Fever After A Blood Transfusion
A febrile reaction occurring during or shortly after a blood transfusion, most commonly caused by recipient antibodies against donor leukocyte antigens or cytokines accumulated in stored blood products.
This lecture by Dr. YY Hwang (Haematology, QMH) is a critical GC lecture covering everything that can go wrong when you give someone blood products. The framing is clinical and practical: a patient on the ward spikes a fever mid-transfusion — what do you do? From that common scenario, the lecture radiates outward to cover all blood products, acute reactions (febrile, haemolytic, allergic, TRALI, TACO), delayed/chronic complications (delayed haemolytic reactions, TA-GVHD, iron overload, infections), massive transfusion complications, and prevention strategies including Patient Blood Management. [1]
Why this matters for exams: Transfusion reactions are a perennial SAQ/MCQ favourite. The 2025 Fourth Summative SAQ directly asked about risks and complications of blood transfusion and massive transfusion. [2] Past MCQs test irradiated blood products, CMV-negative products, and the distinction between TACO and TRALI. [3]
Learning Objectives (from the lecture): [1]
- Different kinds of blood products
- Acute adverse reactions after transfusion
- Chronic complications from transfusion
- How to prevent complications from transfusion
Blood products listed in the lecture: Red cells, Platelet concentrates, Fresh Frozen Plasma, Cryoprecipitate, Cryoprecipitate-reduced plasma, Leucocytes (buffy coat). [1]
| Product | Storage Temp | Shelf Life | Volume/Unit | Key Points |
|---|---|---|---|---|
| Packed Red Cells | 4°C | 42 days | ~330 mL | Additive: citrate-phosphate-dextrose-adenine (CPDA) |
| Platelet Concentrates | Room temp (20–24°C) | 4–5 days | Variable | Requires constant agitation; highest risk of bacterial contamination (stored at RT) |
| Fresh Frozen Plasma (FFP) | −30°C | Months (frozen) | ~250 mL | Contains ALL coagulation factors; must be thawed before use |
| Cryoprecipitate | −30°C | Months (frozen) | ~15–20 mL | Rich in fibrinogen, Factor VIII, vWF, Factor XIII |
| Leucocytes (buffy coat) | Room temp (20–24°C) | 8 hours | Variable | Must be irradiated to prevent TA-GVHD |
Why storage temperature matters: Platelets stored at room temperature support bacterial growth far more than red cells at 4°C — this is why bacterial contamination is most common in platelet transfusion. [1][4]
Why agitation matters for platelets: Without agitation, platelets aggregate and become non-functional. The short shelf life (4–5 days) further limits supply and increases wastage.
Why FFP must be thawed: Coagulation factors are preserved in the frozen state. Thawing takes ~30 minutes — important for emergency planning. Once thawed, FFP should be used within 24 hours.
High Yield: Platelet Contamination
The categories of risk from the lecture: Volume, Infections, Immunological, Electrolytes, Vascular, Iron load. [1]
This is a clean framework for any exam question asking "what are the risks of blood transfusion" — memorize these six categories.
