Haemolytic disease of the fetus and newborn — branching viva

Branch 1 — Mechanism and prevention

The examiner opens: "Explain how this woman became sensitised and how it could have been prevented." A strong candidate traces the fetomaternal haemorrhage that exposed her to fetal RhD-positive cells, the maternal immune response producing anti-D IgG, and the fact that this crosses the placenta from about 16 weeks via the neonatal Fc receptor to bind and destroy fetal red cells. The prevention is antenatal and postnatal anti-D immunoglobulin to Rh-negative mothers, which suppresses sensitisation, and anti-D after any sensitising event such as a miscarriage — the Crowther Cochrane reviews established the evidence base. [1]

Branch 2 — Fetal surveillance and the MCA-PSV threshold

The examiner pivots: "How will you monitor this fetus?" The candidate states that once a clinically significant antibody is identified, serial antibody titres or quantitative anti-D levels are monitored, and at the laboratory-specific critical threshold, serial middle cerebral artery peak systolic velocity Doppler begins. The candidate names the validated non-invasive threshold: MCA-PSV above 1.5 multiples of the median for gestational age detects moderate-to-severe fetal anaemia (Mari, NEJM 2000), and the SMFM Clinical Guideline #8 codified this, retiring serial amniocentesis with delta-OD450. When the threshold is exceeded or hydrops develops, fetal blood sampling is performed with preparation for intrauterine transfusion. [3] [4]

Branch 3 — The postnatal ladder

The examiner presses on the newborn: "The infant is jaundiced at 12 hours. What is your plan?" The candidate recognises that first-24-hour jaundice is haemolysis until proven otherwise, takes cord blood for blood group, direct antiglobulin test, haemoglobin and bilirubin, plots the bilirubin on an hour-specific nomogram, and starts intensive phototherapy as the bilirubin approaches the threshold. If the bilirubin continues to rise toward exchange despite phototherapy, intravenous immunoglobulin 0.5 to 1 g per kilogram is given as an adjunct, and exchange transfusion is performed at the threshold or with signs of acute bilirubin encephalopathy. The candidate notes that haemolysis lowers the phototherapy and exchange thresholds. [5] [8]

Branch 4 — Anti-Kell and the deceptive variant

The examiner closes on the atypical: "How would your surveillance differ if the antibody were anti-Kell?" The candidate explains that anti-Kell binds the Kell antigen on erythroid progenitors and directly suppresses marrow erythropoiesis, so anaemia is disproportionate to haemolysis, reticulocytes are low, and bilirubin under-represents the severity. The MCA-PSV remains the surveillance tool, but the threshold to transfuse is lower because the marrow cannot compensate, and a reassuring bilirubin must never delay intrauterine transfusion when the MCA-PSV signals anaemia. [4]