Summary
Blood transfusion is lifesaving but carries real risks. Reactions are classified by timing (acute vs delayed) and by mechanism (immune vs non-immune vs infectious).
- Acute (< 24 hours): acute hemolytic (ABO mismatch), febrile non-hemolytic, allergic/anaphylactic, TRALI, TACO, septic.
- Delayed (> 24 hours): delayed hemolytic, transfusion-associated graft-versus-host disease (TA-GVHD), iron overload, alloimmunization, infections (HBV, HCV, HIV).
The first step in any suspected reaction is to stop the transfusion immediately, keep the IV line open with normal saline, and send the blood bag + patient sample back to the blood bank.
Classification
Group reactions by timing first — acute reactions appear during or within hours of transfusion, while delayed reactions show up days to weeks later.
| Classification of Transfusion Reactions | |
| Acute | Within 24 hours |
| Acute hemolytic (AHTR) | ABO incompatibility – clerical error |
| Febrile non-hemolytic (FNHTR) | Cytokines / recipient anti-HLA Abs |
| Allergic / Anaphylactic | IgE to plasma proteins (anaphylaxis → IgA deficiency) |
| TRALI | Donor anti-HLA → non-cardiogenic pulmonary edema |
| TACO | Volume overload → cardiogenic pulmonary edema |
| Septic | Bacterial contamination (esp. platelets) |
| Delayed | After 24 hours |
| Delayed hemolytic (DHTR) | Anamnestic minor antigen response (Kidd, Rh) |
| TA-GVHD | Donor lymphocytes attack recipient – fatal |
| Iron overload | Chronic transfusion (thalassemia, SCD) |
| Alloimmunization | Antibodies to RBC / HLA / platelet antigens |
| Infections | HBV, HCV, HIV, CMV, malaria |
Acute Hemolytic Transfusion Reaction (AHTR)
Mechanism: recipient's preformed IgM antibodies against ABO antigens on transfused RBCs → complement activation → intravascular hemolysis. Almost always caused by a clerical error (wrong unit, wrong patient).
Onset: within minutes of starting transfusion.
Clinical features:
- Fever, chills, flank or back pain
- Hypotension, tachycardia (shock)
- Hemoglobinuria → dark/red urine
- DIC, acute kidney injury
- In an anesthetized patient: oozing from surgical wound + hypotension may be the only clue.
Labs: ↑ LDH, ↑ indirect bilirubin, ↓ haptoglobin, positive direct Coombs (DAT), hemoglobinuria, schistocytes if DIC.
Management:
- STOP transfusion immediately.
- Maintain IV access with normal saline — keep urine output > 100 mL/hr.
- Send the blood unit + a fresh patient sample to blood bank.
- Supportive: vasopressors, treat DIC, dialysis if AKI.
| Important – فكرة سؤال | |
|
Fever + flank/back pain + dark urine + hypotension within minutes of starting transfusion = Acute Hemolytic Transfusion Reaction (ABO mismatch). First step: STOP the transfusion, send the bag back, start IV normal saline to protect the kidneys. أي مريض يبدأ بحمى + ألم أسفل الظهر + بول داكن + هبوط ضغط أثناء النقل ⇐ أوقف النقل فوراً. |
تذكر |
Febrile Non-Hemolytic Reaction (FNHTR)
The most common transfusion reaction.
Mechanism:
- Cytokines (IL-1, IL-6, TNF) released from donor WBCs during storage, OR
- Recipient anti-HLA antibodies reacting with donor leukocytes.
Onset: 1–6 hours after transfusion starts.
Features: fever (↑ ≥ 1 °C), chills, headache, malaise. No hemolysis, no hypotension, no respiratory distress.
Management: stop the transfusion (must rule out AHTR first) → give antipyretics (acetaminophen). Reaction is self-limiting.
Prevention: use leukoreduced blood products for future transfusions.
Allergic and Anaphylactic Reactions
Mild allergic (urticarial) reaction
- Type I hypersensitivity to donor plasma proteins.
- Onset within minutes — urticaria, pruritus, flushing. No fever, no hypotension.
- Management: pause transfusion → give antihistamines (diphenhydramine). If symptoms resolve, transfusion can be resumed slowly.
Anaphylactic reaction
- Classic patient: IgA-deficient recipient with anti-IgA antibodies reacting against IgA in donor plasma.
- Onset: seconds to minutes.
- Features: hypotension, shock, bronchospasm, wheeze, stridor, angioedema.
- Management: STOP transfusion → IM epinephrine, IV fluids, airway support, antihistamines, steroids.
- Prevention: future transfusions with washed RBCs (plasma removed) or products from IgA-deficient donors.
| Note |
| Selective IgA deficiency is the most common primary immunodeficiency. Most patients are asymptomatic — but they are at lifelong risk of anaphylaxis from any blood product containing IgA. |
TRALI and TACO
Both cause dyspnea + bilateral pulmonary infiltrates within 6 hours of transfusion — but the mechanism and management are opposite. Distinguishing them is a classic exam question.
- TRALI (Transfusion-Related Acute Lung Injury) — leading cause of transfusion-related mortality. Think "ARDS triggered by transfusion." Hypotension, fever, no signs of fluid overload.