A patient receiving red cell transfusion develops a kick of fever, now 38.5°C, with half a unit remaining. Doctor, what should you do? [1]
This is the clinical anchor of the lecture. The three differential diagnoses for fever during/after transfusion are: [1]
- Infection — bacterial contamination of the blood product
- Haemolytic reaction — ABO incompatibility
- Febrile non-haemolytic transfusion reaction (FNHTR)
Immediate Management Algorithm (from lecture + senior notes) [1][4][5]
- STOP the transfusion and spigot off the unit
- Vitals and resuscitation — ABC approach
- Recheck identity — patient wristband vs. blood unit label vs. blood form (clerical check)
- Save blood bag and IV set for investigation, but keep IV line patent with normal saline
- Workup: CBC, clotting, RFT, haemolytic screen (LDH, haptoglobin, bilirubin, urine Hb), T&S, crossmatch, DAT, blood culture (from patient AND from blood bag)
- Classify the reaction and manage accordingly (see below)
Exam Tip: SAQ Management Steps
The management of acute transfusion reaction is a classic SAQ. The steps above (stop, vitals, recheck, save, workup) are the markscheme backbone. [5]
Acute Adverse Reactions: Detailed Breakdown
ALWAYS A MEDICAL ERROR. Can be fatal. [1]
Pathophysiology (from first principles): [1]
- Recipient has naturally occurring IgM and IgG anti-A and anti-B antibodies
- These are complement-fixing antibodies → when they bind transfused incompatible red cells, the classical complement pathway is activated → intravascular haemolysis
- Free haemoglobin released into plasma:
- Activates platelets
- Induces vascular inflammation
- Binds nitric oxide → causes smooth muscle dystonia (vasoconstriction/vasodilation disturbance)
- Complement activation liberates potent anaphylatoxins (C3a, C5a) → degranulates mast cells → histamine release → vasodilation, hypotension
- Cytokines released from phagocytes (TNF, IL-6, IL-8) → systemic inflammatory response
- Activates the coagulation system → DIC
Renal failure may result from vasoconstriction, hypotension, or DIC — NOT from free haemoglobin itself. [1]
This is a critical point the lecturer emphasizes. Students often assume free Hb directly causes renal failure by "clogging tubules" — the lecture explicitly states the mechanism is haemodynamic and coagulopathic.
Clinical Features: [1]
- Abrupt onset of "sense of impending doom"
- Flushing, fever, rigors
- Loin/back pain (renal capsule distension from vasoconstriction)
- Vomiting, shock
- Haemoglobinuria ("coca-cola urine") [4]
- May develop DIC and acute renal failure
Management: [1]
- STOP the transfusion
- Intensive care often indicated
- Aggressive fluid resuscitation
- Alkaline diuresis (sodium bicarbonate to alkalinize urine → prevents Hb precipitation in renal tubules)
- Dopamine infusion to preserve renal perfusion
Prevention: [1]
- ALWAYS do Type and Screen properly
- ALWAYS give group-specific blood
- This is a systems/human error — bedside identity checks are the final safety net
ABO Incompatibility = Always a Medical Error
ABO incompatible haemolytic transfusion reaction is ALWAYS a medical error. It is caused by wrong patient identification, wrong labelling, or wrong blood issued. It can be fatal. Prevention is entirely about process: proper patient identification, proper sample labelling, proper bedside checking before transfusion. [1]
- Most common in platelet transfusion (room temperature storage) [1]
- Patient will be very septic, extremely ill [4]
- Common organisms: Pseudomonas fluorescens, Yersinia (psychrophilic organisms that can grow at 4°C in red cell units), Gram-negatives [5]
What to do: [1]
- Inspect the blood product for any visible damage or discolouration
- Microbiological workup of the patient (blood cultures from patient)
- Send the remaining blood product for culture + alert blood bank
Differentiating from other febrile reactions: [4]
- Septic reaction → patient is extremely ill, high fever (rise ≥ 1.5°C), often rigors, hypotension
- FNHTR → patient is generally well, mild fever (rise < 1.5°C)
Incidence: Red cells 1–12.4%; Platelets up to 30%. [1]
Definition: Rise of body temperature by 1°C or more during or within several hours of transfusion. [1]
Mechanism: [1]
- Leucoagglutinins in the recipient bind to transfused leucocytes, activating monocytes → release of cytokines with pyrogenic properties
- Leucoagglutinins could be anti-HLA class I or granulocyte-specific antibodies
- Additionally, plasma factors (cytokines: TNF-α, IL-1α/β, IL-6) accumulate during storage in the blood bag
- Correlates with: number of residual leucocytes, storage time, storage temperature, rate of infusion
- Highest in platelet concentrates [1]
- Chills, fever, dyspnoea, hypotension or hypertension, rigors
- Usually 30 min–2 hr after starting transfusion
- Mild fever, usually 1–2°C rise
- FNHTR is the most common cause of transfusion fever
- After excluding ABO incompatibility and bacterial contamination:
- Give paracetamol
- Fever is NOT a contraindication for transfusion — may continue at slower rate if rise < 1.5°C [4]
- Prevention: leucocyte-reduced (leucodepleted) blood products
FNHTR: Most Common Cause of Post-Transfusion Fever
Incidence: mild allergic reactions 3%; anaphylaxis 1 in 20,000 transfusions. [1]
- Range from urticaria to anaphylaxis
- Allergic reactions towards transfused proteins
- IgE mediated
- Beware of IgA-deficient and haptoglobin-deficient patients — they can develop severe anaphylaxis because they form antibodies against IgA/haptoglobin present in donor plasma [1]
Why IgA-deficient patients are at risk: ~1 in 700 people are IgA deficient. Some develop anti-IgA antibodies. When they receive blood products containing donor IgA, an anaphylactic reaction ensues. Management: use washed red cells (removes plasma proteins) or products from IgA-deficient donors.
