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Thread: Are you Rh-negative blood? Then you have to know this! (if you are Rh positive, too)

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    Post Are you Rh-negative blood? Then you have to know this! (if you are Rh positive, too)

    (for boys and girls)
    http://www.nlm.nih.gov/medlineplus/e...cle/001600.htm

    Erythroblastosis fetalis

    Alternative names

    Hemolytic disease of the newborn due to Rh incompatibility
    Definition

    Erythroblastosis fetalis is a severe anemia that develops in an unborn infant because the mother produces antibodies that attack the fetus' red blood cells. The antibodies are usually caused by Rh incompatibility between the mother’s blood type and that of the fetus (that is, the mother and baby have different blood types).

    The severity of this condition can vary widely. In some instances this can lead to death of the baby. It can be treated in utero (before birth) by medication or intrauterine transfusion. When the child is born, signs may include an enlarged liver and/or spleen, generalized edema (swelling, anasarca), jaundice, and anemia. After birth, depending on the severity, a transfusion may be performed.

    See also Transfusion reaction.

    Rh incompatibility

    Alternative names

    Kernicterus; Rh-induced hemolytic disease of the newborn; Hydrops fetalis

    Definition

    Rh incompatibility is a condition which develops when there is a difference in Rh blood type between that of the pregnant mother (Rh negative) and that of the fetus (Rh positive).

    Causes, incidence, and risk factors

    During pregnancy, red blood cells from the fetus can get into the mother's bloodstream as she nourishes her child through the placenta. If the mother is Rh negative, her system cannot tolerate the presence of Rh positive red blood cells.

    In such cases, the mother's immune system treats the Rh positive fetal cells as if they were a foreign substance and makes antibodies against the fetal blood cells. These anti-Rh antibodies may cross the placenta into the fetus, where they destroy the fetus' circulating red blood cells.

    First-born infants are often not affected (unless the mother has had previous miscarriages/abortions, which could have sensitized her system) as it takes time for the mother to develop antibodies against the fetal blood. However, second children who are also Rh-positive may be harmed.

    Rh incompatibility can cause symptoms ranging from very mild to fatal. In its mildest form, Rh incompatibility causes hemolysis (destruction of the red blood cells) with the release of free hemoglobin into the infant's circulation.

    Hemoglobin is converted into bilirubin, which causes an infant to become yellow (jaundiced). The jaundice of Rh incompatibility, measured by the level of bilirubin in the infant's bloodstream, may range from mild to dangerously high levels of bilirubin.

    Hydrops fetalis is a complication of a severe form of Rh incompatibility in which massive fetal red blood cell destruction (a result of the Rh incompatibility) causes a severe anemia resulting in fetal heart failure, total body swelling, respiratory distress (if the infant has been delivered), and circulatory collapse. Hydrops fetalis often results in death of the infant shortly before or after delivery.

    Kernicterus is a neurological syndrome caused by deposition of bilirubin into the brain (CNS) tissues. Kernicterus develops in extremely jaundiced infants, especially those with severe Rh incompatibility.

    It occurs several days after delivery and is characterized initially by loss of the Moro (startle) reflex, poor feeding, and decreased activity. Later, a high-pitched shrill cry may develop along with unusual posturing, a bulging fontanel, and seizures. Infants may die suddenly of kernicterus.

    If they survive, they will usually later develop decreased muscle tone, movement disorders, high-pitched hearing loss, seizures, and decreased mental ability.

    Rh incompatibility develops only when the mother is Rh negative and the infant is Rh positive. Special immune globulins, called RhoGAM, are now used to prevent this sensitization. Hydrops fetalis and kernicterus have decreased markedly in frequency as a result of these preventive measures.

    Symptoms
    Signs and tests

    Mild Rh incompatibility:
    Hydrops fetalis:
    Kernicterus -- Early:
    • high bilirubin level (greater than 18 mg/cc)
    • extreme jaundice
    • absent Moro (startle) reflex
    • poor suck
    • lethargy
    Kernicterus -- Mid:
    • high-pitched cry
    • arched back with neck hyperextended backwards (opisthotonos)
    • bulging fontanel (soft spot)
    • seizures
    Kernicterus -- Late (full neurological syndrome):
    Treatment

    Since Rh incompatibility is almost completely preventable with the use of RhoGAM, prevention remains the best treatment. Treatment of the already affected infant depends on the severity of the condition.

    Mild:
    Hydrops fetalis:
    • amniocentesis to determine severity
    • intrauterine fetal transfusion
    • early induction of labor
    • a direct transfusion of packed red blood cells (compatible with the infant's blood) and also exchange transfusion of the newborn to rid the blood of the maternal antibodies that are destroying the red blood cells
    • control of congestive failure and fluid retention
    Kernicterus:
    • exchange transfusion (may require multiple exchanges)
    • phototherapy
    Expectations (prognosis)

    Full recovery is expected for mild Rh incompatibility. Both hydrops fetalis and kernicterus represent extreme conditions caused by hemolysis. Both have guarded outcomes. Hydrops fetalis has a high mortality rate.

    Complications
    • neurological syndrome with mental deficiency, movement disorder, hearing loss, speech disorder, and seizures
    Calling your health care provider

    Call your health care provider if you think or know you are pregnant and have not yet seen a doctor.

    Prevention

    Rh incompatibility is almost completely preventable. Rh negative mothers should be followed closely by their obstetricians during pregnancy.

    If the father of the infant is Rh positive, the mother is given a mid-term injection of RhoGAM and a second injection within a few days of delivery.

    These injections prevent the development of antibodies against Rh positive blood. This effectively prevents the condition.

    Erythroblastosis fetalis, photomicrograph


    Antibodies from an Rh negative mother may enter the blood stream of her unborn Rh positive infant, damaging the red blood cells (RBCs). The infant responds by increasing RBC production and sending out immature RBCs that still have nuclei. This photograph shows normal RBCs, damaged RBCs, and immature RBCs that still contain nuclei.

    Antibodies

    Antigens are large molecules (usually proteins) on the surface of cells, viruses, fungi, bacteria, and some non-living substances such as toxins, chemicals, drugs, and foreign particles. The immune system recognizes antigens and produces antibodies that destroy substances containing antigens.

    Intrauterine transfusion


    Erythroblastosis fetalis is a condition manifested by anemia that develops in an unborn infant when maternal antibodies, usually caused by Rh incompatibility between the mother's blood type and that of the fetus, attack the red blood cells of the fetus. An intrauterine transfusion of blood may be indicated.

    Coombs’ test - indirect

    Alternative names

    Indirect antiglobulin test
    Definition

    The indirect Coombs' test measures the presence of antibodies to red blood cells in the blood (see also Coombs' test - direct).

    Why the test is performed

    The indirect Coombs' test detects circulating antibodies against red blood cells (RBCs). The major use of this test is to determine if the patient has antibodies in the blood capable of attaching to RBCs. (These antibodies are other than the major ABO system or the Rh type).

    The test is only rarely used to diagnose a medical condition but is essential for use by laboratories such as blood banks. Blood banks use the indirect Coombs' test is to determine whether there is likely to be an adverse reaction to blood that is going to be used for a blood transfusion.

    Normal Values

    No agglutination (i.e., the absence of clumping of red blood cells) is normal.

