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PA21.1-6 | Transfusion Reactions & Investigation — Part 3

Delayed Transfusion Reactions

Four-panel infographic explaining delayed haemolytic transfusion reaction, transfusion-associated graft-versus-host disease, TA-GVHD prevention by irradiation, and chronic transfusion iron overload.

Delayed Transfusion Reactions

Panel A: Delayed haemolytic transfusion reaction showing prior sensitisation, low undetectable antibody titre, 2-14 day anamnestic IgG response, IgG-coated donor RBCs, splenic macrophages, extravascular haemolysis, falling Hb, mild jaundice, low-grade fever, positive DAT.. Panel B: TA-GVHD showing viable donor T lymphocytes engrafting in an immunocompromised host and attacking skin, gut, liver, and bone marrow, with fever, rash, diarrhoea, hepatitis, pancytopenia, and mortality >90%.. Panel C: Prevention of TA-GVHD showing gamma irradiation of cellular blood products inactivating donor lymphocytes, with leukoreduction alone marked as insufficient.. Panel D: Iron overload showing repeated transfusions, approximately 200 mg elemental iron per unit, iron deposition in liver, heart, and endocrine pancreas, causing cirrhosis, cardiomyopathy, diabetes, and treatment with iron chelation therapy..

1. Delayed Haemolytic Transfusion Reaction (DHTR)

Occurs 2–14 days post-transfusion. Mechanism: an anamnestic (secondary) immune response — the patient was sensitised to a red cell antigen (most commonly Rh, Kidd, Duffy, Kell systems) by a previous transfusion or pregnancy. Titre was too low to detect pre-transfusion; re-exposure boosts IgG antibody production.

Mechanism: IgG-coated donor cells are removed by splenic macrophages — extravascular haemolysis (less catastrophic than AHTR).

Features: Falling Hb, mild jaundice, low-grade fever, positive DAT. Usually self-limiting. Detect with post-transfusion DAT and antibody screen.


2. Transfusion-Associated Graft-versus-Host Disease (TA-GVHD)

Occurs 1–6 weeks post-transfusion in severely immunocompromised patients (haematological malignancies, bone marrow transplant, congenital immunodeficiency).

Mechanism: Viable donor T-lymphocytes engraft and mount a GvH attack against host tissues.

Features: Fever, rash, diarrhoea, hepatitis, pancytopenia (marrow aplasia) — mortality >90%.

Prevention: Gamma-irradiation of cellular blood products kills donor lymphocytes. Leukoreduction alone is NOT sufficient.


3. Iron Overload

Each unit of blood contains ~200 mg elemental iron. Patients receiving chronic transfusions (e.g., thalassaemia, sickle cell disease) accumulate iron in the liver, heart, and endocrine organs — haemosiderosis → cirrhosis, cardiomyopathy, diabetes.

Treatment: Iron chelation therapy (desferrioxamine, deferasirox).


4. Post-Transfusion Purpura (PTP)

Rare. Occurs ~7–10 days post-transfusion. Antibody (usually anti-HPA-1a) destroys both donor AND recipient platelets → severe thrombocytopenia → purpura, bleeding.

Side-by-side comparison showing extravascular haemolysis in spleen versus intravascular haemolysis in blood vessels with labeled cellular mechanisms and clinical features.

Extravascular vs Intravascular Haemolysis: Mechanisms and Clinical Features

Panel A: Spleen cross-section showing red pulp macrophages, IgG-coated RBCs, phagocytosis process, spherocytes in circulation, mild jaundice indication. Panel B: Blood vessel lumen showing complement cascade (C5b-9), direct RBC lysis, free hemoglobin in plasma, kidney with hemoglobinuria.

CLINICAL PEARL

TA-GVHD vs AHTR — the overlooked danger:

Both can be fatal, but TA-GVHD is uniquely silent in its early phase and is virtually 100% preventable with irradiation. The clinical pearl: always check for immunocompromise before ordering blood products. A patient on aggressive chemotherapy, a post-BMT recipient, or a premature neonate — these patients MUST receive irradiated (and often CMV-negative, leukodepleted) products. Asking 'is this patient immunocompromised?' before every transfusion costs nothing; missing it costs everything.