Management: Mild → antihistamine, may restart slowly. Severe/anaphylaxis → IM adrenaline, steroids, antihistamines, saline-washed RBCs for future transfusions. [5]
Hypotension and vasodilation due to reactions towards bradykinins or prekallikrein activator in plasma products. [1]
- Bedside filtration of blood products exposes plasma to charged synthetic surfaces → activates the contact pathway → generates bradykinin
- Mainly a concern in patients on ACEI — ACE normally degrades bradykinin, so patients on ACEI cannot clear the excess bradykinin → exaggerated hypotension [1]
This is a subtle but testable point. If an exam stem mentions a patient on ACEI developing isolated hypotension during transfusion without other features, think hypotensive transfusion reaction.
TACO is the leading cause of transfusion-related mortality. (SHOT 2018) [1]
Occurs in 1–8% of transfusions. [1]
Why it happens: Blood products are essentially a volume load. If the patient's cardiovascular system cannot handle the extra volume (elderly, heart failure, renal impairment), they develop pulmonary oedema.
At-risk groups: [1]
- Elderly
- Renal impairment
- Heart failure
Prevention (from the lecture): [1]
- Avoid unnecessary transfusion
- Transfuse ONE unit of red cells and reassess (restrictive approach)
- Control transfusion rate
- Judicious use of diuretics (e.g., furosemide between units)
- Close monitoring of haemodynamic and fluid status
FFP and TACO: [1]
- Plasma volume in adult ≈ 40 mL/kg
- To achieve haemostasis, 25–30% factor level is adequate → replacing 1/3 to 1/4 of plasma volume is enough
- Typical dose of FFP: 10–15 mL/kg → equivalent to ~2 units in an average patient
- This represents a significant volume challenge
- Infuse at 1–3 mL/kg/hour with close monitoring and diuretics
Incidence: 1 in 65,000 FFP infusions. [1]
- Non-cardiogenic pulmonary oedema — this is what differentiates it from TACO
- Chills, fever, dyspnoea, and hypotension within 1–2 hours of transfusion
- Onset of respiratory distress defined to be within 6 hours of initiation of transfusion [1]
- Radiological evidence of new bilateral pulmonary infiltrates in the absence of circulatory overload
- Pathogenesis: leucocyte antibodies in donor plasma (usually anti-HLA or anti-HNA antibodies from multiparous female donors) react with recipient's neutrophils in the pulmonary vasculature → neutrophil activation → endothelial damage → capillary leak
TACO vs TRALI — Critical Exam Discriminator:
| Feature | TACO | TRALI |
|---|---|---|
| Mechanism | Volume overload (cardiogenic) | Donor antibodies vs recipient WBCs (non-cardiogenic) |
| BNP/NT-proBNP | Elevated | Normal/low |
| JVP | Raised | Normal/low |
| CXR | Pulmonary oedema + cardiomegaly | Bilateral infiltrates, NO cardiomegaly |
| Timing | Any time during/after transfusion | Within 6 hours |
| Response to diuretics | Improves | Does NOT improve |
| Fluid balance | Positive | May be neutral |
| Blood pressure | Hypertension common | Hypotension common |
| Management | Diuretics, slow/stop transfusion | Supportive, ventilatory support |
Prevention of TRALI: Use only male donors in preparation of FFP — multiparous female donors are more likely to have anti-HLA antibodies from prior pregnancies. [1]
Delayed / Subacute Adverse Reactions
Usually due to minor blood group incompatibility, e.g., Kidd antigen. [1]
Mechanism: [1]
- Initial antibody titre is too low to be detected in the T&S
