Objective To evaluate the effects of serial intravascular transfusions on RhD-alloimmunized fetuses with ascites/ hydrops at the time of the first transfusion by measuring multiple hematological/biochemical blood variables. Methods Thirty-one singleton pregnancies were referred for management of RbD alloimmunization. Seven fetuses bad hydrops on presentation and were transfused immediately. The remainder underwent weekly ultrasound examinations, and fetal blood sampling and transfusion were performed on development of ascites. In the 104 samples collected overall from the 31 fetuses, glucose, uric acid, urea, creatinine, total protein, total and direct bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltransferase, alkaline phosphatase, lactic dehydrogenase, amylase, pseudo-cholinesterase (PCHE), creatine kinase, triglycerides and cholesterol were measured and compared with a reference range for non-anemic fetuses. Results The median gestational age at first transfusion was 26 (range, 18-34) weeks. There were three fetal losses after the first transfusion, two of which were due to procedure-related complications; one further loss occurred. At the first transfusion fetal hematocrit, pO(2), total protein, PCHE, creatinine and urea concentrations were significantly decreased compared to reference data, while total and direct bilirubin, AST, ALT, amylase, triglyceride and uric acid concentrations were increased. In all surviving fetuses ascites/hydrops bad disappeared by the second transfusion. Fetal pO(2), total protein, AST, ALT and PCHE concentrations bad normalized by the third transfusion. Correction of fetal anemia did not affect the other variables. Conclusions RbD-alloimmunized fetuses with ascites/hydrops at the time of the first transfusion bad a survival rate of 87%. Alterations of several biochemical fetal blood indices are present at the first sampling/transfusion, but most variables normalize with intravascular transfusions. Copyright (C) 2005 ISUOG. Published by John Wiley Sons, Ltd.