[Pediatrics; erythroblastosis fetal].
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A retrospective survey of Winnipeg Rh laboratory data from January 1, 1981 to December 31, 1984 determined that, despite placental localization, 2.6% of 974 women having amniocenteses performed at 16 to 18 weeks' gestation for genetic reasons and 2.3% of 1215 women having amniocenteses performed between 32 and 38 weeks' gestation had fetal-maternal transplacental hemorrhages greater than or equal to 0.1 mL of fetal red cells due to placental trauma. In 1.6 and 1.8%, respectively, the fetal transplacental hemorrhages were greater than or equal to 1 mL. Four of 99 alloimmunized women undergoing 257 amniocenteses for determination of severity of fetal erythroblastosis had fetal transplacental hemorrhages all greater than 5 mL of fetal red cells. The 1.9% incidence of fetal transplacental hemorrhages after amniocentesis in alloimmunized women is 83% less than the 11.2% incidence that occurred in the authors' institution from February 1963 to December 1966. However, in three of the four women, there was a very rapid rise in Rh antibody titer and increased severity of Rh fetal disease. Only the alloimmunized woman who meets strict criteria, indicating that her fetus is at risk of fetal death, should be subjected to amniocentesis, and then only after careful placental localization by ultrasound. Because fetal transplacental hemorrhages occur after amniocentesis despite ultrasound placental localization, 300 micrograms of Rh immune globulin should be administered to all unimmunized Rh negative women after amniocentesis.
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Intra-uterine transfusion may be a life-saving procedure in severe cases of rhesus isoimmunization. Yet it may be technically difficult and poses a real hazard to the fetus. This material consists of 51 intra-uterine transfusions performed in 34 severe rhesus (anti-D) isoimmunized pregnant women. The selection of patients was based upon an evaluation of the severity of fetal erythroblastosis (past obstetric history, serological and amniotic fluid examinations). The major criterion for selection was the concentration of amniotic fluid bilirubin. The technique employed was based upon a fluoroscopic television control system. The most serious complications were blood-stained amniotic samples in 15% of the amniocenteses and vaginal leaking of amniotic fluid and preterm labour after the performance of the intra-uterine transfusions in 33%.
Immunohematologic and clinical data, i.e., antibody profile, location of the placenta, mode of cordocentesis, obtained from 48 pregnant patients with irregular erythrocyte antibodies during the last 2 years have been retrospectively evaluated. All fetuses of the patients received intrauterine transfusions for the treatment of fetal erythroblastosis. In 16 (33%) patients (group I) a secondarily induced antibody was detected after the onset of intrauterine transfusion therapy. 32 (67%) patients (group II) did not further develop new antibody specificities. Group I exhibited a significantly different distribution in the location of the placenta (p < 0.05; chi 2 test) as compared with a nonselected control group of pregnant women. In group I a 5-fold higher rate of anterior than posterior placenta location was found. The mode of cordocentesis differed significantly (p < 0.01; chi 2 test) between group I and group II patients. In group I a significantly higher rate of transplacental punctures than in group II had been performed. This has to be considered to be causative for the secondary sensitization. Therefore, the secondary induction of antibodies by invasive intrauterine interventions in our patients depended indirectly on the location of the placenta and directly on the mode of the puncture (trans- vs. paraplacental access).
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