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Select INCORRECT statements with reference to Rh grouping:
A. Erythroblastosis foetalis occurs when foetus is Rh-ve and mother is Rh+ve
B. Rh antigen is observed on RBCs of the majority of humans
C. Before blood transfusion Rh group should also be matched
D. Erythroblastosis foetalis occurs in second or subsequent pregnancies
Options
1
A and C only
2
A only
3
B and D only
4
C and D only
Correct Answer
Option 2: A only
Solution
1

Erythroblastosis foetalis mechanism:

Rh-NEGATIVE mother + Rh-POSITIVE foetus → problem

NOT: Rh-ve foetus + Rh+ve mother (statement A says this — WRONG)

2

A ❌ INCORRECT — Wrong: foetus Rh-ve, mother Rh+ve causes NO problem.

B ✅ CORRECT — ~85% humans are Rh+ve (have D antigen)

C ✅ CORRECT — Rh matching essential before transfusion

D ✅ CORRECT — Erythroblastosis affects 2nd/subsequent Rh+ve pregnancies

Only A is INCORRECT statement
Erythroblastosis = Rh-ve MOTHER + Rh+ve FOETUS (not the reverse)
Theory: Human Physiology
1. Rh Blood Group System

Rh (Rhesus) blood group system is second most important after ABO in clinical medicine. Named after Rhesus monkeys (Landsteiner and Wiener, 1940). D antigen: most important Rh antigen clinically. Rh-positive (Rh+): has D antigen on RBC surface. ~85% of people worldwide. Rh-negative (Rh-): lacks D antigen. ~15% of people. Unlike ABO: Rh-negative people do NOT naturally have anti-D antibodies. They develop anti-D only AFTER exposure to D antigen (sensitisation). This is why first transfusion of Rh+ve blood to Rh-ve person is usually safe (no antibodies yet), but the second transfusion can be dangerous (antibodies formed after first exposure cause haemolytic reaction).

2. Erythroblastosis Foetalis — Mechanism

Erythroblastosis foetalis (haemolytic disease of the newborn, HDN) occurs when: Mother is Rh-NEGATIVE (no D antigen) AND foetus is Rh-POSITIVE (has D antigen). During first Rh+ve pregnancy: small amount of foetal Rh+ve RBCs cross placenta into mother (especially at delivery) → mother makes anti-D IgM antibodies (sensitisation). Usually no problem in first pregnancy. During second (or subsequent) Rh+ve pregnancy: mother already has anti-D IgG antibodies (memory cells produce IgG quickly). IgG crosses placenta → attacks foetal Rh+ve RBCs → haemolysis → foetal anaemia, hyperbilirubinaemia (jaundice), heart failure, hydrops foetalis. Severe cases: stillbirth. Neonatal effects: jaundice (from bilirubin), kernicterus (bilirubin deposits in brain → intellectual disability). STATEMENT A IS WRONG: it says foetus Rh-ve + mother Rh+ve → this causes NO problem because Rh-ve foetus has no D antigen to sensitise mother.

3. Prevention of Erythroblastosis

Prevention: RhoGAM (Rho(D) immune globulin, anti-D immunoglobulin). Given to Rh-negative mothers: after delivery of Rh+ve baby (within 72 hours). After miscarriage, ectopic pregnancy, amniocentesis, CVS, trauma in pregnancy. Mechanism: the injected anti-D antibodies destroy any foetal Rh+ve RBCs in the mother's circulation before they can stimulate the mother to form her own anti-D antibodies → prevents sensitisation. This is PASSIVE immunisation — the antibodies are given, mother does not make her own. No RhoGAM needed if father is also Rh-negative (foetus cannot be Rh+ve). Treatment of HDN: Intrauterine transfusion: in severe cases, Rh-ve blood transfused to foetus in utero. Exchange transfusion of neonate: replace baby blood with Rh-ve blood to remove antibodies and bilirubin. Phototherapy: UV light converts bilirubin to water-soluble form → excreted. IVIG: intravenous immunoglobulin to slow RBC destruction.