- Transfusion of incompatible red cells provokes an anamnestic (memory) immune response
- Over days, antibody titre rises → sensitizes transfused RBCs → extravascular haemolysis (mainly in spleen)
- Onset of haemolysis: 4–5 days after transfusion (can be 3–21 days) [6]
Clinical features: [1]
- Fever, jaundice, and rapid drop in Hb
- Often clinically silent (< 10% clinically diagnosed) [6]
- NO intravascular haemolysis features (no haemoglobinuria)
Investigations: [1]
- CBP, reticulocyte count, manual blood film
- Haptoglobin, methaemalbumin, direct/indirect bilirubin, LDH
- Direct antiglobulin test (DAT), Indirect antiglobulin test (IAT)
- Extended red cell phenotype (of pre-transfusion sample)
Management: Generally self-limiting. Avoid future transfusion with the implicated red cell antigen. [6]
Acute vs Delayed Haemolytic Reaction
Acute: ABO incompatibility → IgM complement-fixing → intravascular haemolysis → haemoglobinuria, shock, DIC, renal failure. ALWAYS a medical error. Delayed: Minor blood group (e.g., Kidd) → IgG → extravascular haemolysis → fever, jaundice, Hb drop 4–5 days later. Often clinically silent. [1]
Mortality: 90%. [1]
Mechanism: [1]
- Transfused allogeneic (donor) lymphocytes attack the recipient
- Causes marrow aplasia, diarrhoea, rash, and hepatitis
- 4 to 30 days after transfusion
Who is at risk: [1]
- Immunocompromised recipients: preterm infants, bone marrow transplant recipients, congenital immunodeficiency
- Immunocompetent recipients receiving blood from a donor who is HLA-homozygous at a locus shared with the recipient — the recipient's immune system fails to recognize the donor lymphocytes as foreign because they share one HLA haplotype, but the donor lymphocytes CAN recognize the recipient's "other" haplotype as foreign
Prevention: Irradiation of blood products — gamma irradiation (or X-irradiation) inactivates donor lymphocytes while preserving red cell and platelet function. [1]
Irradiation of blood products before transfusion in all immunocompromised patients. [1]
Past Paper: MCQ on Irradiated Blood Products
A 2023 MCQ asked: A post-allogeneic stem cell transplant patient needs transfusion. CMV seropositive but CMV antigen negative. What blood product? Answer: One unit of irradiated red cell (option C). NOT CMV-negative (patient is already CMV seropositive — the horse has bolted). Irradiation is mandatory post-transplant to prevent TA-GVHD. [3]
Massive Transfusion Complications
Massive transfusion = > 1 total blood volume in 24 hours (or > 10 units packed RBCs). [5]
Citrate is present in stored red cells as anticoagulant. [1]
- Massive rapid transfusion → citrate toxicity
- Risk is higher in infants and patients with liver impairment (liver metabolizes citrate)
- Citrate chelates calcium → lowers ionized calcium → QT prolongation and arrhythmia
- Treatment: replace calcium with 10% calcium gluconate (10 mL for every 1 litre of citrated blood) [1]
Potassium is released from red cells with storage. [1]
- Extracellular potassium in a unit of red cells stored for 28 days ≈ 10.2 mmol
- Risk of hyperkalaemia in infants and patients with renal impairment [1]
Why potassium leaks with storage: During storage, the Na⁺/K⁺-ATPase pump on red cell membranes gradually fails → K⁺ leaks out of cells into the supernatant. Older units = more K⁺. This is why fresh blood is preferred for neonatal transfusion.
