Prenatal Information and Courses from MediaLab, Inc.

Gestational diabetes is diabetes that develops during pregnancy. After delivery, the woman may remain a diabetic, develop diabetes in the future, or never again experience any hyperglycemia. Risk assessment and screening for diabetes is routine in prenatal care because of the pregnancy complications and mortality associated with gestational diabetes.

IEF's greatest advantage is its high resolution, resulting in greater separation of solutes. IEF of serum proteins results in many more bands; these bands are sharper because each pH region is very narrow. Performing IEF is easier because the placement of sample application is not important. The sample and ampholytes can be mixed before application; the ampholytes will migrate, create the gradient, and then the proteins separate and migrate.Some isoenzymes and variant hemoglobins in prenatal screening are separated with IEF. Detection of oligoclonal bands in gamma-globulin is a newer use of IEF. IEF is commonly used as one of the separations in two-dimensional electrophoresis.

When hemoglobin S (HbS) has been detected using a primary screening method, it is then crucial to determine if the HbS is homozygous, heterozygous, or is another variant. Additional procedures that may be needed include isoelectric focusing (IEF) or high performance liquid chromatography (HPLC).Observation of RBC morphology and use of sickle cell screening may provide initial information for this diagnosis, but may be negative in some sickle cell disorders.Polymerized chain reaction (PCR) methods are being used in prenatal diagnosis of sickle cell disorders.

Prenatal treatment of severe HDFN due to anti-D consists of in utero transfusions. Because of significant risks, transfusion is indicated only if fetal monitoring suggests significant hemolytic disease. 1. Intrauterine Transfusion (IUT)IUTs are done when fetal monitoring indicates severe HDFN and the fetus is too premature for early delivery. IUTs involve the intraperitoneal infusion of packed red cells. The success of the procedure depends on absorption of the red cells through the subdiaphragmatic lymphatic vessels of the fetus. 2. Intravenous transfusion (IVT)Because there may be erratic and inconsistent absorption of intrauterine transfusions in severely hydropic fetuses, IVTs were developed. IVTs involve transfusing donor RBC directly into the umbilical vein.

ABO HDFN is the most common type of HDFN, in that anti-A is the antibody most often found bound to the red cells of a newborn. While the disease is usually so mild as to not require treatment, severe HDFN is possible. EtiologyABO HDFN is caused by maternal IgG anti-A or anti-B, which can be produced as a result of prior pregnancy or prior inoculation (some common inoculations contain A or B substances). In Caucasians, most often the mother is group O and the child is group A, although other combinations are possible. Group O people tend to produce IgG ABO antibodies more commonly than other blood groups.Just as in other types of HDFN, maternal IgG antibody crosses the placenta and destroys fetal red cells.SymptomsTypical symptoms of ABO HDFN include mild anemia and especially jaundice appearing in the first 24 hours. In rare severe cases the infant can have the more severe symptoms of Rh HDFN, except that prenatal death is unlikely. Rationales to explain the mild nature of ABO HDFN include Fewer A and B antigens on fetal cells Poorly developed fetal A and B antigens Presence of A and B antigens on cells and tissues other than red cells

Tests done routinely as part of perinatal testing programs vary from country to country and within countries. Below is one example of routine serologic tests typically done when pregnant females lack clinically significant antibodies. Other test protocols exist.Tests on Mother ABO, Rh*, and antibody screen at first prenatal visit; Test for weak D, if initial Rh typing appears to be D-negative (Optional -not mandated by blood safety standards); D-negative females: Tested again (ABO, Rh, and antibody screen) at ~ 28 weeks gestation prior to administration of RhIg (depending on the country) and again at delivery.* The mother, putative father, and fetus can be typed for D using DNA methods, if available.

Numerous studies have shown that, if administered correctly, RhIg is effective at preventing D immunization. To work, RhIg must be given in sufficient dose, and it must be given before Rh immunization has begun.Unfortunately, despite RhIg's proven efficacy, some women still make anti-D in the perinatal period. Such 'failures' are mainly (but not totally) due to human error. Examples of how women may still produce anti-D some 40+ years after the implementation of RhIg prophylaxis: Immunization to D occurred before RhIg was administered, e.g., before 28 weeks gestation*; Immunization to D occurred after the administration of RhIg at 28 weeks and before delivery because an antenatal FMH occurred that was too large for residual passive anti-D to give protection; Female was already immunized from a prior pregnancy but anti-D was too weak to be detected in antibody screen tests prior to RhIg administration; RhIg dosage was insufficient to clear a larger fetal bleed at delivery (e.g., FMH screen or quantification was not done or a false negative occurred); Incorrect calculation of RhIg dosage; RhIg administered too late , e.g., well after 72 hours of delivery; Antenatal RhIg not given, e.g., mother had no or limited access to prenatal care, or did not seek it, and a FMH occurred during pregnancy; Failure of physician to carry out prenatal blood testing; RhIg not given due to laboratory clerical or technical error in Rh typing the mother or child; RhIg not given in cases such as abortions, ectopic pregnancies, and trauma (e.g., car accidents). * Because anti-D production before 28 weeks is rare (the order of 0.24% to 0.31%), RhIg's use earlier in pregnancy is not recommended. It is not cost effective and would expose most women to an unneeded blood product.