Award Lectures and Special Reports
Special Report: Transfusion Risks
RICHARD H. WALKER, M.D.
The benefits of blood transfusion must be considered and evaluated in terms of risk factors relating to the adverse effects of
transfusion. Transfusions may result in either serious or troublesome complications. Although the risk of transfusion-associated acquired immune deficiency syndrome (AIDS) is of paramount concern in the patient population, it has been virtually
eliminated because of testing of donor units for antibody to
human immunodeficiency virus. Serious and troublesome adverse effects of blood transfusion are listed and ranked in order
of approximate frequency. About 20% of all transfusions result
in some type of adverse effect. The major serious risk of blood
transfusion today continues to be transfusion-associated viral
hepatitis. This entity is usually subclinical but frequently results in serious chronic liver disease. Transfusions should be
avoided unless patient care would be compromised if withheld.
(Key words: Blood transfusion; Adverse effects) Am J Clin
Pathol 1987; 88: 374-378
BLOOD TRANSFUSIONS provide a vital therapeutic
modality, but they may be associated with adverse effects in some recipients. Although most of such complications are clinically occult, they can be serious in terms
of outcome. The most common of the serious risks continues to be viral hepatitis. Until recently, 1-2% of all
transfused units resulted in transfusion-associated viral
hepatitis despite the use ofan all-volunteer donor source
and testing for the hepatitis B surface antigen (HBsAg).
Although posttransfusion hepatitis is usually subclinical,
about 50% of these patients have chronic active hepatitis
or chronic persistent hepatitis develop and approximately 10% progress to cirrhosis.2
In the summer and fall of 1986, blood banks instituted testing of blood donor units for antibody to hepatitis B core antigen (anti-HBc) and/or alanine aminotransferase (ALT), using positive or abnormal results as
indirect indicators (surrogate markers) for the virus(es)
of non-A, non-B hepatitis. Available information suggests that elimination of donor units with positive results for anti-HBc and elevated ALT will reduce the
incidence of posttransfusion hepatitis by about
40-50%. 23
Received September 23, 1986; received revised manuscript and accepted for publication December 8, 1986.
Address reprint requests to Dr. Walker: William Beaumont Hospital, Royal Oak, Michigan 48072.
William Beaumont Hospital, Royal Oak, Michigan
Current known transfusion risks are listed in Table 1.
The frequency estimates are approximations that are
subject to wide variation, depending upon the source of
the donor population, the diligence and careful observations of the blood bank laboratory staff members and
transfusion service, the mix of blood and blood components used, the accuracy of reporting, and the recipient
population.
Approximately 20% of all transfusions result in some
adverse effect in the recipient. No patient should be denied a transfusion if it is clearly indicated, but transfusions should be avoided if safe alternatives exist.
Comments
(1) Clinical icteric hepatitis is quite uncommon after
transfusion, but until recently 5-6% of all blood recipients (the usual recipient receives 3-4 units) had subclinical/anicteric posttransfusion hepatitis develop, as documented by abnormal liver function tests and liver
biopsy. 1 ' 2 - 417,19 - 23 " Only about 10-20% of these cases
are result from the hepatitis B virus.3 Eighty to 90% are
non-A, non-B hepatitis. Chronic hepatitis follows in
about half of these patients, and approximately 10%
have cirrhosis develop.2 Since the implementation of
testing donor units for anti-HBc and ALT (the surrogate
markers for non-A, non-B hepatitis virus carriers) in the
summer and fall of 1986, the risk of posttransfusion
hepatitis is now estimated to be about 1 in 200 transfusions, or 1-2% of recipients, but data are not available
yet for a reliable estimate. 23 The incubation period for
posttransfusion hepatitis is 2-26 weeks after transfusion.
(2) Circulatory overload is often unrecognized as a
sequela of blood transfusion. It is more common in infants and in adults older than the age of 60. The onset
may be delayed for up to two hours after transfusion.
This complication can be minimized by the use of red
blood cells rather than whole blood and by the control of
the rate of transfusion.
374
AWARD LECTURES AND SPECIAL REPORTS
Vol. 88 • No. 3
375
Table 1. Adverse Effects of Blood Transfusions
Approximate Frequency*
Adverse Effects
Ratio
Percentage
Serious adverse effects
Viral hepatitis (clinical and subclinical cases)
Circulatory overload
Acute lung injury
Acute hemolytic transfusion reactionf
Anaphylactic hypotensive reaction
Hemosiderosis!