Investigation of a Suspected Transfusion Reaction

A six-step flowchart shows the investigation of a suspected transfusion reaction from stopping the transfusion through patient stabilisation, clerical recheck, return of the unit, fresh sample collection, and laboratory evidence of haemolysis.

Investigation of a Suspected Transfusion Reaction

Panel A: STOP transfusion immediately; blood bag; transfusion line; emergency stop symbol; suspected reaction.. Panel B: Maintain IV access; cannula kept in place; airway, breathing, circulation assessment; vital signs; resuscitation access.. Panel C: Clerical recheck; patient wristband; blood group; unit label; request form; compatibility report; magnifying glass verification.. Panel D: Return blood unit, giving set, and all labels to blood bank; do not discard; unit re-examination for haemolysis, Gram stain, and culture.. Panel E: Fresh patient samples from a different vein; clotted sample for repeat ABO/Rh grouping, repeat crossmatch, serum haemolysis; EDTA sample for DAT; archived pre-transfusion sample for repeat DAT and grouping.. Panel F: Evidence of haemolysis; pink/red plasma haemoglobinaemia; urine haemoglobinuria with haem-positive dipstick and no RBCs on microscopy; increased LDH, bilirubin, free haemoglobin; decreased haptoglobin.. Bottom strip: Blood bank tests: repeat ABO/Rh grouping, repeat crossmatch, DAT, visual haemolysis inspection, direct Gram stain, and culture..

PA21.4 specifically requires you to enumerate the investigation steps — meaning an ordered, actionable sequence. Memorise the following algorithm:

Step 1 — STOP the transfusion immediately.
Do not wait to confirm — suspicion alone is sufficient to stop.

Step 2 — Maintain IV access; assess and stabilise the patient.
Check: airway, breathing, circulation. Record vital signs. Do NOT remove the cannula — you need access for resuscitation and fresh samples.

Step 3 — Clerical recheck.
Verify the patient's wristband and blood group vs the unit label, request form, and compatibility report. Most AHTR are caused by clerical error — this step is both investigative and immediately diagnostic.

Step 4 — Return the unit + giving set + all labels to the blood bank.
Do NOT discard anything. The blood bank will re-examine the unit for haemolysis, repeat typing, and perform direct gram stain and culture.

Step 5 — Collect fresh samples from the patient (from a different vein).
• Clotted sample: repeat ABO/Rh grouping, repeat crossmatch, serum for haemolysis
• EDTA sample: direct antiglobulin test (DAT)
• Pre-transfusion sample (from the blood bank archive): repeat DAT and grouping

Step 6 — Check for evidence of haemolysis.
• Visual inspection of plasma: pink/red = haemoglobinaemia
• Urine dipstick + microscopy: haemoglobinuria (haem-positive, no RBCs on microscopy)
• Serum LDH, bilirubin, free Hb: all elevated in haemolysis
• Haptoglobin: decreased (binds free Hb)

Step 7 — Blood culture.
One set from the patient + one from the blood unit residue (for septic reaction).

Step 8 — Monitor renal function and coagulation.
• Urine output, creatinine, urea — renal failure in AHTR
• Prothrombin time, aPTT, fibrinogen, D-dimer — DIC in AHTR

Flowchart showing eight sequential steps for investigating transfusion reactions, from stopping transfusion through patient monitoring.

Stepwise Investigation Protocol for Transfusion Reactions

Steps 1-4: Initial response: STOP transfusion (red highlight), stabilize patient with IV access, perform clerical recheck (orange highlight for importance), return blood unit to bank. Steps 5-8: Investigation phase: collect fresh samples for DAT/grouping/crossmatch, assess haemolysis via plasma/urine/LDH, obtain cultures from patient and unit, monitor renal function and coagulation.

SELF-CHECK

After stopping a suspected acute haemolytic transfusion reaction, what is the SINGLE MOST IMPORTANT immediate clerical action that is simultaneously investigative and preventive of further harm?

