Can You Continue a Transfustion After Treatment for Allergic Transfusion Reaction

Summary

Blood component transfusions are usually safe and, given extensive screening and pretransfusion testing, serious adverse events are uncommon. When acute reactions occur they are typically mild, with the most common reactions including fever and rash. Rarely, more severe reactions can occur, causing respiratory distress, hemolysis, or shock. As there is significant overlap between the manifestations of mild transfusion reactions and the early stages of severe transfusion reactions, the first step is to stop the blood transfusion while assessment is performed. For minor transfusion reactions, it may be possible to restart the transfusion at a slower rate once more serious diagnoses have been excluded. Patients may also experience delayed transfusion reactions days to weeks after a transfusion. Delayed transfusion reactions typically have a more insidious presentation than acute reactions, and identifying them requires a high degree of clinical suspicion.

See also "Transfusion."

Overview

Immunological transfusion reactions

Overview of immunological transfusion reactions
	Background	Clinical features	Management
Acute hemolytic transfusion reaction (AHTR)	Frequency: 1 in 105,000–200,000 transfusions [1] Mechanism: Donor RBCs are destroyed by preformed recipient antibodies (typically due to ABO incompatibility ) and/or by other nonimmune-mediated forces (e.g., mechanical shear), leading to intravascular hemolysis.	Onset: Rapid; during or up to 24 hours after transfusion Fever , chills, nausea, flushing Signs of shock Respiratory distress signs Signs of hemolysis	Immediately stop transfusion and notify the blood bank. Perform Direct Coombs test on recipient blood. Repeat blood typing and crossmatching of the donor blood. Start immediate hemodynamic support (i.e., IV fluid resuscitation, vasopressors and inotropes as needed). Treat complications, e.g., hyperkalemia, DIC, renal failure.
Febrile nonhemolytic transfusion reaction (FNHTR)	Frequency: 1 in 900 transfusions (more common in children) [1] [2] Mechanism: Cytokines released from old or lysed donor WBCs provoke an inflammatory reaction in the recipient.	Onset: During or up to 6 hours after transfusion Fever, chills, malaise, flushing, headache	Stop transfusion until AHTR has been ruled out. Use leukoreduced blood products for prevention. Consider acetaminophen for symptoms.
Anaphylactic transfusion reaction	Frequency: 1 in 30,000 transfusions [1] Mechanism: type I hypersensitivity reaction to donor plasma proteins (due to preformed recipient antibodies)	Onset: Sudden; during or up to 3 hours after transfusion Clinical features of anaphylaxis	Immediately stop transfusion. Epinephrine IM Immediate hemodynamic support Airway management
Minor allergic transfusion reaction	Frequency: 1 in 1200 transfusions (more common in children) [1] [2] Mechanism: allergic reaction to components in donor plasma (due to preformed recipient antibodies)	Onset: during or up to 4 hours after transfusion Pruritus , urticaria	Stop transfusion initially. Use diphenhydramine for symptoms. Restart transfusion slowly under close observation if anaphylaxis has been ruled out and symptoms resolved.
Transfusion-related acute lung injury (TRALI)	Frequency: 1 in 60,000 transfusions [1] [3] Mechanism: activation of primed granulocytes in recipient's lungs by donor blood components leads to an inflammatory cascade, culminating in lung injury and NCPE [4]	Onset: Sudden; during or up to 6 hours after transfusion Features resembling ARDS Respiratory distress signs Signs of increased work of breathing Fever, hypotension	Immediately stop transfusion and notify blood bank. Respiratory support: e.g., lung-protective ventilation Hemodynamic support.
Delayed hemolytic transfusion reaction (DHTR)	Frequency: 1 in 22,000 transfusions [1] Mechanism: delayed anamnestic response to specific donor RBC antigens (e.g., Rh(D) antigen) leads to extravascular hemolysis mediated by recipient antibodies.	Onset: days or weeks after transfusion Most commonly asymptomatic Features may include mild fever, j aundice, signs of a nemia	No acute therapy required (self-limiting) Direct Coombs test to prevent future reaction
Post-transfusion purpura	Frequency: 1 in 57,000 transfusions [1] Mechanism: delayed anamnestic response to platelet antigens leads to antibody-mediated destruction of both donor and recipient platelets. [5]	Onset: 5–10 days after transfusion Petechiae, purpura	IVIG therapy

