVHD and
alloimmunization
 PRBCs and FFP are not common sources of bacterial  Granulocyte and granulocyte-macr op hag e colony-stimulati ng
contamination factors are clinically useful to hasten leukocyte recovery in
 Some gram-negative bacteria can grow at 1° to 6°C have been patients with leukopenia related to high-dose chemotherapy
 Erythropoietin
implicated in infections related to PRBC transfusion
o Stimulates erythrocyte production in patients with anemia of
 Yersinia, Pseudomonas , Serratia, Acinetobacter , and
chronic renal failure and other conditions, thus avoiding or
Escherichia species.
reducing the need for transfusion
 Platelet concentrates stored at room temperature, are more o Can also stimulate erythropoiesis in the autologous donor to
likely to contain skin contaminants such as gram-positive enable additional donation
organisms, including coagulase-negativ e staphylococci  Gene therapy approaches in patients with sickle cell or major
 It is estimated that 1 in 1000 2000 platelet components is con- thalassemia offers the potential of dramatically reducing their
taminated with bacteria. transfusion needs
 Risk of death due to transfusion-associated sepsis is estimated  Stem cell-derived blood cells such as RBCs or platelets may in
to be in the order of 1 in 200,000 400,000 platelets products the future become a suitable alternative to very rare blood donors
 Pathogen-reduced platelets have been available and offer an  Patient blood management programs can improve the
alternative to prevent transfusion-transmitted bacterial infection therapeutic index of transfusion medicine
 Recipients of transfusion contaminated with bacteria may
SOURCES
develop fever and chills, which can progress to septic shock
and DIC

o May occur abruptly, within minutes of initiating the
transfusion, or after several hours

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