Transfusion reactions
Stop the transfusion, keep IV open with saline, check the clerical identity, call the blood bank, send the remaining unit + post-transfusion labs (DAT, hemolysis labs, culture if febrile).
Stop, then sort
Fever, chills, hives, flushing, infusion-site pain, , oliguria, dyspnea, wheeze, crackles, hypoxia, angioedema, new bleeding, nausea — any of these during a transfusion is a reaction until the workup says it is not (;832). Call Book: blood bank x63623 / p21829.
- 1
Stop the unit
Keep the IV open with saline. ABCs. Vitals every 15 minutes. Notify the blood bank. Clerical identity check — the usual cause of ABO disaster is a wristband.
- 2
Decide if it can restart
Isolated urticaria, or isolated temperature ≤39°C with no other signs: treat symptoms; resume once they resolve, per protocol.
- 3
Labs that match suspicion
CBC, BMP, LFTs, and the transfusion-reaction order set. Hemolysis: DAT, bilirubin, LDH, haptoglobin, crossmatch, UA, smear. Sepsis: Gram stain and culture of the patient and the bag. TRALI/TACO: JVP, NT-proBNP, ABG, portable CXR.
Acute reactions (<24 h)
| Reaction (per-unit risk) | Bedside picture | Mechanism | Treatment / prevention |
|---|---|---|---|
| Acute hemolytic (AHTR) 1/76,000–137,000 | 15 min to 2–4 h: fever/chills, nausea, tachycardia, hypotension, back/flank pain, bleeding, DIC. Hemoglobinuria, positive DAT, ↑ bili/LDH, spherocytes | ABO/Kidd: preformed antibody → intravascular hemolysis (IgM), cytokine/complement storm. Rh/Kell/Duffy: milder extravascular hemolysis | IVF ± diuresis for UOP >0.5–1 mL/kg/h. Watch hypotension, AKI, DIC. Mortality tracks volume transfused. Prevention: careful identity and crossmatch |
| Febrile non-hemolytic (FNHTR) 1/14 platelets; 1/200–2,500 RBC | 1–4 h: low-grade fever, chills/rigors, headache, flushing. Hemolysis workup negative; still send blood cultures | Donor WBCs make TNF-α, IL-1, IL-6. RBC: recipient anti-HLA activates donor WBCs. Platelets: cytokines generated during room-temperature storage | Acetaminophen ± meperidine for rigors. Prevention: leukoreduction. Little evidence for routine premedication |
| Bacterial sepsis 1/75,000 platelets | 15–60 min: high fever, rigors, abdominal symptoms, hypotension/. Gram stain/culture of patient and bag | Bacteria >> viruses. RBCs: Yersinia, Pseudomonas (endotoxin GNRs). Platelets (20–24°C storage): Staph epidermidis and other GPCs | Antibiotics. Quarantine other products from the same donation. Routine screening is the prevention |
| Urticaria 1/33–100 | Anytime: localized or diffuse hives and erythema. No workup needed if isolated | IgE against donor plasma proteins | Pause, second-generation antihistamine, resume if hives resolve. Prevention: washed products. No evidence for routine premedication |
| Anaphylaxis 1/20,000–50,000 | Minutes: hypotension, angioedema, urticaria, wheeze, GI symptoms. Consider IgA deficiency; serial tryptase | IgE in a recipient lacking IgA or haptoglobin. Bradykinin flushing/hypotension in patients on ACE inhibitors or negatively charged filters (albumin PLEX) | ABCs, oxygen, IVF ± pressors, epinephrine IM every 15 min, methylprednisolone 125 mg, diphenhydramine 25–50 mg, H2 blocker. Future: washed products |
IVIG reactions (5–15% of infusions)
- Inflammatory: fever, chills, flushing, headache, myalgias — antibody/antigen interaction, often with a concurrent infection.
- Anaphylactoid: urticaria, flushing, chest pain, nausea, hypotension — mechanism unclear, possibly kinin-mediated.
- Treat with fluids and symptomatic care. Prevent by slowing and spacing infusions.
TRALI versus TACO
Both declare themselves 1–6 hours in with dyspnea and pulmonary edema. The difference is hydrostatic versus inflammatory, and the first drug is not the same.
TRALI — 1/12,000 RBC; 1/38,000 platelets
- Dyspnea ± fever, hypotension, normal JVP, normal NT-proBNP
- Bilateral infiltrates, non-cardiogenic edema (ARDS picture)
- Two-hit: recipient neutrophils primed by pre-transfusion stress; donor anti-HLA/HNA antibodies or bioactive lipids then attack them
- Support: oxygen, notify blood bank, intubate if needed. Do not lead with diuretics
- Prevention: male-donor plasma (fewer anti-HLA/anti-PMN antibodies); defer donors implicated in prior TRALI
TACO — 1/100 RBC
- Dyspnea, hypertension, elevated NT-proBNP, S3, cardiogenic edema
- Infusion rate or volume the recipient cannot process — elderly, HF, CKD, chronic anemia
- Sit up, oxygen, IV diuretics, ± nitrates, NIV
- Prevention: slower rate (~1 mL/kg/h), volume-reduced products, do not stack units 'because the Hb is 6.8'
Delayed reactions
| Reaction | Timing and picture | Mechanism | What to do |
|---|---|---|---|
| Delayed hemolytic (DHTR) 1/2,000 | ~3 days (classically 3–10): fever, falling Hb, jaundice, flu-like illness, hemoglobinuria. Positive DAT, ↑ bili/LDH, spherocytes, low haptoglobin | Anamnestic IgG against a previously seen antigen (Kidd, Duffy, Kell) → extravascular hemolysis | Supportive. Delayed serologic transfusion reaction is the same alloantibody without hemolysis |
| TA-GVHD — rare, typically immunosuppressed | 5–10 days (sometimes 2–6 weeks): fever, rash, mucositis, diarrhea, hepatitis, pancytopenia | Donor T cells attack a non-HLA-matched recipient who cannot reject them — immunosuppression or a first-degree-relative donor | Prevention is irradiation. Treatment after the fact is grim — this is why related-donor units are irradiated |
| Post-transfusion purpura — rare, women >>> men | 5–12 days: purpura, mucocutaneous bleeding, platelets <10k, anti-HPA-1a | HPA-1a-negative women immunized by pregnancy or prior transfusion, then exposed to common HPA-1a-positive donor platelets | First-line IVIG; second-line PLEX. Future platelets: HPA-1a-negative |
Acute immune
AHTR, FNHTR, urticaria, anaphylaxis, TRALI, IgA-related anaphylaxis.
Delayed immune
DHTR, TA-GVHD, post-transfusion purpura.
Non-immune
Cold toxicity, citrate toxicity, bacterial sepsis, TACO, viral infection.