| Complication | Mechanism | Risk Groups | Prevention/Treatment |
|---|---|---|---|
| Hypothermia | Cold blood infused rapidly | All massive transfusion | Blood warmer |
| Citrate toxicity | Citrate chelates Ca²⁺ → ↓iCa → arrhythmia | Infants, liver impairment | 10% Ca gluconate (10 mL per 1L blood) |
| Hyperkalaemia | K⁺ leaks from stored RBCs | Infants, renal impairment | Use fresher units, monitor K⁺ |
| Dilutional coagulopathy | Packed RBCs lack clotting factors/platelets | All massive transfusion | Balanced resuscitation: RBC:FFP:Plt ≈ 1:1:1 |
Long-Term / Chronic Complications
Infectious risks include: Hepatitis C, Hepatitis B, HIV, Malaria, Zika, West Nile Virus, HTLV, vCJD, Trypanosoma, Syphilis, Hepatitis E, Japanese Encephalitis, CMV. [1]
Prevention: [1]
- Voluntary donation and donor deferral (screening questionnaires, travel history, risk behaviour)
- Universal pathogen inactivation (emerging technology, not yet universal)
- Nucleic acid testing (NAT) for HIV, HBV, HCV to shorten the "window period"
CMV specifically: [1]
- Prevention of transfusion-transmitted CMV infection — use of CMV-negative products
- Important for: seronegative pregnant women, neonates, seronegative transplant recipients with seronegative donors
- Leucodepletion also reduces CMV risk (CMV resides in leucocytes)
1 unit of blood = 200 mg iron. Daily excretion of iron = 1 mg. [1]
This means the body has essentially no mechanism to actively excrete excess iron. A chronically transfused patient (e.g., thalassaemia major) accumulates iron relentlessly.
Consequences of iron overload: [1]
- Iron accumulation in liver → liver fibrosis and HCC
- Heart → heart failure
- Endocrine organs → diabetes mellitus
- Growth retardation and hypogonadism (pituitary gonadotroph iron deposition → hypogonadotrophic hypogonadism) [7]
Monitoring: [1]
- Serum ferritin
- MRI T2 of liver and heart* (gold standard for quantifying organ iron)
- Liver biopsy (rarely needed now with MRI)
Treatment: Iron chelation therapy [1]
- Deferoxamine (subcutaneous/IV), deferasirox (oral), deferiprone (oral)
The safest transfusion is not to transfuse at all. [1]
The lecture lists these prevention strategies: [1]
- Voluntary donation, donor deferral → reduce infection transmission risk
- Universal pathogen inactivation (investigational)
- Prestorage leucocyte reduction (aim: < 0.5 × 10⁹ leucocytes per unit) → reduces FNHTR, CMV transmission, HLA alloimmunization
- Bedside filtration
- Premedication — antihistamine and steroid (for patients with history of allergic reactions)
- Use only male donors in preparation of FFP → reduces TRALI risk
- Irradiation of blood products in all immunocompromised patients → prevents TA-GVHD
- Alternatives to allogeneic blood:
- Iron supplementation (treat iron deficiency before resorting to transfusion)
- Acellular volume expanders (crystalloids, colloids)
Patient Blood Management (PBM) — Three Pillars [1]
| Pillar | Strategy |
|---|---|
| 1st Pillar: Optimize Haematopoiesis | Treat iron/B12/folate deficiency, use EPO, address underlying cause of anaemia |
| 2nd Pillar: Minimize Blood Loss | Surgical haemostasis, cell salvage, antifibrinolytics (tranexamic acid), restrictive phlebotomy |
| 3rd Pillar: Optimize Patient-Specific Tolerance of Anaemia | Restrictive transfusion thresholds, optimize cardiopulmonary reserve, timely decision-making |
Patient Blood Management - Three Pillars
The three pillars of Patient Blood Management: (1) Optimize haematopoiesis, (2) Minimize blood loss, (3) Optimize patient-specific tolerance of anaemia. This is the modern framework to reduce unnecessary transfusion. "The safest transfusion is not to transfuse at all." [1]
From related GC material and senior notes: [8]
