Blood groups and transfusion
Blood groups and transfusion: ABO, Rh, compatibility, components and reactions
ABO and Rh antigens and antibodies, compatibility testing, blood components and storage, and transfusion reactions, for FCPS Part 1. Covers haemolytic disease of the newborn, anti-D, Coombs tests, TRALI and TACO, and massive transfusion problems.
One of the most tested topics in past papers
The ABO system
| Group | Red cell antigen | Plasma antibodies | Can receive red cells from |
|---|---|---|---|
| O | None (H only) | Anti-A and anti-B | O only |
| A | A | Anti-B | A, O |
| B | B | Anti-A | B, O |
| AB | A and B | None | A, B, AB, O |
- ABO antibodies are naturally occurring, mainly IgM, formed in the first months of life against similar sugar antigens on gut bacteria and food. Being IgM, they fix complement strongly and cause intravascular haemolysis.
- Group O red cells are the universal red cell donor; group AB is the universal recipient. For plasma the rule reverses: AB plasma has no antibodies and suits anyone.
- A and B antigens are made by glycosyltransferases adding a sugar to the H antigen. The rare Bombay phenotype (hh) lacks H and makes anti-H, so these people can receive only Bombay blood.
- In most Pakistani surveys, group B is the most common and AB the least common.
- ABO haemolytic disease of the newborn (mother O, baby A or B) is common but usually mild: most anti-A and anti-B are IgM, which cannot cross the placenta, and fetal A and B antigens are weakly expressed and also present on other tissues that absorb antibody.
The Rh system
- The D antigen is the important one; most people (over 90% in Pakistan) are D-positive.
- Anti-D is not naturally present. It forms only after exposure to D-positive cells (transfusion, pregnancy) and is IgG, which crosses the placenta.
- Rh haemolytic disease of the fetus and newborn: a D-negative mother is sensitised by fetal cells, usually at the first delivery. In a later D-positive pregnancy her IgG anti-D coats fetal red cells (type II hypersensitivity), causing anaemia, hydrops fetalis, and after birth severe unconjugated jaundice and kernicterus.
- Prevention: anti-D immunoglobulin to D-negative women at about 28 weeks, within 72 hours of delivering a D-positive baby, and after sensitising events (miscarriage, ectopic pregnancy, abdominal trauma, amniocentesis, external cephalic version). The Kleihauer–Betke test measures the fetal cells in maternal blood to set the dose. Coexisting ABO incompatibility partly protects, because maternal anti-A or anti-B destroys fetal cells before D can sensitise.
| Feature | ABO | Rh (D) |
|---|---|---|
| Antibody | Naturally occurring | Only after exposure |
| Class | Mainly IgM | IgG |
| Crosses placenta | No (mostly) | Yes |
| HDN | Common, mild, can occur in first pregnancy | Severe, usually second and later pregnancies |
| Transfusion reaction | Immediate intravascular | Delayed extravascular |
Pretransfusion testing
- Group and screen: ABO and D type of the recipient, plus screening recipient plasma for clinically significant antibodies (anti-Kell, anti-Duffy, anti-Kidd).
- Crossmatch: recipient plasma against donor cells.
- Direct antiglobulin (Coombs) test: antibody or complement already on the patient's red cells (autoimmune haemolysis, HDN, transfusion reactions).
- Indirect Coombs test: free antibody in plasma (antenatal screening, crossmatching).
- Bedside identity check is the most important safety step; most fatal ABO reactions are clerical errors.
Blood volume
Blood volume is about 70 mL/kg in adult men, 65 mL/kg in women, about 80–85 mL/kg in infants and 90–100 mL/kg in neonates. A 5 kg infant therefore has about 420 mL, so a small loss is a large proportion of the circulation.
Blood components and storage
| Component | Storage | Use |
|---|---|---|
| Red cells | 2–6 °C, about 35–42 days | Anaemia, bleeding |
| Platelets | 20–24 °C with agitation, 5–7 days | Thrombocytopenic bleeding; cold causes clearance and loss of function; highest risk of bacterial contamination |
| Fresh frozen plasma | −25 °C or below | Multiple factor deficiency: DIC, massive transfusion, liver disease with bleeding |
| Cryoprecipitate | Frozen | Fibrinogen, factor VIII, vWF, factor XIII |
- Stored red cells change with time: potassium rises as it leaks from cells, 2,3-BPG falls (left-shifted curve, less oxygen release), pH falls, platelets and labile factors V and VIII decline, and citrate is present.