    What abnormal results mean

    An abnormal indirect Coombs' test may indicate the presence of an antibody against an antigen that the body views as foreign:
    If you have antibodies against your own red cells, the indirect Coombs' test results may be abnormal if there are excess antibodies beyond what your red blood cells can absorb. This may indicate autoimmune hemolytic anemia or drug-induced hemolytic anemia.

    What the risks are
    • Fainting or feeling light-headed
    • Multiple punctures to locate veins
    • Excessive bleeding
    • Hematoma (blood accumulating under the skin)
    • Infection (a slight risk any time the skin is broken)
    Special considerations

    Veins and arteries vary in size from one patient to another and from one side of the body to the other. Obtaining a blood sample from some people may be more difficult than from others.


    -----------------------------------
    http://www.emedicine.com/med/topic3529.htm

    Erythrocyte Alloimmunization and Pregnancy

    Last Updated: October 5, 2004 Synonyms and related keywords: maternal alloimmunization, isoimmunization, hydrops fetalis, blood transfusion, fetomaternal hemorrhage, therapeutic abortion, spontaneous, ectopic pregnancy, tubal pregnancy, abdominal trauma, obstetric procedures, amniocentesis, chorionic villus sampling, CVS, percutaneous umbilical blood sampling, PUBS, cordocentesis, external cephalic version, ECV, manual removal of the placenta

    AUTHOR INFORMATION
    Author: Susan Tran, MD, Staff Physician, Department of Obstetrics and Gynecology, Kaiser Foundation Hospitals of San Francisco

    INTRODUCTION AND BACKGROUND
    Maternal alloimmunization, also known as isoimmunization, occurs when a woman's immune system is sensitized to foreign erythrocyte surface antigens, stimulating the production of immunoglobulin (Ig) G antibodies. The most common routes of maternal sensitization are via blood transfusion or fetomaternal hemorrhage (transplacental passage of fetal erythrocytes) associated with delivery, trauma, spontaneous or induced abortion, ectopic pregnancy, or invasive obstetrical procedures (see Causes of maternal alloimmunization). In the event of a pregnancy subsequent to becoming alloimmunized, these antibodies can cross the placenta and, if the fetus is positive for the erythrocyte surface antigens, result in hemolysis of fetal erythrocytes and anemia. This, in turn, can lead to potentially disastrous consequences for the fetus, such as hydrops fetalis, a high-output cardiac failure syndrome.


    IgG antibody–mediated hemolysis of fetal erythrocytes, known as hemolytic disease of the fetus and newborn, varies in severity and can have a variety of manifestations. The degree of anemia can range from mild to severe with associated hyperbilirubinemia and jaundice. In severe cases, hemolysis may lead to extramedullary hematopoiesis and reticuloendothelial clearance of fetal erythrocytes. This may result in hepatosplenomegaly; decreased liver function; and ensuing hypoproteinemia, ascites, and anasarca. When accompanied by high-output cardiac failure and pericardial effusion, this condition is known as hydrops fetalis. This syndrome is often fatal despite intensive neonatal care, including emergent exchange transfusion.

    Cases of hemolysis in the newborn that do not result in fetal hydrops can still lead to kernicterus. This is a neurological condition observed in infants with severe hyperbilirubinemia and is due to the deposition of unconjugated bilirubin in the brain. The absence of placental clearance and immature fetal bilirubin-conjugating ability can lead to symptoms that manifest several days after delivery and include poor feeding, inactivity, loss of the Moro reflex, a bulging fontanelle, and seizures. The 10% of infants who survive may develop spastic choreoathetosis, deafness, and mental retardation.

    Causes of maternal alloimmunization
    • Blood transfusion
    • Fetomaternal hemorrhage
      • Antepartum
      • Intrapartum
    • Abortion

      • Therapeutic
      • Spontaneous
    • Ectopic pregnancy


    • Abruption


    • Abdominal trauma


    • Obstetric procedures

      • Amniocentesis
      • Chorionic villus sampling
      • Percutaneous umbilical blood sampling
      • External cephalic version
      • Manual removal of the placenta


    Among the antigens capable of causing maternal alloimmunization and fetal hemolytic disease, the Rh blood group system is the most common. In particular, the D antigen of the Rh blood group system (Rh D) causes the most cases of severe hemolytic disease. The Rh system was discovered in 1940 when Landsteiner and Weiner performed their landmark experiments wherein rhesus monkey erythrocytes were injected into rabbits and guinea pigs. The resultant antisera was mixed with blood samples from white persons, and agglutination was observed in 85% of the samples (Rh D positive). The remaining 15% of the samples were Rh D negative, and this finding corresponds remarkably to the currently known prevalence of Rh D–negative white individuals.

    Following this discovery, Levine determined that hemolytic disease of the fetus and newborn was usually caused by Rh incompatibility, ie, the fetal stimulation of Rh antibody development in an Rh D–negative woman. In 1953, Chown verified that the passage of fetal Rh D–positive erythrocytes into the maternal circulation caused Rh immunization. In 1960, the administration of Rh D Ig, now called anti-D immune globulin or RhoGAM, was demonstrated to prevent Rh D alloimmunization, leading to the licensing of anti-D Ig in 1968 for use in North America. Anti-D Ig administration has been enormously successful in preventing maternal alloimmunization.

    Approximately 17% of Rh D–negative women who deliver an Rh D–positive fetus will become alloimmunized if not administered anti-D Ig. Because anti-D Ig prophylaxis has reduced the risk of sensitization to less than 1% of susceptible pregnancies, other alloantibodies have increased in relative importance. These include antibodies to other antigens of the Rh blood group system (ie, c, C, e, and E) and other atypical antigens known to cause severe anemia, such as anti-Kell (ie, K, k), anti-Duffy (ie, Fya), and anti-Kidd (ie, Jka, Jkb).

    Despite the dramatic success of anti-D Ig prophylaxis protocols, prevention is not universal and 0.27% of susceptible women still become Rh D alloimmunized. One reason for this is failure to follow recommended protocols. Furthermore, a 0.1-0.2% rate of spontaneous immunization occurs despite prophylaxis. These cases have been commonly observed in pregnancies in which no prior overt sensitizing events have occurred. Finally, alloimmunization involving atypical blood groups (eg, Kell and c blood groups) is not yet preventable. Therefore, understanding and using available predictive measures and treatment modalities for hemolytic disease of the fetus and newborn is essential, as is ensuring that the Rh-alloimmunized pregnancy is properly managed.

    Various predictive measures are currently available to estimate the severity of fetal disease. Briefly, these include amniotic fluid spectrophotometric measurements of bilirubin to estimate the degree of hemolysis and anemia, perinatal ultrasonography to assess fetal well-being and to identify findings consistent with hydrops (eg, edema, ascites, effusions), fetal percutaneous umbilical blood sampling (PUBS) to measure fetal hematocrit directly, and Doppler ultrasonography to measure the velocity of blood flow in various fetal arteries as an index of fetal anemia.

    For the fetus that has hydrops, or at least fetal anemia, the development of in utero therapy has been relatively successful. Intrauterine fetal transfusion (IUT), which includes intraperitoneal fetal transfusion (IPT) and direct intravascular fetal transfusion (IVT), has been used for 30 years. Prior to the availability of real-time ultrasound, fetuses that were felt to be anemic were administered IPTs of Rh-negative blood. The first of these was performed in 1963 and led to a reduction in morbidity and mortality in severely affected fetuses.