A. Send the patient's urine for haemoglobin dipstick

B. Order an urgent complete blood count

C. Verify the patient's identity band and blood group against the unit label and compatibility report

D. Collect blood for direct antiglobulin test (DAT)

Reveal Answer

Answer: C. Verify the patient's identity band and blood group against the unit label and compatibility report

The majority of AHTRs result from clerical error — a mismatch between the patient's identity and the unit issued. Rechecking the patient's wristband against the unit label and crossmatch report is the immediate clerical action that identifies whether a clerical error occurred AND prevents further transfusion of the wrong unit to any patient. Urine haemoglobin (A) and DAT (D) are important laboratory steps but come after stopping and stabilising. CBC (B) is useful for trend monitoring but is not the most urgent single action.

Prevention — the Bedside Imperative

Four-panel transfusion medicine infographic showing bedside patient and blood unit verification, ABO haemolysis mechanism, a 10-second pre-transfusion checklist, and reaction-specific prevention strategies.

Preventing Fatal Transfusion Reactions at the Bedside

Panel A: Bedside scene with clinician, patient wristband, packed red cell unit, donor group label, compatibility label, and crossed-out chart-only verification.. Panel B: ABO-incompatible donor red cells, anti-A/anti-B antibodies, complement activation, red cell agglutination, intravascular haemolysis, and free haemoglobin.. Panel C: Four-step bedside check: two identifiers, group and compatibility match, expiry and bag integrity, one unit at a time with re-check before any switch.. Panel D: Reaction-prevention pairs: AHTR with strict ABO/Rh verification, FNHTR with leucoreduction, TRALI with high-risk donor deferral, TACO with slow transfusion and loop diuretic, TA-GVHD with irradiated cellular blood components..

The majority of ABO haemolytic deaths are preventable. The bedside pre-transfusion check is a non-delegable clinical duty:

  1. Two-identifier rule: Confirm patient name + date of birth (or hospital number) on the wristband — NOT from memory or a chart.
  2. Unit label check: Donor group and compatibility label must match the patient's group.
  3. Expiry and integrity: Inspect the unit for discolouration, clots, or bag leaks — signs of bacterial contamination.
  4. Right patient, right time: Transfuse one unit at a time; do not switch units mid-transfusion without re-checking.

A 10-second bedside check before every unit is the single most powerful intervention to prevent the most fatal transfusion reaction. No technology substitutes for this.

Additional system-level prevention strategies:

ReactionPrevention
AHTRStrict ABO/Rh pre-transfusion verification
FNHTRLeucoreduction
TRALIDefer high-risk donors (multiparous women with anti-HLA antibodies)
TACOSlow transfusion; loop diuretic in at-risk patients
TA-GVHDGamma-irradiation of cellular products
Iron overloadIron chelation in chronic transfusion patients
SepticBacterial screening of units; good collection technique

SELF-CHECK

A 7-year-old boy with acute lymphoblastic leukaemia receiving induction chemotherapy requires a packed red cell transfusion. Which special preparation of the blood product is MANDATORY to prevent a potentially fatal complication?

A. Washed red cells to prevent IgA-mediated anaphylaxis

B. Gamma-irradiated blood to prevent transfusion-associated graft-versus-host disease

C. CMV-negative blood only

D. ABO-matched platelets to prevent post-transfusion purpura

Reveal Answer

Answer: B. Gamma-irradiated blood to prevent transfusion-associated graft-versus-host disease

Severely immunocompromised patients — including those on intensive chemotherapy — cannot destroy viable donor T-lymphocytes. These T-cells engraft and attack host tissues, causing TA-GVHD with >90% mortality. Gamma-irradiation kills donor lymphocytes and is mandatory for all cellular products given to immunocompromised patients. Washed red cells (A) are indicated for IgA-deficient patients. CMV-negative blood (C) is also recommended for immunocompromised patients and transplant recipients but does not prevent TA-GVHD. Platelet matching (D) does not prevent TA-GVHD.