- Irradiation stops donor lymphocytes dividing (prevents transfusion-associated GVHD); leucodepletion reduces febrile reactions and CMV transmission; washing removes plasma proteins (IgA deficiency).
Transfusion reactions
| Reaction | Timing | Cause | Features |
|---|---|---|---|
| Acute haemolytic | Minutes | ABO mismatch; IgM and complement lyse donor cells in vessels | Fever, rigors, loin pain, hypotension, dark urine (haemoglobinuria), DIC, renal failure. Stop the transfusion at once, keep the line open with saline, recheck identity |
| Febrile non-haemolytic | During or soon after | Cytokines or antibodies to donor white cells | Fever alone; commonest; reduced by leucodepletion |
| Allergic | Minutes | IgE against plasma proteins | Urticaria, itching |
| Anaphylaxis | Minutes | IgA-deficient recipient with anti-IgA | Bronchospasm, hypotension |
| TRALI | Within 6 hours | Donor anti-HLA or anti-neutrophil antibodies | Non-cardiogenic pulmonary oedema, fever, hypotension |
| TACO | Within hours | Volume overload | Pulmonary oedema with hypertension, raised JVP |
| Delayed haemolytic | 5–10 days | Anamnestic IgG to minor antigens (Kidd, Rh) | Falling Hb, jaundice, positive direct Coombs |
| Transfusion-associated GVHD | 1–2 weeks | Donor lymphocytes engraft | Rash, diarrhoea, pancytopenia; usually fatal |
- Bacterial contamination (often of platelets) causes high fever and septic shock during transfusion.
- Repeated transfusion over years (thalassaemia) causes iron overload, needing chelation.
Massive transfusion
Defined as replacing one blood volume in 24 hours or half in 3 hours.
- Dilutional coagulopathy: give plasma, platelets and cryoprecipitate in balanced ratio.
- Hypocalcaemia: citrate binds ionised calcium (tingling, long QT, hypotension); give calcium.
- Hyperkalaemia: potassium from stored cells causes tall peaked T waves and arrhythmia, especially with rapid infusion of old blood.
- Hypothermia: cold blood chills the heart and worsens coagulopathy; blood is warmed to 37 °C to prevent hypothermia and arrhythmias.
- Acidosis, and later metabolic alkalosis as citrate is metabolised to bicarbonate.
Remember O red cells and AB plasma suit anyone; ABO antibodies are natural IgM, anti-D is acquired IgG.
Exam trap TACO comes with hypertension and fluid overload; TRALI with hypotension and normal filling pressures.
Exam trap A direct Coombs test looks at antibody on cells; an indirect Coombs test looks for antibody in plasma.
How FCPS asks about this
- Fever, loin pain, hypotension and dark urine minutes into a transfusion: ABO mismatch; stop it immediately.
- Why ABO HDN is mild: ABO antibodies are mostly IgM and fetal antigens are weak.
- Anti-D timing: 28 weeks and within 72 hours of delivery or a sensitising event; Kleihauer test sets the dose.
- Anaphylaxis to transfusion: IgA deficiency with anti-IgA antibodies.
- Storage of platelets: 20–24 °C with agitation; cryoprecipitate is richest in fibrinogen.
- Tall T waves after multiple transfusions: hyperkalaemia; tingling and long QT: citrate-induced hypocalcaemia.
- Blood volume of a 5 kg infant: about 420 mL (80–85 mL/kg).
Test yourself on this topic
5 of the 86 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A bleeding patient with DIC has fibrinogen of 0.8 g/L. Which blood component is the richest source of fibrinogen?
Answer: Cryoprecipitate
Cryoprecipitate is made by thawing FFP slowly at 4 °C; the precipitate is rich in fibrinogen, factor VIII, von Willebrand factor, factor XIII and fibronectin. It is used to replace fibrinogen (e.g. below 1.5 g/L in major haemorrhage, DIC, obstetric bleeding). FFP contains all coagulation factors at plasma concentrations. Prothrombin complex concentrate contains factors II, VII, IX and X (warfarin reversal). Platelets are given for thrombocytopenia or platelet dysfunction.
Blood components
- Cryoprecipitate: fibrinogen, VIII, vWF, XIII
- FFP: all factors
- PCC: II, VII, IX, X (warfarin reversal)
- Platelets: low count or dysfunction
Remember Cryo for fibrinogen.
Why the other options are wrong
- Platelet concentrate Platelets, little fibrinogen.
- Packed red cells No clotting factors.
- Albumin 20% No clotting factors.