    With advances in ultrasound, PUBS and direct intraumbilical transfusions became a possibility and then a reality. PUBS was first used for an IUT directly into the umbilical vein in 1982. Currently, this is the mainstay of treatment for anemic and hydropic fetuses remote from term. Of course, the best management of fetuses near term with these issues is delivery in a tertiary hospital with a level 3 neonatal intensive care unit.

    Patient Education For excellent patient education resources, visit eMedicine's <A href="http://www.emedicinehealth.com/collections/CO1602.asp" target=_blank>Pregnancy and Reproduction Center. Also, see eMedicine's patient education article Ectopic Pregnancy.

    DEMOGRAPHICS

    The prevalence of the Rh D–negative blood type is dependent on ethnicity (see Rates of Rh negativity among ethnic and racial groups), with white persons having the highest prevalence (approximately 15%) and Asian persons and American Indians having the lowest (<5%). Because the Rh antigen is derived from what is essentially a 2-allele locus with complete penetrance, the prevalence of the phenotype can be used to calculate the prevalence of the genotypes and overall allele frequency. From the Hardy-Weinberg equation, with p equal to the probability of the dominant allele (ie, D) and q equal to the probability of the recessive allele (ie, the absence of D), the genotypes can be calculated. The Hardy-Weinberg equation is as follows:




    p2 + 2pq + q2 = 1

    (Given that p + q = 1, p2 = prevalence of the homozygous dominant genotype, 2pq = prevalence of heterozygous genotype, p2 + 2pq = prevalence of dominant phenotype, and q2 = prevalence of the homozygous recessive genotype and the recessive phenotype)

    In the white race, a rate of Rh-negative blood type of 15% corresponds to the recessive phenotype but also the prevalence of the homozygous recessive genotype (q2). Thus, q = square root (0.15) » 0.4, or 40%. Because p + q = 1, p = 0.6. Thus, the other 2 genotypic frequencies are p2 = 0.36 for homozygous dominant and 2pq = 0.48 for heterozygous. These genotypic frequencies are helpful when counseling patients about the probability that their fetus will have Rh-positive blood.
    • Rates of Rh negativity among ethnic and racial groups
      • White - 15-16%
      • African American - 8%
      • African - 4%
      • Basque (region of Spain/France) - 30-35%
      • Asian - Less than 1%
      • Asian American - 1%
      • American Indian/Inuit - 1-2%
      • Eurasian - 2-4%


    Of the existing Rh antigens, the D antigen is the most immunogenic. Three pairs of Rh antigens are known, with varying gene frequencies and possible combinations (see <A href="http://www.emedicine.com/med/topic3529.htm#targetC">Rh gene frequencies in 2000 unrelated white adults). Interestingly, with respect to the c and e alleles of the Rh locus, both c and C as well as d and E antigens are known. With respect to the D allele, d actually refers to the absence of the D allele; no particular d antigen is known. When referring to the different alleles, the terms little and big are used. For example, a patient with the cDE complex would be considered to have little c, big d, big e antigens.

    Approximately 10% of white pregnancies are Rh incompatible. However, because the risk of alloimmunization in a susceptible Rh D–negative woman is significantly affected by 3 factors, less than 20% of Rh D–incompatible pregnancies actually lead to maternal alloimmunization. These factors are (1) the volume of fetomaternal hemorrhage, (2) the degree of maternal immune response, and (3) concurrent ABO incompatibility.
    • Rh gene frequencies in 2000 unrelated white adults (with gene complex and percent)
      • CDe - 41%
      • c(d)e - 39%
      • cDE - 16%
      • cDe - 2.2%
      • C(d)e - 1.1%
      • c(d)E - 0.6%
      • CDE - 0.08%
      • C(d)E - 0%


    Fetomaternal hemorrhages have been demonstrated to occur in as many as 75% of pregnancies, with the frequency increasing as gestation advances and with most cases occurring during delivery. If transplacental passage of fetal erythrocytes is suspected, the rosette screening test is used to determine the presence of a fetomaternal hemorrhage. When a large hemorrhage is suspected, the Kleihauer-Betke test is used to quantify the volume of hemorrhage so that an appropriate dose of anti-D Ig can be administered. Fifteen to 50% of births produce hemorrhage volumes sufficient to cause alloimmunization. This volume of fetal blood, which, in more than 50% of intrapartum cases can be as small as 0.1 mL and in rare cases can exceed 30 mL, varies depending on the degree of maternal immune response. As many as 30% of Rh D–negative individuals have been demonstrated to not become alloimmunized, even when challenged with large volumes of Rh D–positive blood. ABO blood group status also affects the risk of alloimmunization. With an ABO-compatible fetus, the overall risk of alloimmunization if not treated with anti-D Ig is approximately 16%. However, in an ABO-incompatible fetus, the risk is only 1.5-2%. The protective effect conferred by ABO incompatibility is believed to be due to maternal destruction and subsequent clearance of the ABO-incompatible fetal erythrocytes before Rh sensitization can occur.

    TREATMENT FOR PREGNANT PATIENTS WHO ARE RH D NEGATIVE

    The primary goal of caring for a pregnant patient who is nonimmunized Rh D negative is prevention of alloimmunization. Every patient should have her ABO blood group, Rh type, and antibody screen (indirect Coombs test) checked at the first prenatal visit of each pregnancy. Patients who are found to be Rh D negative with concurrent negative results from antibody screens are candidates for anti-D Ig prophylaxis unless the Rh status of the father of the baby is negative and the paternity certain. In theory, if the Rh D status of the father is known, the patient can be counseled regarding the risk of the fetus having the Rh D antigen; however, because of a 3-5% rate of unknown or false paternity, discussing this issue privately with the patient is of the utmost importance. Anti-D Ig is absolutely contraindicated only in those patients with a documented hypersensitivity to anti-D Ig.


    Exogenous administration of Ig to suppress an immune response, as in the case of anti-D Ig prophylaxis, is known as antibody-mediated immune suppression. Although several theories have been proposed to explain the mechanism of action of antibody-mediated immune suppression, the most likely mechanism is via central inhibition, wherein Rh Ig coats fetal erythrocytes, which are then sequestered in the spleen and lymph nodes. The local increase in antigen-antibody complexes interrupts the commitment of B cells to plasma cell clones, thereby suppressing the primary immune response. Additionally, these antigen-antibody complexes stimulate the release of cytokines by immune effector cells that inhibit the proliferation of antigen-specific B cells.

    The standard dosing regimen of anti-D Ig is 300 mcg intramuscularly at both 28 weeks' gestation and postpartum within 72 hours of delivery. The 300-mcg dose was determined in 1963 by Pollack et al following experiments in which male volunteers who received Rh D-positive erythrocytes were administered varying doses of anti-D Ig to prevent alloimmunization. In the early days of anti-D Ig prophylaxis, most fetomaternal hemorrhages were known to occur during delivery, and, thus, anti-D Ig was administered only in the postpartum period. This continues to be the regimen used in many other countries.

    Although this produced a dramatic decrease in the prevalence of alloimmunization, Bowman et al observed that despite this postpartum anti-D Ig prophylaxis, 1-2% of susceptible women continued to become sensitized. They concluded that these women were experiencing fetomaternal hemorrhages prior to delivery, and they conducted experiments in which antepartum doses were added to the prophylaxis regimen. This resulted in a reduction in the number of sensitized women from 1.8% to 0.1% and eventually led to a regimen that includes the additional dose at approximately 28 weeks' gestation, which is used today in the United States.

