Learn about blood transfusion contraindications, including when not to transfuse. Understand acute reactions like AHTR & their management.
SECTION 3: CONTRAINDICATIONS & ADVERSE EFFECTS --- HOW TO OPEN "Thank you. Before any transfusion, we must ask two questions — does this patient truly need blood, and what could go wrong? My section answers both." --- PART 1 — CONTRAINDICATIONS First, understand this:There are no absolute contraindications in a life-threatening emergency. If someone is dying from blood loss — you transfuse. Period. But outside emergencies, transfusion carries real risks. So the rule is: Only transfuse if the benefit clearly outweighs the risk. --- The Relative ContraindicationsThink of them in a simple way — "Can I fix this without blood?" 1. Anaemia with a treatable cause If the anaemia is from iron deficiency, B12 or folate deficiency — give the supplement. Transfusion doesn't fix the root problem. It just buys time and adds risk. 2. Stable patient, Hb above 7–8 g/dL Evidence shows no benefit. You're exposing the patient to transfusion risks for nothing. 3. Severe decompensated heart failure The heart is already struggling. Extra volume from transfusion can cause pulmonary oedema — this is TACO, which we'll cover shortly. If you must transfuse, go very slow and co-administer a diuretic. 4. Uncontrolled hypertension Transfusion increases circulating volume and can worsen BP further. Stabilise BP first. 5. Autologous blood available Always prefer the patient's own blood — zero risk of immune reaction or infection transmission. 6. Religious objection — Jehovah's Witnesses Informed refusal must be respected legally and ethically. Offer alternatives: tranexamic acid, IV iron, erythropoietin, cell salvage. 7. Active febrile illness If the patient is already febrile, you cannot distinguish a transfusion reaction from the existing fever. Postpone unless urgent. 8. High alloantibody load These patients have developed antibodies to many RBC antigens from previous transfusions or pregnancies. Crossmatching is difficult and haemolytic risk is high. Extended phenotype matching is required. 9. Hyperkalaemia or renal failure Stored pRBCs leak potassium over time — up to 50 mmol/L by day 42. In a patient who already can't excrete potassium, this can cause dangerous hyperkalaemia or even cardiac arrest. Use the freshest unit available. --- Presenting this section, say: "As you can see, most of these contraindications share a common thread — the existence of a safer alternative. Our job as clinicians is to exhaust those alternatives before reaching for blood." --- PART 2 — ACUTE TRANSFUSION REACTIONS Before you go into each reaction, understand this framework:Every reaction has: - A cause (why it happens) - A mechanism (how the body reacts) - Features (what you see) - Management (what you do) - And the first action for almost every acute reaction is the same: STOP THE TRANSFUSION IMMEDIATELY. --- 🔴 1. AHTR — Acute Haemolytic Transfusion Reaction The most dangerous acute reaction. Understand it first:ABO incompatibility means the patient is receiving blood their immune system recognises as foreign. Here's what happens step by step: - Patient has pre-formed IgM antibodies against the donor's ABO antigens (e.g. a group A patient receives group B blood) - IgM binds to the foreign red cells - This activates the complement cascade — starting from C1 all the way to the membrane attack complex (MAC) - MAC punches holes in the donor RBC membranes → intravascular haemolysis — the red cells burst inside the blood vessels - Haemoglobin is released into the plasma → passes into urine → haemoglobinuria (red/dark brown urine) - The complement activation and cell destruction trigger systemic inflammation → fever, hypotension, shock - Released RBC contents and inflammatory mediators activate the coagulation cascade → DIC (Disseminated Intravascular Coagulation) - How does DIC happen here? When red cells lyse, they release thromboplastin (tissue factor) into the bloodstream. This triggers widespread, uncontrolled clotting throughout the body. All the clotting factors get consumed trying to manage this. The patient ends up with clots forming everywhere AND simultaneously bleeding — because there are no clotting factors left. This is DIC. - The complement fragments also cause renal vasoconstriction + haemoglobin deposits in tubules → acute kidney injury - Features: - Fever, rigors - Severe back and loin pain — classic, due to renal involvement - Red/dark brown urine — haemoglobinuria - Hypotension, tachycardia - Bleeding from multiple sites — DIC - Renal failure - Management: - STOP transfusion immediately - Maintain IV access — give IV fluids aggressively - Keep urine output above 1 mL/kg/hr to flush the kidneys - Treat DIC with FFP and platelets - Renal support if needed — dialysis in severe cases - Send the blood bag back to the bank with a patient sample — investigate the error - Report as a critical incident - Mortality: 10% if more than 200 mL of incompatible blood has been transfused. Cause of the error?Almost always clerical — wrong label, wrong patient, wrong bag. This is why bedside identity checks exist. --- 🟡 2. FNHTR — Febrile Non-Haemolytic Transfusion Reaction The most common reaction. Understand it:No red cell destruction here. Instead, the recipient's antibodies react with donor white cell (leukocyte) antigens , or cytokines that accumulated in stored blood trigger an inflammatory response. Features:- Fever — temperature rise of more than 1°C - Chills and rigors - No haemolysis — urine is clear, no DIC, no kidney failure - Management: - Slow or stop the transfusion - Give paracetamol - Critically — rule out AHTR first. Both present with fever. AHTR will kill; FNHTR won't. Check for back pain, urine colour, haemodynamic instability. - If AHTR excluded and symptoms are mild, you can resume slowly - Prevention: Leukoreduction — removing white cells before transfusion dramatically reduces this reaction. --- 🔴 3. TRALI — Transfusion-Related Acute Lung Injury Leading cause of transfusion-related death. Understand it:This is an immune-mediated lung reaction , not fluid overload. Here's the mechanism: - Donor plasma contains anti-HLA or anti-HNA antibodies (especially from multiparous female donors — pregnancy causes sensitisation to fetal antigens) - These antibodies enter the recipient's bloodstream and bind to the recipient's neutrophils - Activated neutrophils migrate into the pulmonary capillaries and release toxic granules - This damages the alveolar-capillary membrane → fluid leaks into the alveoli → non-cardiogenic pulmonary oedema - Lungs fill with fluid — but the heart is fine and there is no fluid overload - Features: - Sudden severe breathlessness - SpO₂ drops below 90% - Bilateral pulmonary infiltrates on chest X-ray — "white-out" - Fever, hypotension - No raised JVP, no peripheral oedema — distinguishes from TACO - Management: - STOP transfusion - High-flow oxygen; may need mechanical ventilation - NO diuretics — this is NOT fluid overload. Diuretics will make the patient worse. - Supportive care — ICU if needed - Prevention: Use plasma-poor products from male donors or screened female donors. Female donors who've been pregnant may have anti-HLA antibodies. Memory distinction: TRALI = lungs fail, no fluid overload, NO diuretics. TACO = lungs fail, fluid overload, GIVE diuretics. --- 🟡 4. TACO — Transfusion-Associated Circulatory Overload Common and frequently underdiagnosed. Understand it:Simply — the heart cannot handle the extra volume being transfused. This is pure hydrostatic pulmonary oedema . More common in elderly, heart failure patients, renal failure, infants. Features:- Hypertension — distinguishes from TRALI (which causes hypotension) - Tachycardia - Pulmonary oedema — breathlessness, crackles - Elevated BNP/NT-proBNP - Raised JVP, peripheral oedema - Management: - STOP transfusion - Sit patient upright - Furosemide IV — remove the excess fluid - Oxygen - Prevention: Transfuse slowly — 2 to 4 hours per unit. Give a diuretic between units in high-risk patients. --