4. Blood Group Matching for Transfusion

Before any blood transfusion: ABO typing: determine patient and donor ABO group. Rh typing: determine D antigen status (Rh+ or Rh-). Antibody screen: detect unexpected antibodies in patient serum. Crossmatch: mix patient serum with donor RBCs → check for agglutination. ABO compatibility: most critical. ABO mismatch → immediate haemolysis → potentially fatal. Rh compatibility: Rh-negative patients should receive Rh-negative blood whenever possible. Rh+ve patients can receive Rh-ve blood (no problem). Rh-ve patients CAN receive Rh+ve blood once (no antibodies yet) but will be sensitised → risky. Emergency: when no time for full crossmatch → use O negative blood (universal donor for RBCs). O-negative blood: no A, B antigens, no D antigen → compatible with almost anyone. Extended matching: for patients needing multiple transfusions (sickle cell, thalassaemia) → match more Rh antigens (C, c, E, e) and other blood groups (Kell, Duffy, Kidd).

5. Rh Factor and Pregnancy Management

Standard antenatal care for Rh-negative women: Blood type and Rh factor tested at first antenatal visit. Father blood group tested if possible. Anti-D antibody screening at booking and 28 weeks. If no antibodies: prophylactic anti-D immunoglobulin at 28 weeks (and 34 weeks in some protocols) AND within 72 hours of any sensitising event. If antibodies present: monitor antibody level (titre). If rising titre or ultrasound signs of foetal anaemia → intrauterine transfusion or early delivery. Middle cerebral artery Doppler: detects foetal anaemia non-invasively (high peak systolic velocity of MCA indicates anaemia). Cord blood at birth: Rh type and Coombs test. Direct Coombs (DAT): detects antibodies on foetal RBCs. Positive DAT → maternal antibodies coating foetal RBCs → HDN. Kleihauer-Betke test: measures amount of foetal blood in maternal circulation after delivery → determines anti-D dose needed.

6. Other Clinically Important Blood Group Systems

Over 35 blood group systems recognised by ISBT. Clinically important ones: Kell system: K and k antigens. K antigen is highly immunogenic (second most important after D). Anti-K causes haemolytic transfusion reactions and HDN. Source of K antigen: often blood transfusion. Duffy system: Fya and Fyb. Duffy-negative individuals (DARC null — common in West Africa) resistant to Plasmodium vivax malaria (Duffy antigen is the receptor for P. vivax invasion). Kidd system: Jka and Jkb. Notorious for delayed haemolytic transfusion reactions (antibody levels drop over time and undetectable → transfusion given → rapid anamnestic response → delayed haemolysis). MNSs system: glycophorin A (MN antigens) and glycophorin B (Ss antigens). Lewis system: Le antigens related to secretor status. ABO-related. P system: P1 antigen. Anti-P1 is common, usually clinically insignificant. H system: H antigen on chromosome 19. Bombay phenotype (hh) has no H antigen → cannot make A or B antigens.

7. Coombs Test — Direct and Indirect

Coombs test (antiglobulin test) detects antibodies against RBCs. Direct Coombs test (DAT): detects antibodies already bound to RBCs in vivo. Take patient RBCs → add anti-human immunoglobulin (Coombs reagent) → agglutination = positive. Used to diagnose: HDN (maternal antibodies on foetal RBCs), autoimmune haemolytic anaemia (patient antibodies on own RBCs), transfusion reaction. Indirect Coombs test (IAT): detects antibodies in serum. Take patient SERUM → incubate with known RBCs → wash → add Coombs reagent → agglutination = antibodies present. Used in: antibody screening before transfusion, crossmatching, antenatal antibody screening in pregnant women. Key distinction: Direct = antibodies ON cells (in vivo coated). Indirect = antibodies IN serum (looking for them in vitro).

8. Haemolytic Transfusion Reactions

Haemolytic transfusion reaction: most serious complication of blood transfusion. Acute haemolytic reaction: usually ABO incompatibility. Pre-formed antibodies immediately attack donor RBCs → intravascular haemolysis. Symptoms within minutes: fever, chills, back/flank pain, haemoglobinuria (dark red urine), shock, DIC, acute kidney injury. Most often caused by clerical error (wrong blood given to wrong patient). Fatal in 1 in 600,000 transfusions. Delayed haemolytic reaction: usually non-ABO alloantibodies (Kidd, Duffy, Kell, Rh). Antibody level undetectable before transfusion → transfusion given → anamnestic response → antibody rises → destroys donor RBCs. Occurs 3-14 days after transfusion. Symptoms: unexplained drop in haemoglobin, fever, positive DAT. Usually less severe than acute. Febrile non-haemolytic reaction: most common reaction. Caused by antibodies to donor WBCs or platelets, or cytokines in stored blood. Fever, chills but no haemolysis. Prevented by leukoreduction (removing WBCs from blood products).