    In settings in which a fetomaternal hemorrhage can be calculated, 10 mcg of anti-D Ig should be administered for every milliliter of fetal blood in the maternal circulation. Thus, the 300-mcg dose is more than adequate for a typical fetomaternal hemorrhage and covers hemorrhage volumes of up to 30 mL of whole fetal blood. In the less than 1% of cases in which the volume of fetomaternal hemorrhage exceeds 30 mL, using the Kleihauer-Betke test to quantitate the volume of fetomaternal hemorrhage and administering the appropriate amount of anti-D Ig (10 mcg/mL fetal blood) is necessary.

    Following delivery, if the infant is found to be Rh negative, the postpartum dose may be omitted. However, if any doubt remains concerning whether to administer anti-D Ig, always administer unless contraindicated. If the fetus if found to be Rh positive, administer anti-D Ig and take care to screen for excess fetomaternal hemorrhage, particularly if cesarean delivery or manual removal of the placenta occurred because both would increase the risk and volume of fetomaternal hemorrhage.

    Because delivery of an Rh D–positive fetus is not the only means by which transplacental passage of fetal blood can occur, anti-D Ig prophylaxis for nonimmunized women who are Rh D negative is also warranted (1) in cases of first- and second-trimester bleeding, (2) in cases of spontaneous or elective abortion, (3) prior to any invasive procedure (eg, amniocentesis), (4) in evidence of subchorionic or retroplacental hematoma upon ultrasound, and (5) in cases of intrauterine fetal death. Patients who experience antepartum bleeding or intrauterine fetal death in the third trimester should have a Kleihauer-Betke test to determine whether more RhoGAM, beyond the prophylactic dose at 28 weeks' gestation, is necessary. If so, patients can be administered 10 mcg anti-D Ig per estimated milliliter of whole fetal blood in the maternal circulation.

    Because fetal Rh antigens are present as early as the 30th day after conception, anti-D Ig is indicated with ectopic pregnancy and with therapeutic and spontaneous abortions. The risk of alloimmunization in susceptible women undergoing therapeutic or spontaneous abortion is 4-5% and 1.5-2%, respectively. For pregnancies less than or equal to 12 weeks' gestation, 50 mcg of anti-D Ig is sometimes administered because the entire blood volume of the fetus is usually less than 5 mL. However, pregnancies exceeding 12 weeks' gestation or pregnancies in which the gestational age is unknown should receive the full 300-mcg dose.

    Invasive obstetrical procedures, such as chorionic villus sampling and amniocentesis (respective risks of alloimmunization of at least 14% and 7-15%), also necessitate anti-D Ig prophylaxis at the time of the procedure. While a dose of 50 mcg is adequate for first-trimester procedures, the 300-mcg dose should be used for both second- and third-trimester procedures. Additionally, if amniocentesis is performed within 72 hours of delivery, as is often the case with fetal lung maturity determinations, withholding the postpartum anti-D Ig until the fetal Rh status is established postpartum is possible. However, if delivery is to be delayed for more than 72 hours, anti-D Ig should be administered.

    Although not an invasive obstetrical procedure, external cephalic version is associated with fetomaternal hemorrhage in 2-6% of cases, irrespective of procedure success. In this situation, administering an additional dose or checking for antibody status from the 28-week gestation prophylactic dose and performing a Kleihauer-Betke test shortly afterward to check for fetomaternal hemorrhage is reasonable. Although the above guidelines have been dramatically successful in reducing the prevalence of Rh D alloimmunization since the introduction of anti-D Ig prophylaxis in 1968, improper management of nonimmunized Rh D–negative patients continues to be problematic. Potential errors and oversights that can result in the patient becoming Rh D alloimmunized include failing to type every patient with the potential for transfusion or fetomaternal hemorrhage, not screening for fetomaternal hemorrhage, not administering anti-D Ig when indicated, or administering an inadequate dosage of anti-D Ig.

    TREATMENT FOR PATIENTS WHO ARE ALLOIMMUNIZED

    The goals in managing the alloimmunized pregnancy are 2-fold. First is the detection of fetal anemia prior to the occurrence of fetal compromise. After detection, the goal is to minimize fetal morbidity and mortality by correcting this anemia until fetal lung maturity and delivery can be achieved.


    The advent of exchange transfusion for the treatment of Rh (D) hemolytic disease of the fetus and newborn by Wallerstein in 1945 dramatically reduced perinatal mortality. However, because this intervention is only used after the fetus is delivered, those fetuses experiencing severe anemia, particularly those that became hydropic, might not survive to term delivery. In fact, elective preterm delivery and subsequent emergency exchange transfusion was the standard of care for the fetuses of alloimmunized patients in the early 1960s. Unfortunately, the inability to predict the severity of fetal disease and to manage the complications of prematurity at the time resulted in perinatal mortality rates as high as 25%.

    The introduction of measures to predict the severity of fetal disease greatly reduced perinatal mortality rates and augmented survival rates. The decision to use specific interventions should be dictated by the degree of fetal disease. Consider fetal D antigen status, maternal antibody titers, and prior obstetrical history in order to individualize and optimize management of an alloimmunized pregnancy. If indicated, the fetus can be assessed and monitored further using amniotic fluid analysis, ultrasound and Doppler studies, and fetal blood analysis.

    Assessing fetal risk for Rh D–positive status

    Upon confirming maternal Rh D alloimmunization, determining if the fetus is at risk is important (see Image 1) because an Rh D–negative fetus will be unaffected and requires no intervention irrespective of maternal titers. With certain paternity, if the father is Rh D negative, the fetus is also absolutely Rh D negative. If the father is Rh D positive, he can be homozygous for the D allele or heterozygous. If he is homozygous for the D allele, then the fetus is absolutely Rh D positive.

    If paternity is uncertain, as in 3-5% of pregnancies, or if the father is heterozygous for the D allele, determining fetal D antigen status via polymerase chain reaction assays of fetal cellular elements in amniotic fluid or chorionic villi is currently possible. Because of the small risk associated with amniocentesis, noninvasive means of determining fetal D antigen status via molecular analysis of fetal nucleated erythroid progenitors found in maternal blood will hopefully be developed and decrease the need for invasive testing.

    The need for absolute certainty regarding paternity in these settings cannot be overemphasized because the outcomes can be disastrous if the fetus is misdiagnosed as Rh D negative. Because of this, emphasize this point with patients after they have been isolated from anyone who has accompanied them on their prenatal visit.



    Methods for determining fetal status in patients who are alloimmunized

    In pregnant women who are known to be Rh D alloimmunized or for whom the prenatal antibody screen result is positive, a titer determination is necessary to assess the risk to the fetus and to guide the decision-making process. In general, women with titers higher than 1:4 should be considered Rh alloimmunized. However, the threshold for invasive fetal testing varies at different institutions and is generally 1:16 or higher because these titers have been associated with fetal hydrops. Titers tend to correlate more reliably with the severity of fetal disease in the first sensitized pregnancy than in subsequent pregnancies. As such, first sensitized pregnancies in which antibody titers are 1:8 or lower can be managed by monitoring serial maternal antibody titers. This is usually performed monthly, although some clinicians recommend testing antibody titers every other week beyond fetal viability.

