So while Suzanne was in utero, her mother's antibodies to her Rh+ blood passed through the placenta and into Suzanne's circulation. The antibodies caused hemolysis of Suzanne's blood, and she ramped up production of blood cells in her bone marrow to compensate. The new blood cells (baby red cells are called reticulocytes) are bigger, and babies are usually born with thick blood anyway. This gives the heart a heavy load to push, and can cause "high output heart failure" before the fetus is born.
There are lots of other complications that can occur. The mass lysis of red blood cells causes anemia and jaundice in the fetus. Bilirubin released from red blood cells into the plasma can cause irreversible brain damage and retardation. The brain area damaged is the basal ganglia. I haven't found anything too specific about the effects on the basal ganglia but I am particularly interested in this question. Any fetus that has fought long against it's mother's immune system will have an enlarged liver and spleen, and may be grossly bloated with ascites and water on the brain. Many babies with all this trouble are stillborn or die soon after birth. But not Suzanne. She's a fighter.
So Suzanne was born with erythroblastosis fetalis. She was born late--supposed to be an October baby but born in November. She "wouldn't come out". I wonder about this. Did her mother's body fail to push her out because she was being immunologically rejected? Or??? She was "taken by Ceasarian" in her mother's and sister's words. She was a "blue baby", but so far the family lore has told me no more about her appearance at birth.
Her sister told her that they sucked out her blood and gave her someone else's. Her sister freaked her out by saying she is not of the same blood because of it. "I don't know whose blood you got" and "I don't know who you are." Not very nice... Suzanne did receive exchange blood transfusions. They pulled out her blood to reduce the bilirubin overload (and jaundice), and replaced her lysed blood with someone else's intact blood. In 1955. And she survived. She is here today, teaching me about medicine. From spondylolytic spondylolisthesis to erythroblastosis fetalis in one person.
Her mother resented her. First of all, she hadn't been born on schedule. Second, she had to be "taken by Ceasarian", which isn't a pretty surgery now but back then, egad. Third, she needed this blood and apparently they had a hard time coming up with the right type for her. But it was urgent, I am sure. Suzanne's mother never once breast fed her. And she grew up to have allergies galore. That's another whole medical topic. Her mother never stopped telling her how much trouble she was. She feels right at home when I tell her she's trouble.
The story goes on. The way you are born, and the way you are treated just after birth, have a large part in forming you. But it is not the end of the story. As you live you have choices. It amazes me how much this one woman can teach me about medicine. I would not learn it the same way without this person with these stories to piece together.
Something I found in Merck about exchange transfusions:
Exchange transfusion, in which blood from the neonate is removed in aliquots in sequence with packed RBC transfusion, is indicated for hemolytic anemia and some cases of severe anemia with heart failure. It decreases plasma antibody titers and bilirubin levels (when phototherapy fails) and minimizes fluid overload. Serious adverse events (eg, shock, pulmonary edema, or both caused by shifts in fluid balance) are common, so the procedure should be performed by experienced staff. Guidelines for when to begin exchange transfusion differ and are not evidence based.
Among the various forms of congenital dropsy, in which the infants are often prematurely born, erythroblastosis, first described by Schridde  and named by Rautmann , is the least understood. Congenital generalized edema may be the result of cardiac anomalies and diseases, portal obstruction, syphilis of the liver, fetal peritonitis, abnormality of the D. venosus Arantii, deformities of the intestines and diseases of the kidneys. Schridde, in 1910, pointed out a form of congenital general dropsy with hydramnios associated with a pathological blood state.
The disorder is characterized by anasarca and fluid in the cavities, hydramnios and enlargement of the liver and spleen. The latter two organs show the most marked changes, which consist of the accumulation, both inside and outside of the blood vessels, of large numbers of erythroblasts and a smaller number of other marrow cells. The lymph follicles in the spleen are absent and the liver cells are crowded out. Accumulations of lymphoblasts in small numbers may be found in the kidneys, adrenals, and lymph glands. Erythroblasts appear in the blood in greatly increased numbers and they show very often mitotic processes. The heart is often hypertrophied.
Because of the presence of hemosiderin in the spleen and liver, Schridde was led to believe that the disease was due to a severe anemia with compensatory hematopoiesis having no relation to syphilis. Others have assumed that the extramedullary formation of blood corpuscles was due to some form of unknown toxic action. Chiari  described an infant in whom there was no blood pigment in the liver or spleen, and consequently no indications of any antecedent destruction of blood cells. Fischer , in his examination of the older literature, came to the conclusion that many of the cases described as congenital leukemia were probably instances of erythroblastosis.
AND LAST BUT NOT LEAST
from Perinatal Journal 2005; 13(4): 218-222
Here's a case report on a young one who was given intra-uterine transfusions. The title is: The predictive value of middle cerebral artery peak systolic velocity in repeated intrauterine transfusion: a case report. In other words, if Suzanne's situation happened now they'd give the baby good blood until the lungs were mature and it could be born. ...