- Restrictive strategy: Transfuse when Hb < 7 g/dL → associated with better outcomes (lower rebleeding rate, lower mortality at 6 weeks)
- Liberal strategy: Transfuse when Hb < 9 g/dL → poorer prognosis
- Exceptions to restrictive strategy:
- Haemodynamically unstable patients
- Underlying cardiovascular disease (especially ACS) → threshold Hb 8–9 g/dL
In Hong Kong, cross-matching is NOT routinely done — Type and Screen is used instead. [9]
| Step | What It Does | Why |
|---|---|---|
| Type | ABO and Rh typing of patient's red cells | Ensures group-compatible blood |
| Screen | Check patient's serum against panel of RBCs with known antigens by indirect Coombs test | Detects unexpected antibodies (e.g., anti-Kidd, anti-Duffy) |
| Crossmatch | Only if screen is positive; "trial transfusion" of patient serum + donor RBCs | 30–45 min; ensures compatibility when antibodies are present |
- T&S is only valid for 3 days (new antibodies can form) [5][9]
- If screen is positive → "ALERT" symbol on blood bank system → additional testing needed before issuing RBCs [9]
| Reaction | Timing | Mechanism | Key Features | Management | Prevention |
|---|---|---|---|---|---|
| AHTR | Immediate (min) | ABO mismatch, IgM, complement, intravascular haemolysis | Doom, shock, haemoglobinuria, DIC, renal failure | Stop, ICU, fluids, alkaline diuresis, dopamine | Proper T&S, bedside ID checks |
| Bacterial sepsis | During/immediately after | Contaminated product | Very sick, high fever ≥1.5°C | Stop, blood cultures (patient + bag), anti-pseudomonal Abx | Inspect product, platelet storage limits |
| FNHTR | 30 min–2h | Leucoagglutinins, cytokines | Mild fever (↑1°C), chills | Paracetamol, may restart slowly | Prestorage leucoreduction |
| Allergic | During transfusion | IgE vs plasma proteins | Urticaria → anaphylaxis | Antihistamine ± adrenaline | Premedication; washed RBCs for IgA-deficient |
| Hypotensive | During transfusion | Bradykinin (esp. ACEI patients) | Isolated hypotension | Supportive | Avoid bedside filtration in ACEI patients |
| TACO | During/after | Volume overload | APO, raised JVP, ↑BNP | Diuretics, slow/stop transfusion | Slow rate, 1 unit then reassess, diuretics |
| TRALI | Within 6h | Donor anti-WBC Ab | Non-cardiogenic pulm oedema, bilateral infiltrates, hypotension | Supportive, ventilation | Male-only donors for FFP |
| DHTR | 4–5 days (3–21d) | Minor blood group Ab, anamnestic, extravascular haemolysis | Fever, jaundice, ↓Hb, +ve DAT | Supportive, avoid antigen | Extended phenotype |
| TA-GVHD | 4–30 days | Donor lymphocytes attack recipient | Rash, diarrhoea, hepatitis, marrow aplasia, 90% mortality | Largely untreatable | Irradiation |
| Haemosiderosis | Chronic | Iron accumulation (200mg/unit) | Heart failure, cirrhosis/HCC, DM, hypogonadism | Iron chelation | Minimize transfusion |
Past Paper Analysis and Exam Intelligence
Stem: 55yo male, alcoholic cirrhosis, massive haematemesis, hypotension, oliguria, 11 packs transfused.
(a) DDx for hypotension and oliguria: Hypovolaemic shock (ongoing bleeding), Transfusion reaction (AHTR/septic) (b) Aim of blood transfusion: Restore oxygen-carrying capacity / maintain Hb at an adequate level to ensure tissue oxygenation (not to normalise Hb) (c) Three risks of blood transfusion: Infection, Immunological reactions, Volume overload (use the lecture's 6 categories) (d) Three complications of massive transfusion: Hypothermia, Citrate toxicity (hypocalcaemia), Hyperkalaemia (also accept dilutional coagulopathy)
Stem: Post-allogeneic SCT, Hb 6.8, CMV seropositive, CMV antigen negative. Best product? Answer: C — One unit of irradiated red cell. NOT CMV-negative (already seropositive). Irradiation is mandatory to prevent TA-GVHD.