    Should titers ever rise to 1:16 or higher, invasive testing is indicated. This is usually accomplished via amniocentesis for amniotic fluid analysis, but recent research suggests that noninvasive Doppler ultrasonography studies might be used to screen for fetal anemia. Although not reliably accurate in predicting the severity of fetal disease, past obstetrical history can be somewhat prognostic. In general, the severity of fetal disease in a particular pregnancy tends to be similar to, if not more severe than, that of prior pregnancies. Additionally, with a history of a prior hydropic fetus, the chance that the next Rh D–incompatible fetus will also become hydropic if untreated is greater than 80%.

    Analysis of amniotic fluid allows physicians to detect the presence and severity of fetal hemolysis and anemia. Amniotic fluid containing high levels of bilirubin, such as that found in fetuses with severe hemolytic disease, is yellowish-brown. This observation led to the eventual development by Liley in 1961 of a method to predict the severity of fetal hemolysis using spectrophotometric measurements of bilirubin in amniotic fluid. Because the wavelength at which bilirubin absorbs light is 420-460 nm, the amount of shift in optical density from linearity at 450 nm (D OD 450) in serial amniotic fluid samples can be used to estimate the degree of fetal hemolysis. Modification of the Liley curve (see Image 6) to adjust for the relative inaccuracy of D OD 450 readings in the early-to-middle second trimester and the use of serial measurements have improved its accuracy.

    The interface between the different zones has a negative slope; this is secondary to the increased ability of the fetus to metabolize the breakdown products of hemoglobin. Thus, the same value of D OD 450 is more worrisome for hemolysis at a later gestation. Because amniocentesis is an invasive procedure, the risks associated with it include preterm premature rupture of the membranes, fetal bleeding, fetal bradycardia requiring emergency cesarean delivery, chorioamnionitis, preterm labor, spontaneous abortion, and worsening of alloimmunization due to induced fetomaternal hemorrhage.

    Ultrasonographic evaluation of the fetus is a significant part of managing an Rh-incompatible pregnancy. Although it cannot help predict the impending development of hydrops, ultrasound can help unequivocally diagnose the presence of hydrops—a diagnosis that would greatly affect the course of treatment. The sonographic findings consistent with hydrops include ascites, pleural and pericardial effusions, and edema (see Images 1-3).

    Several other sonographic findings have been proposed as possible indicators of the future development of hydrops. These include polyhydramnios, increased placental thickness (>4 cm), dilation of the cardiac chambers, dilation of the umbilical vein, chronic enlargement of the spleen and liver, and visualization of both sides of the fetal bowel wall. However, none of these findings has proven predictive. Currently, the role of ultrasound in the management of Rh-incompatible pregnancies is to assess fetal well-being; diagnose hydrops; and guide amniocenteses, fetal blood sampling, and IUTs. In this capacity, ultrasonography has improved both the safety and success rate of invasive procedures and has helped to minimize invasive testing.

    The use of Doppler flow measurements in various fetal blood vessels has been studied to help predict the severity of fetal anemia. Although Doppler studies have been conducted in a number of fetal blood vessels, investigators have not been successful in demonstrating accurate prediction of fetal anemia until recently. In their studies of the middle cerebral artery in 2000, Mari et al purport that increases in peak velocity of systolic blood flow in the middle cerebral artery can be used to detect moderate and severe anemia in nonhydropic fetuses.

    Further, Pereira et al demonstrated in a small series that Doppler ultrasound had both better sensitivity and specificity than amniocentesis and D OD 450 measurement. Of note, information is available on the ability of this technique to consistently identify milder cases of anemia; therefore, results should be interpreted with caution. Regardless, Doppler flow studies represent a promising noninvasive tool. Of note, Doppler flow studies may ultimately be quite useful for cases of non-D alloimmunization, such as those observed with the Kell antigen, because in these patients, the degree of fetal anemia correlates poorly with the extent of erythrocyte destruction and the D OD 450, rendering amniotic fluid studies ineffective.

    The previously discussed predictive measures are indirect measures of fetal disease. The only definitive means of diagnosing fetal anemia and acidosis is via fetal PUBS, also known as cordocentesis, which was first performed in the early 1980s. PUBS helps provide direct and accurate diagnosis of anemia and fetal acidosis, especially in cases of anti-Kell alloimmunization and before 26-28 weeks' gestational age when D OD 450 values of amniotic fluid are not as reliable. The other advantage of PUBS is that by providing direct access to the umbilical vein, the same procedure can be used to transfuse the fetus. Despite the wealth of information afforded by PUBS, routine umbilical cord blood sampling is not universal because of concerns regarding fetal and maternal complications. These include fetomaternal hemorrhage, fetal loss (0.5-2% per procedure), placental abruption, acute refractory fetal distress, and amnionitis with maternal adult respiratory distress syndrome.

    Management scheme for patients who are alloimmunized with an at-risk fetus

    Traditional management of alloimmunized patients with serial amniocenteses (see Image 5) is based on which zone the D OD 450 measurement falls into on the Liley curve. Evidence from several studies, including Liley's original work, indicates that mild or no hemolytic disease occurs in zone 1; intermediate disease in zone 2 (transitional between mild and severe hemolysis); and severe disease, including the development of hydrops within the week, in zone 3.

    Based on this evidence, once serial measurements are started, if a zone 1 reading is obtained, monitoring the D OD 450 approximately every 3 weeks is reasonable. However, with a trend into zone 2, the frequency of testing should increase to every 1-2 weeks depending the steepness of the slope of the curve and the closeness of the measurement to zone 3. Currently, because the test characteristics of Doppler ultrasound of the peak systolic velocity of the fetal middle cerebral artery seem to be at least as good as amniocentesis, most patients at tertiary institutions are followed with both amniocentesis and ultrasound.

    Once the D OD 450 measurements have entered high zone 2 or zone 3 or the fetus has been diagnosed with hydrops based on ultrasound findings, a decision should be made to either perform a PUBS or deliver if beyond 34 weeks' gestation (32 wk with mature lung indices). A number of important factors must be considered when preparing a patient for PUBS and possible IUT; these include gestational age, the possibility of delivery, fetal maturation with corticosteroids, and the likelihood of transfusion.

    If a patient is beyond viability (24th wk of gestation), a discussion regarding the management of fetal bradycardia should occur. Even though 24 weeks' gestation is considered the cusp of viability, the outcomes are likely to be even more dismal if the fetus is hydropic. In this setting, consultation with a neonatologist is important, as is fully informing the patient of the description and probabilities of different outcomes.

    If the fetus is at a gestational age at which the patient would desire immediate delivery if signs of fetal distress occurred, the procedure may be performed with the patient under epidural or spinal anesthesia to avoid the risks associated with general anesthesia and to decrease the amount of time required to deliver the fetus. In addition, also consider regional anesthesia in the setting of likely transfusion because this procedure can be time consuming and uncomfortable for the patient. Because of the possibility of immediate delivery, a 48-hour course of betamethasone to accelerate fetal maturity, particularly the lungs, is usually administered before the first 2 procedures.

    PUBS and intrauterine transfusions

    The first IUTs were performed intraperitoneally in 1963. However, since the advent of PUBS and intravenous transfusions into the umbilical vein, use of the IPT has diminished in the management of anemic fetuses. Benefits of IVT over IPT include direct measurement of the fetal hemoglobin and acid-base status, lower failure rate (particularly in hydropic fetuses), lower rates of procedure-related morbidity and mortality, and better efficacy at earlier gestational ages. The only benefit offered by IPT is the ability to drain fetal ascites during the procedure, but this is of minimal benefit in hydropic fetuses.