Hemostatic defect:):
Hypothermia^
Bacterial/endotoxin reaction
1 in
200
1 in 10,000
1 in 10,000
1 in 25,000
1 in 150,000
Unknown
Unknown
Unknown
Rare
0.5000
0.0100
0.0100
0.0040
0.0007
Malaria and other parasitic
infections
Graft versus host disease
Acquired immune deficiency syndrome
Total
Troublesome adverse effects
Depression of erythropoiesisf
Leukocyte and/or platelet alloimmunization
Cytomegalovirus seroconversion
Red blood cell alloimmunization!
Epstein-Barr virus seroconversion
Febrile non-hemolytic reaction§
Allergic reaction§
Nonspecific (chill) reaction§
Delayed hemolytic reactionf
Metabolic abnormalities^
Immunologic alterations
Posttransfusion purpura
Total
Rare
Rare
Rare
(3) Acute lung injury or noncardiogenic pulmonary
edema has only recently been recognized as a problem.
It may be the result of the release of biologically active
complement components that mediate inflammation,
causing leukostasis and increased capillary permeability
in the lungs. This phenomenon may be triggered by
leukoagglutinins in the donor plasma.
(4) Acute hemolytic transfusion reactions usually result from a clerical error, resulting in ABO incompatibility, which leads to intravascular hemolysis of the
donor's cells. Immediate hemoglobinemia and hemoglobinuria follow. The reaction often results in disseminated intravascular coagulation. Management consists
of the immediate use of large volumes of intravenous
Ringer's lactate with mannitol and/or furosemide to
achieve a urinary output of at least 100 mL/hour. An
immediate check should be made to be certain that another patient is not also in imminent danger of receiving
the wrong blood because of the same clerical error.
(5) Approximately 1 in 600 persons are deficient in
IgA. Such persons may react to the IgA present in donor
plasma. Reactions have also been attributed to allotypic
differences in IgA types of the recipient and the donor.28
These reactions usually occur immediately after the start
References
1-4.17.19.23,33
40.41
29.40.41
35.40.41
28.40,41
25
8.31
25
26.34,39
34
6
5.7.15.18.22,43
0.5247
Frequent
1 in
10
7 in 100
1 in 100
1 in 200
1 in 200
1 in 1,000
1 in 1,000
1 in 2,500
Unknown
Unknown
Rare
* Frequency given as risk per unit transfused.
t Red blood cell components only.
1
2
3
4
5
6
7
8
9
10
11
12
1 in 190
1 in 5
Comments
10.0000
7.0000
1.0000
0.5000
0.5000
0.1000
0.1000
0.0400
13
14
15
16
17
18
19
20
21
22
23
24
13
10.32
30.36,42
14,24
16
37,40,41
11.38.40.41
40.41
35.40.41
9,20
21,27
12
19.2400
t Massive transfusions only.
§ Common clinical reactions recognized in 2-3% of all recipients.
of the transfusion and can be avoided in patients known
to have this problem by the use of frozen thawed red
blood cells that have had extended washing.
(6) Each unit of red blood cells or whole blood contains about 250 mg of iron. Repeated transfusions in the
nonbleeding patient can result in excessive deposition of
storage iron, which may be harmful in some patients.
(7) Massive transfusion is often associated with diffuse
microvascular hemorrhage and frank uncontrollable
"oozing" from multiple cut surfaces, venipuncture sites,
and mucosal surfaces. The most common cause of this
problem is thrombocytopenia secondary to dilution, but
disseminated intravascular coagulation may also complicate the clinical picture.
(8) The rapid infusion of cold bank blood in massive
transfusions can lower the body temperature and induce
cardiac arrhythmia. Most routine transfusions should be
given with the use of cold bank blood, but with massive
transfusions the blood should be warmed with a controlled in-line warming device.
(9) Cold-loving bacteria, psychrophiles, can survive
and multiply in cold stored bank blood. Their lipopolysaccharide cell wall is pyrogenic and can induce endotoxin shock, which is associated with a very high mortal-
376
WALKER
ity rate. There are isolated case reports of bacteremic
shock resulting from contaminated bank blood.26
(10) The risk of malaria, Chagas' disease, filariasis,
toxoplasmosis, and babesiosis is miniscule because of
the use of donor blood drawn from healthy North
American donors who have been carefully screened by
history.
