An achieved live birth following five-time serial stillbirth by serious Rh alloimmunization

A 41-year-old G6P1 woman presented for first prenatal visit at 26 weeks gestation. It was her sixth pregnancy. The details of the previous four pregnancies cannot be acquired, but all the four pregnancies were ended by stillbirth at approximately 3, 4, 5, and 6 months gestation, respectively, and the fourth fetus was diagnosed with fetal hydrops before death. Three years ago, she was in fifth pregnancy, fetal hydrops was found at 27 weeks gestation. She was hospitalized, laboratory examination showed her blood type was O Rh-negative, and the titer of anti-RhD was 256. Amniocentesis and intrauterine transfusion were suggested to her. Being worried about neonatal adverse outcome, the patient gave up any treatment and was discharged. The fetus was dead 3 weeks later and the patient received induced labor at a village hospital. In her childhood, the patient was hospitalized and received platelet transfusion several times because of immune thrombocytopenic purpura (ITP), and Rh blood type was not analyzed at that time. This was her sixth pregnancy. She was hospitalized at 28 weeks gestation because of high-risk pregnancy. The vital signs were stable. And the BMI was 31 kg/m. OGTT test suggested she had GDM. The titer of anti-RhD was 256. Ultrasound did not find any sign of fetal hydrops. Insulin was used to control the patient’s glycemia. Rh antibody and Doppler ultrasound screening (including the peak systolic velocity in the middle cerebral artery i.e. MCA-PSV, fetal growth, and fetal hydrops) were checked every 1–2 weeks regularly (see Table 1). Anti-RhD titer rose to 512 at 30 weeks gestation, but the MoM of the MCA-PSV did not change obviously, and there was no sign of fetal hydrops from ultrasound. Single-course dexamethasone was used to enhance fetal lung maturity. Serial MCA-PSV, anti-Rh titer and fetal monitoring were screened weekly. At 34 gestational weeks, the titer of antiRhD reached 1,024, emergency caesarean section (CS) was performed. A boy was born with Apgar score 10-10-10 and weight 1.77 kg. The newborn was transmitted to NICU immediately. Laboratory test showed the baby’s blood hemoglobin was 57 g/L, total bilirubin was 292 lmol/L and unconjugated bilirubin was 283 lmol/L. Direct coombs test, indirect coombs test and ABO radiation test were all positive. The titers of anti-D in the newborn’s serum were 0 for IgM and 16 for IgG. No other disorders were found in the preterm infant. After one blood exchange transfusion (1.5 ll for leukocyte privative red blood cells of O, Rh-dccee and 75 ml for blood plasma of AB, Rhnegative) and two times transfusion of O Rh-negative leukocyte privative red blood cells (0.25 and 0.4 ll respectively), the baby was cured and discharged healthy 3 weeks later. The blood type and antibody titers of the patient’s family are shown in Table 2 and the changes of the fetus’s hemoglobin, total bilirubin and unconjugated bilirubin of pre-, intraand post-blood exchanging M. Hou A. Xing (&) Department of Obstetrics and Gynecology, West China Second Hospital, Sichuan University, Chengdu, Sichuan 610041, China e-mail: aiyun-x@126.com