    When preparing to perform a PUBS, a number of details must be accomplished before the procedure itself. As mentioned previously, the patient must have a consultation with a neonatologist and anesthesiologist. The blood for possible transfusion must be typed and cross-matched against the mother's serum to help rule out any other possible hemolytic antibodies. This can require several hours. The large variety of equipment, such as transfusion tubing, a blood warmer, heparinized syringes, and an accurate machine to obtain a rapid hematocrit value, must be prepared and calibrated. Unless the procedure is being performed in a unit that routinely performs these procedures, these issues should be discussed and reviewed in detail with the team of nurses, physicians, and technologists involved in the procedure.

    Once all of the consultants and equipment are prepared, the actual PUBS can be performed. After regional anesthesia is obtained, the patient is placed in the supine position with a left lateral tilt to prevent the uterus from occluding the inferior vena cava. The abdomen is carefully prepared, often using both povidone-iodine solution (Betadine) and alcohol because an intrauterine infection can be as disastrous as hydrops itself. A sterile sleeve is placed over the ultrasound transducer used to guide the procedure.

    The best location for the PUBS is near the umbilical cord insertion into the placenta. This location is relatively stable, and the needle is less likely to be dislodged once access is gained. If the placenta is anterior, the risk of the fetus dislodging the needle is unlikely. However, this risk is increased with a posterior placenta and an active fetus. In this setting, the fetus may be administered a subcutaneous injection of a neuromuscular blocking agent to decrease its activity.

    Once intraumbilical vascular access is gained, stabilizing the needle is enormously important so that access is not lost. This can be accomplished more easily if tubing is attached to the hub of the needle, rather than connecting and disconnecting syringes. A sample of the fetal blood is taken. Usually, part of the sample is used to obtain a rapid hematocrit value from the unit and the rest is sent to the laboratory for confirmation. Usually, the transfusion of Rh D–negative packed erythrocytes is begun even before the hematocrit results are returned, unless some strong possibility exists that the fetus will not require blood.

    The amount to be transfused can be calculated once the hematocrit/hemoglobin results are returned. In general, 30-60 mL/kg of nonhydropic fetal weight is transfused because volumes higher than this may be difficult for the fetus to tolerate. During the transfusion, the turbulent flow of the blood being infused should be monitored via ultrasound to ensure that the needle is still in place. If intravascular access is lost and the transfusion is inadequate, repeat access may be attempted.

    In the setting in which repeat access cannot be gained or with a posterior placenta in which intravascular access could not be gained initially, performing an IPT is reasonable. These transfusions require a greater volume of blood, roughly calculated as the following:



    (number of weeks' gestation – 20) X 10 mL

    If an IPT is attempted, take care to avoid the umbilical vessels and to ensure that intra-abdominal access is indeed intraperitoneal. This can be accomplished by watching the blood as it is transfused into the fetal abdomen.

    Once the transfusion is accomplished, if via IVT a final blood sample is often taken to estimate the final hematocrit value of the fetus, although this measurement will be an underestimation of the hematocrit secondary to the large volume infused during the transfusion. The fetus should be monitored with continuous fetal monitoring for the ensuing 4 hours (both during the procedure and immediately after because decelerations of the fetal heart rate are common and must be managed cautiously). If the initial hematocrit value was extremely low, a repeat procedure may be necessary as soon as within a week; otherwise, the procedure can be performed every 2-4 weeks based on the posttransfusion hemoglobin value. Because the goal is to maintain the fetal hemoglobin value at greater than 9 g/dL and because it drops at approximately 1 g/dL every 3 days, these values can be used to calculate how much time can be allotted until the next procedure. Serial IUTs are usually performed until 34 weeks' gestation, beyond which time the risk of the procedure likely outweighs the benefits. This leads to delivery of the fetus at 34-37 weeks' gestation and, occasionally, even earlier if fetal lung maturity is documented.

    ALLOIMMUNIZATION RELATED TO NON–RH D ANTIGENS


    While alloimmunization to the Rh D erythrocyte antigen has historically been the most common etiology of severe hemolytic disease of newborns, it is becoming a rarity in developed countries because of routine prophylaxis with anti-D Ig. However, hemolysis may also be caused by the presence of antibodies to atypical erythrocyte antigens. Because no screening program or prophylaxis is available for antigen-negative patients of these atypical erythrocyte antigens against whom sensitization can lead to fetal hemolysis, the rate of hemolytic disease related to these more rare antibodies is either stable or rising.


    Commonly, patients with antibodies to the more rare erythrocyte antigens are recognized by the antibody screen performed upon initial presentation to prenatal care. If the results of the screen are positive, the laboratory will then isolate the exact antibody. If the antibody is known to cause hemolysis in the fetus (see Association of atypical erythrocyte antibodies and hemolytic disease of the newborn), such as anti-c, anti-Kell, and anti-E antibodies, these patients are treated similarly to those who are Rh sensitized. Initial management involves monitoring serial maternal antibody titers, which leads to an assessment of the fetus for hemolysis using amniocentesis as indicated by rising antibody titers, ultrasound findings, and, possibly, the results from PUBS.

    If the antibody has not been known to cause fetal hemolysis (see Association of atypical erythrocyte antibodies and hemolytic disease of the newborn), such as anti-Lea and anti-Leb (the Lewis antigens), no reason exists to follow antibody titers. One proposition is that patients with antibodies known to cause only mild hemolysis, such as anti-Hil, anti-Hu, and anti-Vw antibodies, can be treated expectantly because the risk of invasive testing likely outweighs the risk of disease. In the rare case of finding a new erythrocyte antibody, conservative management entails monitoring the patient as if the antibody would cause hemolysis. However, patients should be counseled carefully regarding the risks and benefits of either management plan.

    In only 2 situations are patients not monitored identically to patients who are Rh sensitized. The first is that of alloimmunization to the c, E, or, C antigens. Some concern exists that hemolysis may occur in these patients with a lower than 1:16 titer. Thus, if the initial titer is 1:4 and stable but increases at 26 weeks' gestation to 1:8, assessing with amniocentesis for D OD 450 at that point is reasonable. However, if the patient presents in the first trimester with a 1:8 titer that remains stable at 1:8 throughout the second trimester, continued serial antibody titers are indicated.

    The second situation in which patients should not be treated identically to patients who are Rh sensitized is that of Kell isoimmunization because several cases of severe fetal hemolysis with anti-Kell antibodies have occurred in the setting of low D OD 450 values. The proposed etiology for this is that the anti-Kell antibodies may attack and destroy erythroid precursors that have low levels of hemoglobin. This leads to fetal anemia, but not with the concomitant rise in bilirubin breakdown products, thus leading to relatively normal values of the D OD 450.

    • Association of atypical erythrocyte antibodies and hemolytic disease of the newborn (with disease frequency and antibodies)

      • Common – Kell, c, E
      • Uncommon - e, C, cE, Ce, Cw, Kpa, Kpb, k, Jka, s, Wra, Fya
      • Rare - Biles, Coa, Dia, Dib, Doa, Ena, Fyb, Good, Heibel, Jkb, Lua, Lub, M, Mia, Mta, N, Radin, S, U, Yta, Zd
      • No documented cases - Lea, Leb, P



    ABO incompatibility
    Sensitization to an Rh D–positive fetus is much less likely in the setting of a mother who is making anti-A or anti-B antibodies to the fetal erythrocytes. This is likely because the erythrocytes are cleared by the ABO incompatibility before the maternal immune system has an opportunity to recognize the other foreign antigen, Rh D. This type of ABO incompatibility can also lead to mild fetal hemolysis. Because most of the anti-A and anti-B antibodies are Ig M, which does not cross the placenta, the fetal hemolysis does not lead to severe anemia and hydrops. However, even with mild anemia, the hemolysis may lead to hyperbilirubinemia and even kernicterus; thus, closely monitor the neonate postpartum for jaundice. No particular antepartum management needs to be addressed in the setting of ABO incompatibility.

