Question

Kell Lewis was 19 when she met Kidd Duffy. Raised in the Rasneesh commune in Antelope, Oregon, Kell had a unique view of life; the college sophomore quite enjoyed living in a tent amongst the redwoods while pursuing a degree in graphic arts at Humboldt State University. However, the winter rains put a damper on tent life, so when she met Kidd (a junior in physics, finally finishing off his gen-ed requirements) in her Cubist French films class and learned that he lived in an RV (with a heater) it was love at first sight. The couple’s natural lifestyle soon resulted in pregnancy, and their first child (“Unit One”, affectionately known as “Uni”), a healthy 6 lb, 5 oz. girl, was born “naturally” in a swimming pool, with an astrologer/midwife in attendance. Life moved on, Kidd got his degree, and was accepted into a graduate program at Cal Tech. Kell liked the idea of living somewhere warm, so she and Kidd got married and with Uni they headed south. Life in Pasadena was different – they got tired of cooking Vegan, and Kell shaved her legs, but some things don’t change and soon Kell found herself once again pregnant. However, her first experience of natural childbirth was more than sufficient; this birth would involve doctors and nurses and all sorts of drugs. At this point they learned that while Kidd’s blood type was A positive, Kell’s was A negative. And so, at 18-weeks pregnancy, her obstetrician ordered an indirect Coombs test, and noted that she had a 1:16 titer. Fetal development was closely monitored, and she delivered a healthy 7 lb, 2 oz. boy (“Rutherford”) by induction at 36-weeks. Time moves on – Kidd took a postdoctoral position at the Jet Propulsion Labs, Kell got her realtor’s license, and they bought an SUV for Kell to take Uni and Rutherford to soccer in. More careful now, Rutherford was six years old when Kell realized she was once again “expecting”. At 15-weeks gestation, Kell’s indirect Coombs titer was 1:8, by 19 weeks it was 1:16. Her obstetrician harvested amniotic fluid at 24 weeks and detected the presence of bilirubin (indicative of fetal hemolysis). Further samples at 27 and 29 weeks showed a steady increase in bilirubin, so a blood sample was taken from the umbilical vein. This blood had a hematocrit of 7.4% (normal = 45%). Therefore 85 ml of packed red blood cells (type O, RH-negative) were transfused into the umbilical vein. At 31-weeks another umbilical vein sample was taken, with a hematocrit of 17.1%. Another 75 ml of packed red blood cells (type O, RH-negative) was transfused. From this point the fetus was examined weekly by ultrasound for evidence of hydrops fetalis – which did not occur. At 33-weeks, another umbilical vein sample was taken, with a hematocrit of 20.9%. At this point another 75 ml of packed red blood cells (type O, RH-negative) was transfused. At 34.5-weeks of gestation the fetus was deemed sufficiently mature to sustain extrauterine existence and labor was induced. A normal 5 lb, 7 oz. female (“Brittany”) was delivered. The umbilical vein hematocrit was 31.2%. Brittany developed normally and no further therapeutic measures were required.

Questions:

4. If Kidd’s blood type had been B positive instead of A positive, would the risk of hemolytic disease be greater, lesser or equal? Explain why (this one is a bit counter-intuitive – think about it…).

5. Kell’s sister Clare is also A-negative (she is the one that told you this story about her sister). During her second pregnancy, she had a negative indirect Coombs test, but her serum agglutinated Rh-positive red blood cells. What does this mean, and what do you as her obstetrician do about it?

Answer 1

If Kidd's blood type had been B positive instead of A positive then the risk of Hemolytic Disease be greater .

The child of Rh negative mother (genotype dd) and a Rh positive father (genotype DD) must be Rh positive (Dd).If Rh positive father is Dd the offspring may be Rh positive (Dd) or Rh negative (dd)

If Kell'S (mother) is Rh negative (A negative blood group) and foetus is Rh positive ,serious complication may occur.RBCs Containing 'D' antigen may pass the placenta from the foetus to the mother, either during pregnancy or small amount of foetal blood leaks into maternal responds by forming anti-D which returns to foetal circulation and tends to destroy foetal RBC.The degree of damage done to the foetus depends on the magnitude of the maternal anti-D response and ability of maternal Rh antibodies to cross the placenta.