Nonimmunological transfusion complications

Overview of nonimmunological transfusion complications
Complications		Background	Features	Management
Transfusion-associated sepsis		Incidence: 1:10,000-200,000 transfusions [6] [7] Mechanism: bacterial contamination of blood product	Onset within 4 hours of transfusion Fever, hypotension, rigor, and other signs of SIRS	Immediately stop the transfusion. Start immediate hemodynamic support (e.g., IV fluid resuscitation, vasopressors, and inotropes as needed). Obtain blood cultures from both patient and remaining blood product. Administer broad-spectrum empiric antibiotic therapy for sepsis.
Transfusion-associated circulatory overload (TACO)		Frequency: 1 in 9000 transfusions [1] [3] Mechanism: fluid overload	Onset during or within 12 hours of transfusion Signs of hypervolemia : shortness of breath , S3 gallop , jugular venous distention , hypertension	Respiratory support: e.g. oxygen therapy, mechanical ventilation Consider diuretics to correct volume status.
Massive transfusion-related complications [3]	Hypocalcemia	Resulting from the binding of ionized calcium by citrate (an anticoagulant added to RBC, platelet, FFP, and whole blood transfusion units) See also "Clinical features of hypocalcemia"		Monitoring of ionized calcium Calcium repletion
	Hyperkalemia	Resulting from the lysis of RBCs in stored blood units; the risk is higher with increased transfusion rate and/or volume and longer storage age.		Monitoring of serum potassium See "Therapeutic approach to hyperkalemia."
	Hypothermia	Triggered by the rapid infusion of cold blood products		Prevention: inline blood warming devices
	Coagulopathy	Thought to be multifactorial, including dilution of platelets and clotting factors, hypothermia, and platelet dysfunction [8]		Prevention: Consider using balanced ratio of blood products. [9] See also "Treatment of DIC."
Other		Bloodborne viral, treponemal, and parasitic infections (e.g., HIV, hepatitis B, hepatitis C): uncommon in the US as a result of routine blood donation infection screening protocols [10] Iron overload (secondary hemochromatosis): May occur with repeated blood transfusion, e.g., in thalassemia, sickle cell anemia (see also "Iron overload disease in thalassemia")

Acute transfusion reactions

Acute hemolytic transfusion reaction

Description

Acute hemolytic transfusion reaction (AHTR) is an adverse reaction to blood transfusion that occurs within the first 24 hours after transfusion.

Pathophysiology ^[1]

• ABO incompatibility
• Non-ABO-related
  • Immune-mediated: the destruction of donor RBCs by recipient alloantibodies to non-ABO RBC antigens
  • Nonimmune-mediated: RBC destruction resulting from mechanical, thermal, or osmolar injuries

Clinical features ^[1]

• Rapid onset during transfusion (because of preformed antibodies) or up to 24 hours after the transfusion
• Clinical presentation ranges from asymptomatic to severe.
• Symptoms include: ^[12]
  • Fever , chills, nausea, flushing
  • Hypotension , tachycardia
  • Flank pain or chest pain
  • Dyspnea , tachypnea
  • Hemoglobinuria (due to intravascular hemolysis)
  • Jaundice (due to intravascular hemolysis)
  • Pruritus, urticaria
  • Burning pain at the IV site
  • Patients in a coma or under general anesthesia may present with oozing from wounds or puncture sites.
• Sequelae include:

AHTR is mainly a clinical diagnosis.

Confirmatory testing

Additional laboratory testing

AHTR is a medical emergency.

Stop the transfusion immediately if AHTR is suspected!

Febrile nonhemolytic transfusion reaction

Anaphylactic transfusion reaction

See also "Anaphylaxis."

• Frequency: 1 in 30,000 transfusions ^[1]
• Pathophysiology
  • Type I hypersensitivity reaction in which preformed IgE antibodies on the surface of mast cells bind to donor plasma proteins (commonly donor IgA in recipients with IgA deficiency ), leading to mast cell degranulation
  • Individuals with IgA deficiency should receive IgA-depleted blood products.
• Clinical features: Sudden onset during or up to 3 hours after the transfusion
  • Shock, hypotension , wheezing, respiratory distress
  • Skin reactions (e.g., pruritus, urticaria)
• Diagnosis ^[1]
  • Clinical diagnosis established according to diagnostic criteria for anaphylaxis
  • If the diagnosis is in doubt, consider workup for AHTR, TRALI, and septic transfusion reaction as the presenting features (e.g., hypotension, dyspnea) may be similar.
  • Consider testing the transfusion recipient for serum IgA levels and anti-IgA antibodies.
• Management ^[1]
• Prevention: in patients with a previous history of anaphylactic transfusion reaction ^[1]
  • Use washed blood products (platelets, RBCs) and solvent detergent plasma.
  • Use IgA-deficient blood products for patients with IgA deficiency.
  • The use of prophylactic antihistamines and/or steroids is commonly practiced but lacks supportive evidence. ^{[3] [16]}