    CONCLUSION
    The prevention and treatment of alloimmunization leading to fetal hydrops is a true success story in obstetrics. While this problem only occurred in a minority of pregnancies, the outcomes were disastrous in patients who were affected. With the discovery of the Rh (D) antigen and anti-D Ig and with the fact that prophylaxis with the latter could prevent sensitization to the former 99% of the time, women who are Rh D negative no longer need to fear the complications of alloimmunization. Furthermore, in patients who have become sensitized, close monitoring of antibody titers, the use of D OD 450 to recognize hemolysis, and treatment with IUT have led to a dramatic decrease in perinatal morbidity and mortality rates. Because of the small risks associated with each amniocentesis, hope exists that with continued research into noninvasive modalities to assess fetal anemia, avoiding even these procedures may be possible in the future.






    ---------------------------------------------------------
    http://www.kfshrc.edu.sa/annals/205_206/99-335.htm

    Case Reports

    Recurrent Hydrops Fetalis Due to Kell Allo-immunization





    Vijaymani Baichoo,
    FRCP; Alexander Bruce-Tagoe, FRCPath




    We report a case of recurrent hydrops fetalis caused by Kell allo-immunization. The peculiar features of hemolytic disease of the newborn (HDN) due to anti-Kell allo-immunization are described, discussed and contrasted with those of anti-D allo-immunization. The ideal management protocol is outlined and discussed. It is suggested that a team comprising an obstetrician, a neonatologist and a hematologist or blood transfusion expert should manage pregnancies complicated by Kell allo-immunization.




    Case Report



    A 33-year-old gravida 12 para 11+0 mother presented unbooked, in active labor at 31 weeks of gestation. Her obstetric history was remarkable: two of her previous pregnancies (10th and 11th) had ended in fetal deaths at 24 and 26 weeks of gestation, respectively, due to fetal hydrops. She had undergone cesarean section on two occasions (5th and 6th pregnancies), during the first of which she received blood transfusions at another hospital. Her blood group was "A" Rh negative, and she had been identified to have anti-Kell antibodies in two previous pregnancies (10th and 11th) at Prince Salman Hospital (PSH), Riyadh. No anti-D antibodies were detected then or have been detected since.

    Delivery was by cesarean section, during which marked polyhydramnios was noticed. The infant weighed 2.75 kg, had an Apgar score of 2 at 1 minute, and was hydropic with gross ascites, scalp edema and severe pallor. He was actively resuscitated with endotracheal intubation, positive pressure ventilation, volume expansion and abdominal paracentesis of 100 ml of ascitic fluid to facilitate ventilation.

    The initial investigations of the infant revealed severe anemia (hemoglobin 35 g/l), macrocytosis (MCV 165 fl), low reticulocyte count (0.4%), normal white blood cell count (8.6x109/l) and platelet count (216x109/l). The serum transaminases were normal as was serum bilirubin, but total serum proteins (33 g/l) and serum albumin (17 g/l) were low.



    From the Departments of Pediatrics and Hematology, Prince Salman Bin Abdul-Aziz Hospital, Riyadh, Saudi Arabia.

    Address reprint requests and correspondence to Dr. Baichoo: Al-Corniche Hospital, P.O. Box 3788, Abu Dhabi, United Arab Emirates. E-mail: vjmanib@emirates.net ae.

    Accepted for publication 7 July 2000. Received 29 December 1999.

    Cord blood analysis revealed the infant’s blood group as "O" Rh positive, and the direct Coombs’ test (DCT) was strongly positive. The maternal blood was positive for anti-Kell antibodies in a titer of 1:512, but no anti-D antibodies were detected. The infant and his father were heterozygous Kell positive (K1K2), as indeed was the fourth child, who was born before the mother received her first blood transfusion.

    The infant received a single-volume exchange transfusion with packed "O" Rh negative, Kell (K1) negative red blood cells, followed by a top-up transfusion after 12 hours, as well as supportive treatment. He also required phototherapy for three days for moderate hyperbilirubinemia (maximum serum bilirubin 190
    m mol/l). The infant did well until the age of seven days, when he was noticed to be hypertensive (BP 106/62 mm Hg). Antihypertensive treatment with hydrallazine was started. On the 8th day, he was lethargic, the anterior fontanelle was full and tense, and brain CT scan showed a large intracerebral hemorrhage on the right side, causing compression of the brain stem and the lateral ventricle. The infant died at the age of 10 days.





    Discussion










    The incidence of rhesus hemolytic disease of the newborn (HDN) has diminished significantly due to anti-D prophylaxis. At the same time, HDN caused by other irregular antibodies is being increasingly recognized. After anti-D and anti-c, anti-Kell antibodies can cause moderate to severe hemolytic disease in the fetus and the newborn. Blood transfusion to a Kell-negative woman is an important cause of allo-immunization.

    Isolated reports of Kell allo-immunization have appeared in the literature from 1965, and the earliest large series were published by Caine and Mueller-Heubach in 1986,1 and by Leggat et al. in 1991.2 Kell allo-immunization in women can be caused by pregnancy with a Kell-positive fetus or, more commonly, following transfusion with Kell-positive blood. In white populations, only 0.2% of the people are homozygous Kell positive, 8.7% are heterozygous and 91.1% are Kell (K1) negative. The frequency of anti-Kell antibodies differs in different countries and different populations. The studies from the U.S. quote figures from 3.1% to 22%.3 The prevalence of K1 phenotype in Saudi Arabia is 18%,4 and the prevalence of K1 phenotype in Saudi blood donors in Prince Salman Hospital is 14.7% (Bruce-Tagoe, unpublished data).

    Kell antigens are strong immunogens; they are well developed in the red blood cells of the fetus that inherits the gene, and are present at an early stage of red cell maturation. One remarkable feature of anti-Kell hemolytic disease is that there is selective inhibition of erythroid progenitor cells, resulting in a lack of reticulocytosis and erythroblastosis.5 Another remarkable feature is that the red cell precursors are destroyed at the primitive stage of maturation when they are still poorly hemoglobinized. Their destruction does not, therefore, produce a significant increase in amniotic fluid bilirubin levels.6 The granulocyte-macrophage and megakaryocytic progenitor cells are not affected.

    Anti-Kell and anti-D hemolytic diseases differ in some other important aspects. In the former, unlike the latter, the previous obstetric history is not always predictive of outcome in the index pregnancy, and there is poor correlation between the antibody titers and the outcome. Severe fetal hydrops has been reported with an antibody titer of 1:2.5 Furthermore, in anti-Kell disease amniotic fluid spectrophotometry for bilirubin concentration correlates poorly with disease severity and hyper-bilirubinemia is not a prominent feature in the affected newborns.