(11) Graft versus host disease (GVHD) in recipients
has been reported with increasing frequency in the past
five years. However, this entity is limited to those recipients with severe immunodeficiency disease—particularly those with severe combined immunodeficiency
disease, bone marrow transplant recipients, patients
with neuroblastoma after therapy, and patients with
Hodgkin's disease. Although other diseases with less severe immunodeficiency have been associated with posttransfusion graft versus host disease, such reports are
rare. GVHD can be prevented by treatment of blood
and cell-containing blood components with irradiation
(1,500-5,000 rads) before transfusion.6
(12) The risk of acquired immune deficiency syndrome (AIDS) is of paramount concern for transfusion
candidates, but it is almost nonexistent today as the
result of testing of donors for antibody to human immunodeficiency virus (anti-HIV, also known as antiHTLV-III/LAV). Fewer than 1,000 cases of transfusion-associated AIDS (TA-AIDS) have been reported in
the United States.7 Children are at greater risk of having
TA-AIDS develop than are adults.15 Children and adults
both have about 30 times more risk of having TA-AIDS
develop if they received more than 10 units of blood
compared with recipients who received less than 10
units.15 The incidence of TA-AIDS resulting from blood
transfused between July 1, 1977, and April 1, 1985, may
reach 1 in 40,000 transfusions (less than 1 in 11,000
recipients).18 This estimate assumes an average of 12
million transfusions and 3.4 million recipients per year.5
It approximates the incidence of TA-AIDS before the
advent of the combined use of donor self-deferral and
serologic testing. The risk of TA-AIDS has been virtually eliminated since blood banks began testing donated blood units for anti-HIV (March/April 1985).
However, at the current transfusion rate of about 15
million transfusions per year and a 99% sensitivity for
serologic tests, it has been estimated that between
30-200 units of "presumably infectious" blood would
be available for transfusion each year because of false
negative results.18,2243
(13) Red blood cell transfusions produce a negative
feedback effect on the rate of red blood cell production
in the marrow. This mechanism is mediated by erythropoietin and may result in the patient having a hemoglobin level lower than the pretransfusion value after the
normal clearance of the transfused red blood cells (about
three months).
AJ.C.P. • September 1987
(14) Leukocytes appear to be very immunogenic. Approximately 10% of transfusion recipients have antiHLA-A,B,C antibodies develop.10,32 The additional incidence of DR, non-HLA, and platelet antibodies after
transfusion is unknown but probably significant. Some
of these antibodies are believed to be responsible in certain recipients for febrile nonhemolytic transfusion reactions and the refractory state to platelets after repeated
platelet transfusions.
(15) Cytomegalovirus (CMV) is present within the
leukocytes of most blood donors. Transfusion of these
units can result in either CMV infection or seroconversion with a significant increase in the titer of preexisting
antibody for CMV. CMV infection can be fatal to the
neonate (especially those who weigh less than 1,250 g)
and the immunocompromised patient.42 Recipients of
CMV-positive blood may have severe morbidity develop after bone marrow grafts and renal allografts.
They may also have graft rejection and/or die. High-risk
recipients may be protected by the use of donor blood
with a negative, or less than 1:8, antibody titer against
CMV or by the use of leukocyte-free red blood cells.
(16) At least 1% of all transfused red blood cell units
induce red blood cell antigen alloimmunization in the
recipient.14,24 This risk exists with all red blood cell products. Such immunized patients may then pose future
problems in cross-matching (finding compatible blood)
and hemolytic disease of the newborn. The appearance
of red blood cell antibodies in the serum of the recipient
is usually delayed for several weeks after the transfusion.
(17) The appearance of fever, leukopenia, and splenomegaly two to five weeks after a transfusion may reflect
an infection because of transmission of the Epstein-Barr
virus. Atypical lymphocytes in the blood and a mononucleosis-like clinical picture are characteristic. Such patients may have a positive serologic test for infectious
mononucleosis. Posttransfusion CMV infection can also
produce these clinical findings.
(18) A febrile nonhemolytic reaction (temperature
elevation of 1 °C or more above pretransfusion temperature) is the single most common immediate transfusion
reaction. Although it may be a manifestation of a hemolytic transfusion reaction, it rarely is. Granulocytes in
the transfused donor unit have been implicated as a
major cause of these reactions, but it is probable that
these reactions have more than a single pathogenesis.
The interaction of recipient leukocyte antibodies with
transfused donor leukocytes and the phagocytosis of
donor granulocyte "debris" and nonviable red cells by
recipient macrophages stimulate the recipient macrophages to produce and release macrophages to produce
and release interleukin-1 (IL-1), a source of endogenous
pyrogen.37 It has been suggested that each recipient has a
certain threshold in terms of the number of granulocytes
Vol. 88 • No. 3
AWARD LECTURES AND SPECIAL REPORTS
that must be transfused in order to initiate a febrile response. Recipients who are afebrile at the start of a
transfusion tend to be tolerant to the development of
fever, whereas recipients who are febrile at the onset of
the transfusion, or those who have been febrile in the
preceding 24 hours, are more likely to manifest a temperature elevation. Red blood cell survival as measured
by hemoglobin increment is normal. These reactions
cannot be entirely prevented, but their frequency can be
minimized by the use of leukocyte-poor red blood cells.
