**4.3 Absence of facility for intrauterine transfusion for children with HDFN that are severely anaemic in utero**

The maternal alloantibody D produced as a result of sensitization of the Rh D negative mother to the Rhesus D positive foetal red cells are low molecular weight IgG antibody. This antibody can potentially cross the placenta barrier into the foetal circulation and can destroy the foetal red cells resulting in anaemia, heart failure, hydrops foetalis (fluid retention and swelling) and intrauterine death. In utero the diagnosis of foetal anaemia used to be made by carrying out ultrasound guided foetal blood sampling for analysis of the foetal haemoglobin and haematocrit or amniocentesis-an invasive ultrasound guided procedure with a significant 2% risk of foetal loss associated with entering the amniotic sac and obtaining amniotic fluid which is analysed for product of haemoglobin breakdown. However, non-invasive diagnosis of foetal anaemia can now be made using non-invasive Doppler ultrasound technology by measuring the middle cerebral artery peak systolic velocities (MCA PSV). The foetal anaemia can be managed with intrauterine blood transfusions. Intrauterine transfusion is associated with a number of risks; foetal bradycardia, foetal death, cord haematoma, haemorrhage from the puncture site, miscarriage, preterm labour and vessel spasm. The blood used for such transfusions must meet certain requirements; gamma irradiated red cells to prevent transfusion-associated graft-versus-host disease, haemoglobin S negative, CMV negative and significantly high PCV (0.70–0.85) [105, 106], unit must be C-, D-, E- and K-, leucocyte depleted to less than 1 × 106 leucocytes per unit, less than 5 days old, free from clinically significant irregular blood group antibodies and negative for high-titre anti-A and anti-B haemolysin. If the mother has other alloantibodies apart from D, it is vital that suitable unit negative for the specific antigens to which those maternal alloantibodies are specific are selected. Once the baby is delivered, intensive phototherapy and IV immunoglobulin along with antiglobulin (DAT) test should be carried out. There should also be continuous monitoring of the haemoglobin, haematocrit and bilirubin level. A positive DAT is diagnostic of HDFN and the baby sample should be sent for elution to identify if the antibody coating the foetal red cell is maternal alloantibody. If the bilirubin is not responsive to intensive phototherapy and continues to rise, the associated neonatal anaemia and hyperbilirubinemia can be managed by carrying our exchange blood transfusion (EBT) to prevent bilirubin encephalopathy by removing a significant number of maternal antibodies-coated foetal red cells and excess bilirubin and replacing it with donor red cells. The red cell product used for EBT must meet certain requirements; group O or ABO compatibility (mum and baby), compatible with any maternal antibody, gamma irradiated, collected in saline, adenine, glucose and mannitol (SAGM), fresh less than 5 days old, have high haematocrit (0.5–0.55) to prevent of post-exchange anaemia and polycythaemia and negative for high titre haemolysins. A number of these evidenced-based best practices; facility for intrauterine blood transfusion, facilities for diagnosis of foetal anaemia in utero, maternal alloantibody testing, elution testing, facility for gamma irradiation of blood, CMV testing of donors units, testing of donor units for other clinical significant red cell antigens apart from ABO and Rhesus D, SAGM units and leucodepletion of donor units are often not available in Nigeria and most developing countries. This failure in stewardship by government in these countries limits the delivery of best possible care in the management of HDFN and appropriate transfusion in these patients.
