Rhesus Allo-immunisation

Question 1

What are the principles of antibody mediated disease

Answer 1

Mother exposed to antigen  mother produces an Ab  Ab cross placenta  fetal sequelae

Question 2

Define autoimmunity and alloimmunity. Give examples.

Answer 2

Autoimmunity is antibody against an antigen the mother has herself (thyroid, connective tissue disease, immune thrombocytopenic purpura)

Alloantibody is Ab against antigen mother does not have (red cell alloimmunisation, perinatal alloimmune thrombocytopenia, perinatal alloimmune neutropenia).

Question 3

Red cell allo immunisation, list harmful and harmless types

Answer 3

Harmful: Rhesus D, c, C, E, Kell, Kidd, Duffy, MNS

Harmless: ABO (A, B) IgM doesn’t cross placenta; Lewis IgG fetus don’t have this; P

Question 4

Perinatal allo immune neutropenia –> consequence and treatment.

Answer 4

infection (bacterial sepsis)

Abx & immunoglobulin (NOT white cell infusion b/c will attack self)

Question 5

Consequence of red cell immunisation by severity.

Answer 5

Mild (50%) - mild jaundice

Moderate (25%) - severe jaundice, mild anaemia

Severe (25%) - severe anaemia, hydrops, FDIU

Question 6

Class severity of Red Cell immunisation via Ab Titre

Answer 6

Mild 512

Question 7

Incidence of red cell immunisation in pregnancy

Answer 7

1% all pregnancies

85% AntiD, 15% others (Kell, c, E, Fya)

Question 8

Primary immunisation occurs via?

Answer 8

Blood transfusion

Feto maternal haemorrhage (bleeding = abortion, miscarriage, ectopic, APH); (trauma = amniocentisis, CVS, ext version, MVA)

Occult (usually after 28/40, prophylactic antiD at 28-34 wks 90% prevented)

Delivery

Question 9

Secondary immunisation how does it work?

Answer 9

passively give anti-D, it blocks antigenic sites on foetal RBCs circulating in mother so mother’s WBCs can’t see antigen and cannot initiate antibody production.

Question 10

Who is screened for anti red cell Abs?

Answer 10

Everyone is screened (all pregnancies screened for anti-red cell Ab at first antenatal visit) 1% positive.

Rh-ve women (15% of population) screened at 1st antenatal visit, 28wks AND delivery

Question 11

Mx of woman with anti-red cell antibodies in pregnancy - 1st antenatal visit

Answer 11

confirm pregnancy, gest age, routine screen

iso-immunisation assessment

• risk allocation (Ab titre)
• partner grouping (dd = no issue, DD = treat, Dd = fetal DNA typing via amniocentesis (NO CVS to avoid fetal-maternal haemorrhage) or use free fetal DNA from maternal blood)
• general advice
• booking for maternal fetal medicine subspecialist

Question 12

Mx of woman with anti-red cell antibodies in pregnancy - subsequent antenatal visit

Answer 12

Low risk (Ab titre each visit; deliver 38 wks)

Med risk (Ab titre each visit; U/S from 20wks for MCA; CTG 32 wks b/c MCA PSV less reliable in later pregnancy; deliver at 38 wks)

High risk (U/S from 17wks; fetal blood sampling if MCA PSV increased; intrauterine transfusion if fetal anaemia)

Question 13

Intrauterine transfusion - what type of blood?

Answer 13

Maternal RBC but w/o plasma as Ab inside it

Question 14

Prevention of immunization

Answer 14

Blood transfusion for women (RhD compatible, Kell-ve)

Feto maternal haemorrhage (administer passive anti-D; use at sensitizing events e.g. bleeding/trauma/ routine 28 and 34wks/post delivery; volume use Kleihauer test to estimate haemorrhage amount; timing within 72hrs of event; contraindication if already immunised it won’t help)

Question 15

Principal of passive anti D?

Answer 15

You passively give anti-D, it blocks antigenic sites on foetal RBCs circulating in mother so mother’s WBCs can’t see antigen and cannot initiate antibody production

Question 16

Why doesn’t Anti-D cross the placenta and chew up the fetal cells?

Answer 16

Anti-D crosses the placenta and damages the foetus but it is minimal as it is in low titres. Only low titres required to mop up antigens in mother.