A total of 27 blood specimen of neonates born at the maternity section of central Hospital Porto Novo by the Rhesus Negative mothers were studied for a period of 12 months. The specimen collection were done within 72 hours of birth, mothers pregnant for the first time without a past history of abortion or transfusion were rejected for the study. Ten (10) blood specimens of the neonates were Rhesus blood group negative and were eliminated from the work whereas the remaining seventeen (17) were recorded Rhesus blood group positive.
The results of the 17 specimen of neonates all recorded in mean values showed Hb 17. 23g/dl, Hct 51.56L/L, the mean cell volume was 102.18 FL, mean cell hemoglobin concentration was 33.41% and mean cell hemoglobin recorded 34.12 pg. The red cell count and white cell count were 5.04 × 1012 /L and 16.06 ×109 /L respectively. The platelet count was 316.53 and red cell distribution width of 17.76% was recorded. The differential leucocytes counts were; Neutrophils 65.35%, Lymphocytes 25.71% and MXD (comprises of monocytes, eosinophils and basophils) recorded 13.48%.
The mean results of Bilirubin direct and Bilirubin total were 0.76mg/dl and 4.29mg/dl. The Direct Coombs test (DCT) was positive in one specimen of neonates and this specimen showed Hb value of 13.6g/dl and a total Bilirubin of 27.5mg/dl. All the neonates were of full term with birth weight of 2.5 to 3.5 kg. This work serves as an epidemiological vigilance for haemolytic diseases of the newborn in the Porto Novo province.
The incidence of hemolytic Disease of newborn in Porto Novo district was recorded to be 5.8% considering from this work where only a case gave positive Direct Coombs. Although, this work suffers from scarcity of pregnant mothers of Rhesus blood group negative and affects the research because the specimen collected were small for the time period of the work. The Porto Novo experience also showed that good control system is at work by the medical team and technical staff concerned with the testing of all prospective mothers. Another positive aspect is that anti-D is freely and timely available for mothers of D- positive infants and with persistent effort in this regard, the incidence should continue very low or until there is no more case of hemolytic disease of the newborn.
The term hemolytic disease of the newborn (HDN) is used to describe an immune hemolytic anemia which causes an infant to be born anemic and jaundiced.
However, Rhesus HDN is usually caused by immune anti-D and less commonly by other Rhesus antibodies. It occurs when a RH negative woman with circulating IgG anti-D antibody (formed from a previous Rhesus incompatible pregnancy) becomes pregnant with a RH positive infant and IgG anti-D passes into the fetal circulation, destroying fetal cells. The infant can be born severely anemic and jaundiced. The severity of the disease increases with each RH positive pregnancy. Infants with Rhesus HDN are usually more severely affected than that caused by other antibodies.
Megan Rowley &Clare Milkins (2006) stated that since immunoglobulin G (igG) is the only immunoglobulin that crosses the placenta, only red cells of antibodies of this class are a potential cause of HDN.
In the RH system, antibodies are formed much more readily against the D-antigen than against any other antigens, so over 99% of infants with RH hemolytic disease will be the RH (D) positive offspring of RH (D) negative mothers.
Professor A.V. Hoff brand (1986) reported the incidence of infants affected with RH HDN in the United Kingdom to be about 0.5-0.75% of all births, although the figures are now falling with the success of routine prophylaxis with anti-D. Of the affected infants,10-20% are born dead or dying if no intrauterine treatment is given and over half of the affected infants need treatment, Often urgently, during the neonatal period. Obviously, it is important to detect the antibodies in the mothers’ serum during the antenatal period.
Dr.Sheila Worlledge reported that antibodies due to RH (D) cannot normally be detected during the first pregnancy unless the mother has had previous transfusions and or abortions.
Dr.Nevanlinna has shown that even after five or more pregnancies, the incidence of antibody formation in D- negative women is only about 10.2%.This discrepancy has three basic explanations:
Firstly, not all D-negative women have D-positive children. It can be calculated that in the United Kingdom, about 10% of mating will result in a mother who is D-negative carrying a D- positive fetus and that only 47% of D-negative pregnant for the second time will be carrying a second D-positive child.
Secondly, not all pregnancies are ABO compatible and there is good evidence that ABOincompatibility protects against RH antibody formation.
Professor Murray (1965) calculated that A-incompatibility gave 90% protection and B- incompatibility affords 55% protection against RH immunization.
The first ABO compatible D-incompatible infant seems to result in the primary immunization of about 17% of RH negative women: In about half of these women, the antibodies appear within six months of delivery; the other half, the antibodies will be detectable by the end of the second pregnancy.
Dr.Worlledge (1983) also stated that abortion produces immunization in up to 4% of D- negative women and the incidence seems to be greater if the abortion occurs in the second trimester than in the first.
ANTENATAL ASSESSMENT OF THE MOTHER´S BLOOD.
All mothers should have their ABO and RH (D) groups determined as soon as possible after pregnancy has been diagnosed. Moreover, their sera should be tested for antibodies outside the ABO blood group system, regardless of their blood group. One suitable way is to test them at 37oc with pooled enzyme treated red cells which have been taken from not more than three donors who between them carry all the common blood group antigens except A and B.
If properly done, this test is very sensitive method for detecting RH antibodies.
However, since other antibodies may have equal importance and since some of the antigens against which the react are destroyed by enzyme treatment, at least selected sera should also be tested with the same untreated red cells by the indirect antiglobulin test (IAT). It is customary for this selection to include the sera from all RH negative mothers and all mothers who give a history of past transfusion or unexplained stillborn, jaundiced or anemic infants.
If these investigations are negative, the sera of RH(D) positive mothers need not be reexamined routinely during pregnancy provided the mothers give no history of past transfusions or infants that might have been affected with hemolytic disease of the newborn. RH (D) negative mothers in their first pregnancy are unlikely to form detectable antibodies until after delivery and their sera probably need to be retested only at 30-40 weeks of pregnancy. RH (D) negative mothers in their second or subsequent pregnancy should be tested more frequently and earlier in pregnancy, Suggested times for these investigations are at 20 weeks and two or three times during the third trimester of pregnancy. All RHD negative mothers who seem to be un- immunized during pregnancy should have their sera retested at delivery if prophylactic anti-D is to be given. The sera of all mothers who give a history of past transfusions or stillborn, jaundiced or anemic infants should also be retested frequently during pregnancy. In these situations, the mother’s serum should be tested with the husband´s red cells if no antibodies are found with the pooled cells.
If the preliminary investigations are positive or if positive results are found in any of the subsequent tests, further tests will depend on the specificity of the antibodies. Some antibodies such as anti-Lewis and anti-p1 are almost always Igm and as such will not lead to HDN.
However, their presence should be recorded because they may make subsequent compatibility tests more difficult but the sera need not be titrated. Although haemolytic disease of newborn resulting from anti-D is the most severe form of the disease anti-c can give rise to significant haemolysis inutero sufficient to cause intra uterine death and to warrant investigation in pregnancy. Other antibodies such as RH antibodies, anti-kell, anti-Duffy, anti-E, anti-ce, and anti-Kidd are often IgG and uncommonly give rise to fetal haemolysis of sufficient severity to merit antenatal intervention and if they react by the indirect antiglobulin test, the sera should be titrated against suitable red cells. All pregnant mothers whether D positive or D negative should be screened for red cell antibodies. Further testing depends on the specificity of any antibodies detected, whether they are capable of causing haemolytic disease of the newborn. Antibody titres are now applied, along with the previous history, to decide whether or not to examine the amniotic fluid.