Frequently Asked Questions
1. What exactly is wrong with statement A about erythroblastosis foetalis? ⌄
Statement A says: erythroblastosis foetalis occurs when foetus is Rh-NEGATIVE and mother is Rh-POSITIVE. This is COMPLETELY WRONG — the roles are reversed. Correct situation: Rh-NEGATIVE mother + Rh-POSITIVE foetus. Why: the foetus inherits D antigen (Rh+) from Rh+ve father. Foetal Rh+ve RBCs cross into Rh-ve mother at delivery. Mother (no D antigen, never exposed) now sees D antigen as foreign → makes anti-D antibodies (sensitisation). In subsequent Rh+ve pregnancies: IgG anti-D crosses placenta → attacks foetal Rh+ve RBCs. If foetus were Rh-NEGATIVE (no D antigen): mother would never be sensitised → no antibodies → no disease. A Rh+ve mother would never make anti-D antibodies (she has D antigen, recognises it as self). So A is fundamentally wrong.
2. Why does erythroblastosis foetalis not usually occur in the first pregnancy? ⌄
First pregnancy with Rh+ve foetus: foetal RBCs cross placenta mainly at delivery (not usually during normal pregnancy). Mother is sensitised → makes anti-D IgM antibodies. IgM: large pentameric molecule (molecular weight ~900 kDa) → CANNOT cross the placenta (placenta only allows IgG, ~150 kDa, to cross via FcRn receptors). So in first pregnancy: even if mother makes some anti-D, it is mainly IgM and cannot harm the foetus. After delivery: mother makes IgG anti-D memory. Second Rh+ve pregnancy: IgG anti-D made → crosses placenta → attacks foetal RBCs → HDN. Exception: some sensitising events can rarely cause problems in first pregnancy (large fetomaternal haemorrhage, prior transfusion with Rh+ve blood, threatened miscarriage).
3. What is the prophylactic role of anti-D immunoglobulin? ⌄
Anti-D immunoglobulin (RhoGAM): preparation of pooled anti-D IgG from human donors. Mechanism of prevention: When Rh-negative mother may have been exposed to Rh+ve foetal blood (at delivery, miscarriage, amniocentesis): inject anti-D immunoglobulin within 72 hours. The injected anti-D binds and destroys any foetal Rh+ve RBCs circulating in the mother before they can be processed by the mother immune system. Without the antigen to see, the mother immune system is NOT sensitised → does NOT make her own anti-D memory cells. So next Rh+ve pregnancy is safe. This is passive immunisation (antibodies given) preventing active immunisation (mother making own antibodies). Standard UK protocol: 500 IU anti-D at 28 weeks, 500 IU within 72 hours of delivery. This has almost eliminated HDN due to Rh incompatibility in countries with good antenatal care.
4. What percentage of humans are Rh-positive and Rh-negative? ⌄
Rh-positive (D antigen present on RBCs): approximately 85% of the world population. Rh-negative: approximately 15%. Ethnic variation: Rh-negative frequency: Europeans/Caucasians: ~15-17%. Sub-Saharan Africans: ~3-5%. East Asians (Chinese, Japanese): <1%. Indigenous Americans: very rare (<1%). Basque people (Spain/France): highest frequency ~30-35% Rh-negative. Why ethnic variation: the RHD gene deletion (Rh-negative is due to deletion of the entire RHD gene or mutations making it non-functional) arose at different frequencies in different populations through genetic drift. Rh-negative is most common in European populations. This has practical implications: in some countries, finding compatible Rh-negative blood for Rh-negative patients can be difficult, especially for rarer blood groups.
5. What happens if an Rh-negative patient receives Rh-positive blood? ⌄
First exposure: Rh-negative patient receives Rh+ve blood. Initially: often no immediate reaction (no pre-formed antibodies). BUT: patient is sensitised → immune system makes anti-D IgG antibodies over next 2-8 weeks. These antibodies persist as memory. Consequences: If patient receives Rh+ve blood again: anti-D attacks donor Rh+ve RBCs → delayed haemolytic transfusion reaction. For Rh-negative women of childbearing age: especially problematic — now sensitised → at risk for HDN in future Rh+ve pregnancies. Management: give anti-D immunoglobulin to unsensitised Rh-ve individuals as soon as possible after accidental Rh+ve transfusion (though large doses needed for transfusion vs small foetomaternal haemorrhage). Test: after 2-6 weeks, check for anti-D antibody formation. If already sensitised (anti-D detected): too late for prevention.
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