- TACO (Transfusion-Associated Circulatory Overload) — too much volume, too fast. Hypertension, raised JVP, S3 — classic CHF picture.
| TRALI vs TACO | ||
|---|---|---|
| Feature | TRALI | TACO |
| Mechanism | Donor anti-HLA/neutrophil Abs activate recipient neutrophils → capillary leak | Volume overload → hydrostatic pulmonary edema |
| Onset | Within 6 hours | Within 6 hours (often during transfusion) |
| Edema type | Non-cardiogenic (↑ permeability) | Cardiogenic (↑ hydrostatic pressure) |
| BP | Hypotension | Hypertension |
| JVP / S3 | Normal | Elevated JVP, S3, peripheral edema |
| BNP | Normal | Elevated |
| CXR | Bilateral infiltrates | Bilateral infiltrates + cardiomegaly |
| Treatment | Supportive, O2, mechanical ventilation if needed | Diuretics (furosemide), O2, slow future transfusions |
| Risk group | Any patient | Elderly, CHF, renal failure, children |
Septic (Bacterial Contamination)
Mechanism: bacterial contamination of the blood product → endotoxin release in recipient.
- Most often with platelets (stored at room temperature, ~22 °C).
- Common organisms: Yersinia enterocolitica (in RBCs), Staphylococcus, gram-negatives (in platelets).
Onset: minutes to hours.
Features: high fever, rigors, hypotension, shock — looks like AHTR but without hemoglobinuria or back pain.
Management: STOP transfusion → broad-spectrum IV antibiotics, IV fluids/vasopressors, blood and bag cultures.
Delayed Hemolytic Reaction (DHTR)
Mechanism: anamnestic response — recipient was previously sensitized (prior transfusion or pregnancy) to a minor RBC antigen (most often Kidd, also Rh, Duffy, Kell). Antibody titer was too low to detect on crossmatch. After re-exposure, the titer rises and IgG attacks donor RBCs.
Onset: 2–10 days after transfusion.
Features: mild — low-grade fever, mild jaundice, unexplained drop in hemoglobin after a "successful" transfusion. Extravascular hemolysis (spleen) → no hemoglobinuria.
Labs: positive direct Coombs, ↑ indirect bilirubin, ↓ haptoglobin, ↓ Hb.
Management: usually supportive; identify the offending antibody for future transfusions.
Transfusion-Associated GVHD (TA-GVHD)
Mechanism: viable donor T lymphocytes in the blood product engraft and attack the recipient's tissues.
At risk: severely immunocompromised patients (BMT recipients, hematologic malignancies, congenital immunodeficiency, fetuses) — and transfusions from a first-degree relative (shared HLA alleles let donor T cells escape recognition).
Onset: 4–30 days post-transfusion.
Features: fever, skin rash, diarrhea, hepatitis, pancytopenia (bone marrow is also attacked — distinguishes from BMT-GVHD where marrow is spared).
Outcome: mortality > 90%.
Prevention: irradiation of blood products inactivates donor lymphocytes.
Other Delayed Complications
Iron overload (secondary hemochromatosis)
- Chronic transfusions (β-thalassemia major, sickle cell disease, MDS).
- Each unit of RBCs contains ~250 mg iron — no physiologic excretion.
- Deposits in heart (cardiomyopathy), liver (cirrhosis), pancreas (DM), skin (bronze), gonads.
- Treatment: iron chelators — deferoxamine, deferasirox, deferiprone.
Alloimmunization
- Recipient develops antibodies against donor RBC, HLA, or platelet antigens after repeated transfusion.
- Consequences: future crossmatch difficulty, platelet refractoriness, DHTR.
Infectious transmission (rare in modern banks but tested)
- Per-unit risk (developed countries, approximate): HBV ~1:1 million, HCV ~1:2 million, HIV ~1:2 million.
- CMV — risk for immunocompromised and neonates → use CMV-negative or leukoreduced units.
- Others: HTLV, parvovirus B19, malaria, Chagas, prions (vCJD).
Hypocalcemia & hyperkalemia
- Massive transfusion → citrate (anticoagulant in stored blood) chelates calcium → hypocalcemia (perioral tingling, tetany, prolonged QT).
- Stored RBCs leak potassium → hyperkalemia (esp. with renal failure, neonates).
General Approach and Prevention
If a reaction occurs during transfusion:
- STOP the transfusion immediately.
- Maintain IV access with normal saline through a new line.
- Check vital signs and identify the patient + the unit (re-check labels).
- Send the blood bag, IV tubing, and a fresh patient blood + urine sample to the blood bank.
- Treat according to the suspected reaction type.
Prevention — modify the blood product to match the patient:
| Blood Product Modifications | ||
|---|---|---|
| Modification | Indication | Purpose |
| Leukoreduction | Prior FNHTR; chronic transfusion; CMV-seronegative substitute | Removes WBCs → prevents FNHTR, HLA alloimmunization, CMV transmission |
| Irradiation | Severe immunocompromise; donation from 1st-degree relative; intrauterine transfusion | Inactivates donor T cells → prevents TA-GVHD |
| Washed RBCs | IgA deficiency with anti-IgA Abs; repeated severe allergic reactions | Removes plasma proteins → prevents anaphylaxis |
| CMV-negative units | Pregnant women, neonates, transplant recipients, HIV | Avoids CMV transmission |
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