Rhesus and allo immunisation Flashcards
First antenatal visit steps?
- Confirm pregnancy
- Gestational age
- Routine screening
- Alloimmunisation assessment (risk allocation, partner grouping)
- General advice
- Booking (MFM subspecialist)
If heterozygous partner how to get foetal DNA to detect alloimmunisation?
Foetal DNA typing:
- amniocentesis
- free foetal DNA from maternal blood
Antenatal care for low risk isoimmunisation?
- Antibody titre at each visit (rises quickly if small foeto-maternal haemorrhage)
- Deliver at 38 weeks (avoid late pregnancy maternal -> foetal antibody transfer)
antental care for medium risk isoimmunisation?
- Antibody titre at each visit
- US from 20 weeks (MCA peak systolic velocity
- Cardiotocographs from 32 weeks
- Deliver 38w (or earlier if foetal anaemia)
Antenatal care for high risk isoimmunisation?
- US from 17 weeks
- Foetal blood sampling if MCA PSV increased
- Intrauterine transfusion (if foetal anaemia)
Screening for anti red cell antibodies in pregnancy?
- All at first antenatal visit
- Rh -ve additionally at 28w + delivery
How is immunisation prevented during blood transfusion?
- Rh (D) compatible
- Kell negative blood to women
How is immunisation due to foeto-maternal haemorrhage prevented?
Administration of passive anti D to Rh(D) negative women at times of sensitising events e.g.:
- bleeding in pregnancy (miscarriage, APH)
- trauma (amnio, CVS, MVA)
- routine at 28 and 34w
- post delivery
which parental antibody combination can lead to isoimmunisation of the mother?
RhD- woman is pregnant with foetus of RhD+ father which has inherited RhD
Which events may lead to maternal exposure to foetal RBCs?
- Childbirth
- Delivery of the placenta
- Threatened, spontaneous or elective abortion
- Ectopic pregnancy
- Bleeding a/w placenta previa or abruption
- Amniocentesis
- Abdo trauma
- External cephalic vesion
What occurs if an RhD+ foetus is carried by a previously alloimmuised mother?
Anamnestic response of mother with production of IgG which freely cross placenta, enter foetal circulation, bind antigenic sites on foetal RBCs.
What happens to foetal RBCs bound by maternal antiD?
Haemolysed in the foetal reticuloendothelial system and destroyed via complement pathways
- if foetus can maintain RBC production may not develop anaemia
- if large numbers of RBCs destroyed, foetal anaemia may develop
What are the typical characteristics of the first affected rhesus pregnancy?
- mild aenamia
- elevated bilirubin at birth (UV light therapy, exchange transfusion)
What is the serious sequelae or markedly elevated bilirubin?
Kernicterus - deposition of bilirubin in basal ganglia producing permanent neuro symptoms or even death
Why does foetal oncotic pressure decrease with severe haemolysis?
Foetal haemotopoiesis increases resulting in extra medullary haemotpoiesis (i.e. liver). When liver produces RBCs, synthesis of other proteins decreases leading to lower oncotic pressure.
This + increased intravascular resistance to flow due to haematopoietic islands in liver can cause ascites, pleural effusion or s/c oedema