Consideration should be given to the routine use of this
component for future transfusions in all patients who
have had three previous febrile nonhemolytic transfusion reactions. Experience has documented that most
blood recipients who have had one febrile nonhemolytic
transfusion reaction will not have a second such reaction
when transfused with a blood component that has not
been depleted of leukocytes. However, all patients who
receive outpatient transfusions and home transfusions
should be given leukocyte-poor red blood cells because
of the anxiety and concern of such patients who experience fever during or after these transfusions. A component prepared by an "in-line" leukocyte filter should be
used first. If a patient continues to react to this component, then washed or frozen thawed deglycerolized red
blood cells should be used because these components
contain the least number of leukocytes. Therapy consists of the administration of antipyretics. Opinions
differ as to whether or not the transfusion should be
continued if fever develops during the transfusion. Certainly, one should rule out the possibility of a hemolytic
transfusion reaction, because fever is a common manifestation of such reactions.35 It would seem prudent to
discontinue the transfusion unless it was given for a lifethreatening emergency.
(19) Allergic reactions are commonly manifest by the
onset of urticaria in the recipient. They have been attributed to proteins in the donor plasma acting as immunogens. Some of these reactions may result from recipient anti-IgA of limited specificity reacting with
donor IgA of a different type (allogeneic disparity).38
However, other protein allergens are more often involved, reacting with IgE and/or IgG antibodies of the
recipient. These immediate type hypersensitivity reactions are believed to result from the release of biologically active mediators such as C3a, C5a, histamine,
and/or leukotrienes." They are observed after the transfusion of any plasma-containing component but are
more common with those components containing maximal amounts of plasma (fresh frozen plasma, whole
blood, pooled platelets, etc.). Red blood cell survival is
not compromised, and urticaria is not a manifestation
of a hemolytic transfusion reaction. Therefore, some institutions will continue the transfusion after giving the
recipient an antihistamine, whereas others advocate dis-
377
continuing the blood. Patients with a history of repeated
allergic reactions should be premedicated with an antihistamine before transfusion.
(20) Chills without a documented temperature increase are also relatively frequent. Their cause is unknown. It is likely that more than one cause is operative
and that at least some may be an indication of an
aborted febrile nonhemolytic transfusion reaction.
Transfusions associated with chills in the patient should
probably be discontinued.
(21) Delayed hemolytic transfusion reactions are most
often detected by the blood bank when laboratory tests
reveal either positive results for a direct or indirect antiglobulin test in a patient who previously had such a test
with normal results who has been recently transfused
(within the previous two months). Most such reactions
are recognized five to ten days after the transfusion of
previously "compatible" blood because of the reappearance of an alloantibody that was initially produced
months or years earlier in response to a pregnancy or
transfusion. Such reactions are clinically silent, although
in some patients there may be jaundice or an unexplained decrease in hemoglobin. Experience at this institution with more than 20 such recognized delayed
reactions indicates that they have no serious adverse
effects.
(22) Massively transfused patients are often acidotic
because of tissue damage, hypovolemia, hypotension,
poor tissue perfusion, and hypoxemia. The acidosis,
however, can be corrected by restoration of blood volume and increase of the perfusion of the microcirculation. After restoration of volume, a transient alkalosis
results from the metabolism of citrate, an ingredient of
the donor blood anticoagulant. Hyperkalemia is also
common during the early phase of massive transfusion
therapy, but there is a shift toward hypokalemia with
recovery resulting from the pH change and increasing
renal function.
(23) Experience in centers throughout the world has
documented an improved renal allograft survival rate in
those patients that have received pretransplant blood
transfusions.27 The mechanism is unknown, but an immune basis is likely. Repeated transfusions of blood and
components/derivatives are also known to alter lymphocyte subpopulation ratios and responses in the recipient.21 The effect in renal transplantation is beneficial,
but in other clinical settings such a response may have
no clinical significance or the effect could be detrimental. Further studies in cell biology and the clinical
variables are needed to explore and define this phenomenon.
(24) Posttransfusion purpura is an extremely rare
complication of the transfusion of blood or blood components. The recipients are typically women who are age
45-65 with a history of several pregnancies and/or
WALKER
378
transfusions. There is a rather sudden onset of petechiae
and purpura approximately one week after the transfusion. The cause is either a platelet-specific antibody,
anti-PlA1 or an HLA antibody. The condition is transient, but isolated cases can be serious.
21.
22.
23.
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