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2374 Part XIII: Transfusion Medicine Chapter 138: Blood Procurement and Red Cell Transfusion 2375

access with slow infusion of normal saline, monitoring vital signs, and allergic transfusion reaction (ATR) occur in 1 to 3 percent of transfu-
assessing urine output are key early steps. A blood specimen should be sions of plasma-rich components (i.e., platelets/fresh-frozen plasma)
collected immediately for laboratory evaluation. The component bag and in 0.1 to 0.3 percent for red cells. Severe anaphylactic reactions
should be returned to the blood bank. If severe hemolysis has occurred, are much less frequent and estimated at one in 20,000 to 50,000
therapy focuses on management of hypotension, coagulation disor- transfusions. 7
ders, and renal function. A urine output of approximately 100 mL/h The majority of ATRs are immediate (type 1) hypersensitivity reac-
for 24 hours should be maintained in adults without contraindications. tions, mediated by preformed IgE antibodies binding to soluble proteins
In simple cases, normal saline infusion may be sufficient; however, present within donor plasma. Severe anaphylactic reactions may occur
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diuretics may be necessary in some cases. Intravenous administration after transfusion of blood products to IgA-deficient patients who have
of furosemide (40 to 80 mg) promotes diuresis and improves blood flow anti-IgA antibodies. Most patients labeled as IgA deficient still have
to the renal cortex. In severe cases of hypotension, intravenous dopa- low levels of the immunoglobulin (2 to 4 mg/dL) and will not produce
mine, which dilates renal vasculature and increases cardiac output, can anti-IgA antibodies. The rare patient with complete IgA deficiency
be used. Patients with coagulopathy and active bleeding may require (<0.05 mg/dL) may develop anti-IgA antibodies and thus might experi-
administration of platelets, fresh-frozen plasma, or cryoprecipitate. ence anaphylaxis with transfusion. Anaphylactoid reactions are similar
Prevention The most common basis for AHTRs is a clerical error to anaphylaxis but clinically less severe and caused by non–IgE-medi-
resulting from mistakes in identifying the patient, labeling the pretrans- ated activation of mast cells.
fusions sample, or identifying the correct red cell unit for the patient. 56–58 Clinical Presentation ATRs usually begin during or within an
hour of starting a transfusion, but may not become evident until sev-
Febrile Nonhemolytic Transfusion Reactions eral hours later. Common findings include urticaria, rash, pruritus,
A febrile nonhemolytic transfusion reaction (FNHTR) is defined, arbi- and flushing. More severe reactions occur sooner and may include
trarily, as a temperature increase of 1°C or more during or up to 4 hours angioedema, chest tightness, dyspnea, cyanosis, hoarseness, stridor,
after transfusion. Other possible symptoms include increases in respira- or wheezing. In addition, gastrointestinal symptoms such as abdomi-
tory rate, anxiety, and, more unusually, nausea or vomiting. nal pain, nausea, vomiting, and diarrhea may also occur. Unlike other
FNHTRs are one of the most commonly encountered transfu- acute transfusion reactions, fever is usually absent. Anaphylaxis occurs
sion reactions occurring in approximately 0.12 to 0.5 percent of RBC immediately after starting the transfusion. Symptoms can include bron-
units transfused, and are more likely to occur following transfusion of chospasm, angioedema, respiratory distress, nausea, vomiting, abdomi-
platelets than RBCs. Leukocyte reduction decreases the incidence of nal cramps, diarrhea, shock, and loss of consciousness.
FNHTRs with both whole-blood derived and apheresis platelets. Laboratory Evaluation There is no need for laboratory investiga-
Clinical Presentation Fever is triggered by the action of cytokines tion with simple urticarial and/or localized pruritus. However, the inci-
(e.g., IL-1, IL-6, TNF-α). This may be the result of activation of donor dent should be reported to the blood bank to update the patient’s record
leukocytes by anti-HLA or other antibodies in the recipient, activation for any future transfusions. In anaphylactic reactions, the patient should
of recipient leukocyte and endothelial cells by transfused donor leuko- be tested for complete IgA deficiency; however, a history of anaphylactic
cytes or plasma constituents, or by the passive transfer of cytokines or reactions mandate use of washed red cells and platelets and avoidance of
CD40 ligand (CD154) that accumulated in the unit during storage. plasma transfusions regardless of the results of these tests.
Fever should not be solely attributed to FNHTR until other potential Management Most ATRs are mild, self-limited and respond
life-threatening transfusion reactions or patient-related factors have been well to transfusion discontinuation and, if indicated, administration
excluded. Past transfusion reaction history should be reviewed to deter- of antihistamine (diphenhydramine hydrochloride, usually orally). In
mine if additional measures should be implemented for future transfusions. cases limited to urticaria, the transfusion may be resumed immediately
Laboratory Evaluation The laboratory investigation should con- after symptoms resolve. However, transfusion should never be resumed
centrate on ruling out a septic transfusion reaction. A Gram stain is not when there is a severe reaction. In acute anaphylaxis, fluid resuscita-
a highly sensitive technique in this setting, but may be used to rule-in tion may be needed to maintain blood pressure followed by administra-
bacterial contamination. Rapid qualitative immunoassay tests (e.g., Verax tion of subcutaneous or intramuscular epinephrine (0.3 mL of 1:1000
or BacTx) are highly sensitive for most commonly encountered bacterial dilution), as well as airway management and intensive care. In case of
contaminants and may be used in lieu of Gram stain to screen implicated shock, a higher concentration of intravenous epinephrine (3 to 5 mL of
platelet units. In cases with a high index of suspicion, the unit should be a 1:10,000 dilution) can be administered. Steroids are usually not help-
cultured. If all results are negative and the patient’s presentation is consis- ful in acute crises.
tent with a mild FNHTR, no additional testing is required. Prevention Patients with a history of mild ATRs should not be
Management FNHTRs are typically benign, and usually resolve premedicated with an antihistamine, as this does not reduce the over-
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completely within 1 to 2 hours after the transfusion is discontinued. The all risk of ATRs. Platelets stored in additive solution may be used to
remainder of the transfused unit and a posttransfusion blood sample reduce the risk of a reaction. In IgA-deficient patients with a history of
from the patient should be sent to the laboratory for investigation. Anti- anaphylaxis to transfusion, components from IgA-deficient donors are
pyretics may be administered to shorten the duration of the fever and sometimes available. 59
provide analgesia. Acetaminophen 325 to 650 mg orally for adults or 10
to 15 mg/kg/dose orally for children is effective for this purpose. Transfusion-Related Acute Lung Injury
Transfusing leukoreduced RBCs and/or platelets stored in additive Transfusion-related acute lung injury (TRALI) is a syndrome of acute
solution will significantly reduce the risk of FNHTRs. Premedication hypoxia attributable to noncardiogenic pulmonary edema that occurs
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with antipyretics (acetaminophen) is not helpful. 60,61 within 6 hours of a transfusion. 63,64 TRALI has been the leading cause of
transfusion-related fatalities for several years.
Allergic Transfusion Reactions There are two main hypotheses regarding the capillary leak seen
These are a common adverse reaction of transfusion therapy, ranging in TRALI. The two-hit hypothesis states that underlying patient fac-
from mild forms characterized by localized pruritus and/or urticaria, tors act as a necessary first hit, leading to adherence of primed neu-
to severe anaphylactic or anaphylactoid reactions. The mild forms of trophils to the pulmonary endothelium. The second hit is caused by

Kaushansky_chapter 138_p2365-2380.indd 2375 9/18/15 11:13 AM