| Trap | Why Students Fall For It | Correct Answer |
|---|---|---|
| Choosing CMV-negative blood for CMV seropositive patient | Confusing seropositive with active CMV | If patient is already CMV seropositive, CMV-negative product offers no benefit |
| Saying free Hb causes renal failure in AHTR | Intuitive but wrong per lecture | Renal failure is from vasoconstriction, hypotension, or DIC |
| Calling FNHTR an indication to stop transfusion permanently | Fear of "transfusion reaction" | FNHTR is benign — give paracetamol, may restart at slower rate |
| Confusing TACO with TRALI | Both cause respiratory distress | TACO = cardiogenic (↑BNP, responds to diuretics); TRALI = non-cardiogenic (↓BP, within 6h) |
| Forgetting irradiation for immunocompromised patients | Focus on leucoreduction instead | Leucoreduction ≠ irradiation; irradiation prevents TA-GVHD |
-
SAQ: A patient develops fever during red cell transfusion. List 3 differential diagnoses and outline your immediate management steps. (Bacterial contamination, ABO haemolytic reaction, FNHTR; Stop transfusion, vitals, recheck identity, save bag, workup)
-
SAQ: Describe the pathophysiology of ABO incompatible acute haemolytic transfusion reaction. (IgM anti-A/B → complement activation → intravascular haemolysis → free Hb + anaphylatoxins + cytokines → DIC, shock, renal failure from vasoconstriction/hypotension/DIC)
-
MCQ: Which transfusion complication is the leading cause of transfusion-related mortality? (TACO)
-
SAQ: List 3 complications of massive blood transfusion and explain the mechanism of each. (Hypothermia — cold blood; Citrate toxicity — citrate chelates Ca²⁺; Hyperkalaemia — K⁺ leaks from stored RBCs)
-
MCQ: A patient on ACEI develops isolated hypotension during FFP transfusion with no other features. Most likely cause? (Hypotensive reaction due to bradykinin accumulation)
-
SAQ: A thalassaemia major patient receives regular transfusions. What long-term complication are they at risk of, and how do you monitor and treat it? (Haemosiderosis; Monitor: ferritin, MRI T2; Treat: iron chelation)*
-
MCQ: Differentiate TACO from TRALI. (See table above — BNP, BP, CXR, diuretic response)
-
SAQ: What are the three pillars of Patient Blood Management? (Optimize haematopoiesis, Minimize blood loss, Optimize tolerance of anaemia)
High Yield Summary
Fever during transfusion: Think infection (bacterial contamination), ABO haemolytic reaction, or FNHTR. Always stop, check identity, and work up. AHTR is always a medical error — IgM complement-mediated intravascular haemolysis — manage with ICU, fluids, alkaline diuresis. Renal failure is from vasoconstriction/hypotension/DIC, NOT from free Hb. FNHTR is the most common cause — give paracetamol, may restart. TACO is the #1 cause of transfusion mortality — prevent by transfusing 1 unit then reassessing, especially in elderly/HF/CKD. TRALI is non-cardiogenic pulmonary oedema within 6 hours — caused by donor anti-leucocyte antibodies — prevent by using male-only FFP donors. TA-GVHD has 90% mortality — prevent with irradiation in immunocompromised patients. Massive transfusion complications: hypothermia (use warmer), citrate toxicity (give calcium), hyperkalaemia (use fresh blood). Iron overload: 200 mg iron per unit, 1 mg/day excretion — monitor with ferritin and MRI T2*, treat with chelation. The safest transfusion is not to transfuse at all — Patient Blood Management: optimize haematopoiesis, minimize blood loss, optimize tolerance of anaemia.
Active Recall - Fever After a Blood Transfusion
[1] Lecture slides: GC 049. Fever after a blood transfusion.pdf (all pages) [2] Past papers: 2025 Fourth Summative SAQ.pdf (Q2, p4) [3] Past papers: 2023 Fourth Summative MCQ.pdf (Q45, p17) [4] Senior notes: Block A - Fever after a blood transfusion_ transfusion and related problems.pdf (pp1, 8, 9) [5] Senior notes: Maksim Medicine Notes.pdf (p184) [6] Senior notes: Ryan Ho Haemtology.pdf (p147) [7] Senior notes: Block A - I keep on bumping into people on my side_ pituitary tumours; hypopituitarism.pdf (p18) [8] Senior notes: Block A - Coffee ground vomitus tarry stool upper GI bleeding.pdf (pp13–14) [9] Senior notes: Block A - Introduction to Haematological investigations (CBP, Clotting).pdf (pp24–25)