Minor allergic transfusion reaction

Pulmonary transfusion complications

Massive transfusion-associated complications

Massive transfusion-associated reactions occur following the transfusion of large amounts of RBC units (e.g., > 10 units in 24 hours or ≥ 50% of the patient's blood volume in 4 hours), usually for cases of massive blood loss (e.g., from trauma or surgery). ^{[3] [21]}

• Hypocalcemia ^[3]
  • Resulting from the binding of ionized calcium by citrate (an anticoagulant added to RBC, platelet, FFP, and whole blood transfusion units)
  • Managed with monitoring of ionized calcium and calcium repletion
• Hyperkalemia ^[3]
  • Resulting from the lysis of RBCs in stored blood units; the risk is higher with increased transfusion rate and/or volume and longer storage age.
  • Managed with monitoring of serum potassium and treatment as needed (see "Therapeutic approach to hyperkalemia")
• Hypothermia ^[3]
  • Triggered by the rapid infusion of cold blood products
  • Can be prevented by using inline blood warming devices
• Coagulopathy ^[8]
  • Thought to be multifactorial, including dilution of platelets and clotting factors, hypothermia, and platelet dysfunction
  • Can be prevented by using a fixed ratio of blood products, e.g., a 1:1:1 of RBCs, FFP, and platelets ^[9]
  • See also "DIC."

Septic transfusion reaction

See also "Sepsis."

• Frequency ^[6]
  • Highest with platelet transfusions (approx. 1 in 10,000–50,000 units) ^[7]
  • Lower with other blood products (e.g., RBC: approx. 1 in 200,000 units)
• Microbiology ^{[6] [22]}
  • Contaminated platelets: most commonly gram-positive organisms (e.g., Staphylococcus aureus, Streptococcus spp.)
  • Contaminated RBC: most commonly gram-negative organisms (e.g., Pseudomonas spp., Yersinia spp., Serratia spp.)
• Clinical features
  • Fever, hypotension, rigors, and other signs of SIRS
  • Usually manifests within 4 hours of transfusion
• Diagnosis ^[3]
  • Obtain bacterial cultures and Gram stains of the patient's blood and any recently transfused (within 4 hours) blood products.
  • Consider workup for AHTR and TRALI, as their presenting features (e.g., fever, hypotension, dyspnea) may be similar.
• Management ^[3]
  • Follow initial management steps for acute transfusion reactions.
  • Support hemodynamics with IV fluid resuscitation and vasopressors as needed.
  • Provide initial broad-spectrum empiric antibiotic therapy for sepsis, including antipseudomonal coverage if RBCs were given.

Acute management checklist for acute transfusion reactions

Initial management steps for acute transfusion reactions

• Stop the transfusion.
• Check patient and blood product IDs for compatibility.
• Maintain open IV access with normal saline.
• Draw blood for a repeat ABO typing and crossmatch.
• Perform a full ABCDE assessment and determine reaction severity.

All patients

• Provide symptomatic relief, e.g., oxygen, antihistamines, antipyretics.
• Identify the underlying cause of the reaction.
• Regularly reassess patients for signs of deterioration.
• Consider initial investigations: e.g., CBC, BMP, coagulation studies, hemolysis workup, urinalysis.
• Consider further investigations based on suspected underlying cause: e.g., Direct Coombs test, chest imaging, echocardiogram, BNP

Severe reactions

• Notify the blood bank and/or transfusion services.
• Consider hematology and ICU consult.
• Provide respiratory support and immediate hemodynamic support as needed.

Mild reactions

• Rule out early presentation of severe reactions.
• If symptoms resolve, consider resumption of blood transfusion at a slower rate.

Delayed transfusion reactions

Delayed transfusion reaction refers to an immune-mediated adverse reaction that occurs > 24 hours after the transfusion of blood products (can be weeks to months later). ^[11]

Delayed hemolytic transfusion reaction (DHTR)

• Frequency: 1 in 22,000 transfusions ^[1]
• Pathophysiology
• Clinical features ^[3]
  • Onset days or weeks after transfusion (due to the delay in the anamnestic response)
  • Most commonly asymptomatic
  • May cause:
    • Mild fever
    • J aundice
    • Anemia
    • Chest, abdomen, or back pain
  • May be mistaken for vasoocclusive crises in patients with sickle cell disease (SCD)
• Diagnosis ^{[1] [3]}
  • Positive DAT
  • CBC: to evaluate for anemia
  • Laboratory evidence of hemolysis
• Treatment ^{[1] [3]}
  • Most cases are self-limited ; and thus no acute therapy is usually required .
  • Additional RBC transfusions are preferably delayed (unless severe anemia) until the culprit alloantibodies are identified.
• Prevention ^[3]
  • Primary prevention in individuals requiring chronic transfusions (e.g., thalassemia, SCD): use of antigen-matched RBC units whenever feasible
  • Secondary prevention in individuals with identified alloantibodies: use of antigen-negative RBC units in future transfusions
  • See "Extended RBC phenotype matching."