    The ideal management of Kell hemolytic disease involves a multidisciplinary team effort by Obstetrics, Neonatology, Hematology and Transfusion services personnel. Efforts are directed at: 1) identifying which fetus is severely affected; 2) treating fetal anemia; and 3) determining optimal time for delivery. Once anti-Kell antibodies are identified in a pregnant woman, the titers should be measured, history of previous pregnancies and blood transfusions ascertained, and the Kell status of the husband determined. If the husband is Kell negative, the fetus will be Kell negative, and no further investigations are required. But if the husband is Kell positive, the Kell status of the fetus needs to be determined. This can be done by DNA analysis of fetal cells obtained by chorionic villus sampling as early as 10-12 weeks of gestation. Otherwise, maternal antibody titers need to be monitored every two to four weeks, and ultrasonography performed to identify signs of fetal affection. At 20 weeks of gestation, fetal blood sampling (FBS) is carried out to determine fetal blood group, hematocrit, DCT, reticulocyte count and bilirubin.

    Once allo-immunization has occurred and the fetus has developed severe erythroblastosis, its healthy survival depends on active intrauterine management. If fetal hematocrit on FBS is below 30%, this indicates a need for either intraperitoneal transfusion (IPT) or intravascular
    transfusion (IVT). IVT is the preferred management modality. It allows direct entry of transfused cells into the fetal circulation and can be performed as early as 20 weeks of gestation. The fetal blood group can be confirmed, pre- and post-transfusion hematocrit can be measured, and reversal of hydrops can be achieved irrespective of gestational age. It also allows continuation of pregnancy until 37-38 weeks of gestation, and the timing of transfusion and the delivery can be decided more rationally. IVT can either be a top-up transfusion or an exchange transfusion. A second transfusion should be performed within two weeks of the first transfusion, as it is difficult to predict the rate of fall of hemoglobin initially. Some institutions employ a combination of transfusions, i.e., IVT followed by IPT, as this approach diminishes the frequency of transfusions. Affected infants need top-up transfusions in the early months of life because they are born with virtual absence of reticulocytes and a red cell population consisting mainly of transfused adult red cells.

    The outcome in allo-immunized pregnancies has improved greatly in recent years. With IPT alone, the overall survival rate is 80%. Following IVT, the survival in some centers is 90%, and the survival in hydropic fetuses is 66%. In a recent series, the reversal of hydrops following IVT was about 60%, and the survival in this group was about 86%.7 The long-term follow-up following intrauterine transfusions has shown normal neurological and developmental outcome in 84%-93% of cases.8


    too:
    http://www.blood.co.uk/pdfdocs/blood_matters_13.pdf
    http://jognn.awhonn.org/cgi/content/full/30/6/589



    I have luck to be positive...


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    Post Re: Are you Rh-negative blood? Then you have to know this! (if you are Rh positive, too)

    There seems to be no selective value for Rh- except that, possibly, two Rh- parents may have higher fertility. The reaction of Rh- and Rh+ to each other in a breeding situation would led to the conclusion that these two alleles are from different species, since they do form a type of reproductive isolation.

    This is science-fiction at this point but what if this Rh-, Rh+ were the result of "speciation"? What if Neanderthals were Rh- and passed this on to sapiens through hybridization in extreme Western Europe, their last stronghold? It would have survived there because of increased fertility should both parents possess it but it would have acted as a reproductive barrier for those who did not. Perhaps the incoming Upper Paleolithic people did not have it, the Neanderthals did, and it was one of the reasons Neanderthals died out. Just an idea.

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    Post Re: Are you Rh-negative blood? Then you have to know this! (if you are Rh positive, too)

    (Sorry my english)
    a natural barrier against mixing?

    I read a mother rh- (father rh+) had 7 pregnancies, and her pregnancy losses (three) were all males for this illness. why?
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    Post Re: Are you Rh-negative blood? Then you have to know this! (if you are Rh positive, too)

    The danger is that kleihauer-betke (despite isn't 100% effective) have to be a rutine analisis (and now is not in some places) in all Neonatology rooms, because it should have to be made before 12 hours post-parthian (childbirth) as after that time, fetal red corpuscle make phisiological clearence and you'll cann't detect them.



    "IgG antibody–mediated hemolysis of fetal erythrocytes, known as hemolytic disease of the fetus and newborn, varies in severity and can have a variety of manifestations. The degree of anemia can range from mild to severe with associated hyperbilirubinemia and jaundice. In severe cases, hemolysis may lead to extramedullary hematopoiesis and reticuloendothelial clearance of fetal erythrocytes. This may result in hepatosplenomegaly; decreased liver function; and ensuing hypoproteinemia, ascites, and anasarca. When accompanied by high-output cardiac failure and pericardial effusion, this condition is known as hydrops fetalis. This syndrome is often fatal despite intensive neonatal care, including emergent exchange transfusion".

    With the discovery of the Rh (D) antigen and anti-D Ig and with the fact that prophylaxis with the latter could prevent sensitization to the former 99% of the time, women who are Rh D negative no longer need to fear the complications of alloimmunization.
    Cases of hemolysis in the newborn that do not result in fetal hydrops can still lead to kernicterus. This is a neurological condition observed in infants with severe hyperbilirubinemia and is due to the deposition of unconjugated bilirubin in the brain. The absence of placental clearance and immature fetal bilirubin-conjugating ability can lead to symptoms that manifest several days after delivery and include poor feeding, inactivity, loss of the Moro reflex, a bulging fontanelle, and seizures. The 10% of infants who survive may develop spastic choreoathetosis, deafness, and mental retardation.
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    Post Re: Are you Rh-negative blood? Then you have to know this! (if you are Rh positive, too)

    Quote Originally Posted by Libertad
    (Sorry my english)
    a natural barrier against mixing?

    I read a mother rh- (father rh+) had 7 pregnancies, and her pregnancy losses (three) were all males for this illness. why?

    In Fact, in the past Rhesus factor was a natural barrier against mixing.There is no relation between EF and the baby sex.


    There is a relaction between Rh + and reumatic diseases , but it´s another topic.

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    My partner is Rhesus negative.

    Through the course of her pregnancy, she was given an anti-D injection before and after the birth.

    She never had to have the anti-D injection on the second birth, as my daughter came out with Rhesus negative blood type O as well.

    The birth of my son was not treated with the same course of anti-D, as they thought me Rhesus negative blood type O as well.

    Would that mean for sure that my children are type O blood?
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    Quote Originally Posted by BeornWulfWer View Post
    The birth of my son was not treated with the same course of anti-D, as they thought me Rhesus negative blood type O as well.

    Would that mean for sure that my children are type O blood?
    What is your partner's bloodtype? If both of you are O then your children will also be O. O is recessive to A & B:
    O + O = O(OO)
    A + O = A(AO)
    A + A = A(AA)
    A + B = AB(AB)
    B + B = B(BB)
    B + O = B(BO)
    2 persons with type O(OO) will only have children with type O. Someone who is type A(AO) can have a child with type O if the other parent is O or A(AO) or B(BO). But persons with A(AA), B(BB) or AB(AB) cannot have a child with type O blood.

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    Quote Originally Posted by BeornWulfWer View Post

    Would that mean for sure that my children are type O blood?
    Sorry Ćmeric, that should have said: "Would that mean for sure that I am type O blood?"

    My daughter and son are both type O, as well as my partner.
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    I'm O negative and so is my mother. My father I believe is A, so he must be AO.

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    I am o- blood along with Rh-negative as well.
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