- Prothrombin complex concentrate Vitamin K-dependent factors only.
A woman with the Bombay phenotype needs a blood transfusion after childbirth. Which blood can she safely receive?
Answer: Only Bombay (Oh) phenotype blood
People with the Bombay phenotype lack the H antigen (the precursor of A and B) and form anti-H, anti-A and anti-B antibodies. Group O red cells carry abundant H antigen, so they are destroyed. Only blood from other Bombay individuals is compatible, so relatives are screened and rare-donor registries used. The phenotype is more frequent in parts of South Asia.
Bombay phenotype
- No H antigen
- Has anti-H, anti-A, anti-B
- Group O blood incompatible
- Give Bombay blood only
Remember Bombay blood for Bombay patients.
Exam trap Bombay types as group O on forward grouping; reverse grouping reveals it.
Why the other options are wrong
- Group O Rh-negative blood Group O cells carry H antigen and will be haemolysed.
- Group AB blood Has H antigen.
- Any group with crossmatching Crossmatch will be incompatible with all non-Bombay blood.
- Group O blood washed of plasma The red cells still carry H antigen.
Which blood group's plasma can be given to a patient of any ABO group (universal plasma donor)?
Answer: AB
Red cells and plasma follow opposite rules. For red cells, group O (no A or B antigens) is the universal donor (O negative in emergencies, especially for women of childbearing age) and AB the universal recipient. For plasma (FFP), group AB contains no anti-A or anti-B, so it is the universal plasma donor; group O plasma contains both antibodies and can only go to group O recipients.
Universal donors
- Red cells: O negative donor, AB recipient
- Plasma: AB donor (no antibodies), O recipient
- Rules are opposite for cells and plasma
Remember O gives cells; AB gives plasma.
Why the other options are wrong
- O O plasma has anti-A and anti-B.
- A Contains anti-B.
- B Contains anti-A.
- O Rh-negative O is the universal red cell donor, not plasma donor.
An oocyte is fertilised in the ampulla on the day of ovulation. How long does the embryo usually take to pass through the tube and reach the uterine cavity?
Answer: About 3–4 days
After fertilisation in the ampulla, the embryo is moved toward the uterus by ciliary beating and smooth muscle contraction of the tube. Transit takes about 3–4 days; it is held for a while at the ampullary-isthmic junction and then passes the isthmus as progesterone relaxes it. It reaches the cavity as a morula or early blastocyst around day 4–5 and implants at about day 6–7, when the endometrium is receptive. Delayed transit, for example from tubal damage, favours ectopic implantation.
Tubal transit
- Fertilised in the ampulla
- Transit about 3–4 days
- Arrives as morula or blastocyst
- Implants day 6–7
Remember Three or four days down the tube.
Exam trap Slow transit from tubal damage lets the blastocyst implant in the tube.
Why the other options are wrong
- About 12 hours Too short for transit through the tube.
- About 7–8 days Implantation, not arrival, occurs about 6–7 days after fertilisation.
- About 14 days Far too long.
- About 21 days Far too long.
A woman with untreated thyrotoxicosis feels hot and sweaty even in winter, and her basal metabolic rate is raised. Which of the following actions of thyroid hormone mainly causes this?
Answer: Induced Na⁺/K⁺-ATPase and oxygen use
T3 enters cells and binds nuclear thyroid hormone receptors, changing gene transcription. It increases the synthesis of Na⁺/K⁺-ATPase, the number of mitochondria and uncoupling of oxidation, so ATP is used faster and oxygen consumption and heat production rise in most tissues (brain, spleen and gonads are exceptions). Sympathetic nerve activity is not increased; the adrenergic features come from greater tissue responsiveness to catecholamines. TSH is suppressed in thyrotoxicosis.
Thyroid hormone and heat
- T3 acts on nuclear receptors
- More Na⁺/K⁺-ATPase and mitochondria
- More oxygen use and heat
- Not in brain, spleen, gonads
Remember Thyroid hormone turns up the cell's engine.
Exam trap Thyrotoxic tremor and tachycardia reflect increased sensitivity, not increased sympathetic firing.
Why the other options are wrong
- Increased sympathetic nerve firing Sympathetic outflow is normal; responsiveness is raised.
- Increased TSH-driven thermogenesis TSH is suppressed in thyrotoxicosis.
- Reduced insulin secretion Not the cause of the raised BMR.
- Increased cortisol production Cortisol is not increased.
Where this sits in the CPSP syllabus
- Paper 1: Blood and immunity, Blood groups and transfusion