Platelet transfusions may be administered to patients with life-threatening bleeding but are usually ineffective in increasing platelet counts in patients with posttransfusion purpura.

References

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2. The National Blood Authority's Patient Blood Management Guideline: Module 1 – Critical Bleeding/Massive Transfusion. https://www.blood.gov.au/pbm-module-1. Updated: January 1, 2011. Accessed: February 17, 2021.
3. Bolliger D, Görlinger K, Tanaka KA, Warner DS. Pathophysiology and Treatment of Coagulopathy in Massive Hemorrhage and Hemodilution. Anesthesiology. 2010; 113 (5): p.1205-1219. doi: 10.1097/aln.0b013e3181f22b5a . | Open in Read by QxMD
4. Balvers K, Coppens M, van Dieren S, et al. Effects of a hospital-wide introduction of a massive transfusion protocol on blood product ratio and blood product waste. J Emerg Trauma Shock. 2015; 8 (4): p.199. doi: 10.4103/0974-2700.166597 . | Open in Read by QxMD
5. Green AR. Postgraduate Haematology. John Wiley & Sons ; 2011
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7. Hawkins J, Aster RH, Curtis BR. Post-Transfusion Purpura: Current Perspectives. Journal of Blood Medicine. 2019; Volume 10 : p.405-415. doi: 10.2147/jbm.s189176 . | Open in Read by QxMD
8. Oakley FD, Woods M, Arnold S, Young PP. Transfusion reactions in pediatric compared with adult patients: a look at rate, reaction type, and associated products. Transfusion (Paris). 2014; 55 (3): p.563-570. doi: 10.1111/trf.12827 . | Open in Read by QxMD
9. Semple JW, Rebetz J, Kapur R. Transfusion-associated circulatory overload and transfusion-related acute lung injury. Blood. 2019; 133 (17): p.1840-1853. doi: 10.1182/blood-2018-10-860809 . | Open in Read by QxMD
10. Haass KA, Sapiano MRP, Savinkina A, Kuehnert MJ, Basavaraju SV. Transfusion-Transmitted Infections Reported to the National Healthcare Safety Network Hemovigilance Module. Transfus Med Rev. 2019; 33 (2): p.84-91. doi: 10.1016/j.tmrv.2019.01.001 . | Open in Read by QxMD
11. Levy JH, Neal MD, Herman JH. Bacterial contamination of platelets for transfusion: strategies for prevention.. Crit Care. 2018; 22 (1): p.271. doi: 10.1186/s13054-018-2212-9 . | Open in Read by QxMD
12. AABB: Regulatory for blood and blood components/Donor safety, testing, and labeling. https://www.aabb.org/regulatory-and-advocacy/regulatory-affairs/regulatory-for-blood/donor-safety-screening-and-testing. . Accessed: January 3, 2021.
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14. Parker V, Tormey CA. The Direct Antiglobulin Test: Indications, Interpretation, and Pitfalls. Arch Pathol Lab Med. 2017; 141 (2): p.305-310. doi: 10.5858/arpa.2015-0444-rs . | Open in Read by QxMD
15. Bakdash S, Yazer MH. What every physician should know about transfusion reactions. Can Med Assoc J. 2007; 177 (2): p.141-147. doi: 10.1503/cmaj.061106 . | Open in Read by QxMD
16. Red Blood Cell Transfusion: a pocket guide for the clinician.
17. Norfolk D. Handbook of transfusion medicine, 5th edition. United Kingdom Blood Services ; 2013
18. Bux J, Sachs UJ. The pathogenesis of transfusion-related acute lung injury (TRALI).. Br J Haematol. 2007; 136 (6): p.788-99. doi: 10.1111/j.1365-2141.2007.06492.x . | Open in Read by QxMD
19. Bux J. Transfusion-related acute lung injury (TRALI): a serious adverse event of blood transfusion. Vox Sang. 2005 . doi: 10.1111/j.1423-0410.2005.00648.x . | Open in Read by QxMD
20. D. Goldberg A, J. Kor D. State of the Art Management of Transfusion-Related Acute Lung Injury (TRALI). Curr Pharm Des. 2012; 18 (22): p.3273-3284. doi: 10.2174/1381612811209023273 . | Open in Read by QxMD
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