Hemolitic Newborn Disease

  1. Can anyone help me figure out how to find a website that has information on Hemolitic (sp?) Newborn Disease. I'm not even sure it is called that, but my A&P teacher wants us to do a brief write up on it. I've looked on Yahoo, Google and other search engines but I'm not getting much help on the newborn part. It has to deal with rH with the mom and the baby. We also have to state why it's not a problem anymore. So if anyone could help me that would be great! Thanks!
  2. Visit kcsunshyn8 profile page

    About kcsunshyn8

    Joined: Apr '02; Posts: 72


  3. by   sunnygirl272

    Anemias caused by breakdown of RBCs.

    Rhesus Incompatibility
    Rhesus (Rh) incompatibility may occur when an Rh-negative woman carries an Rh-positive fetus. Maternal isoimmunization occurs after some (incompatible) fetal RBCs cross the placenta and induce an immunologic response with specific maternal anti-Rh antibodies, some of which subsequently cross the placenta into the fetus and lead to hemolysis.

    The first isoimmunization may occur with a miscarriage or in a pregnancy with an Rh-positive fetus. The severity of isoimmunization usually increases in each subsequent pregnancy, and each succeeding infant is likely to be more severely affected. Rh incompatibility usually indicates that antibodies to group D RBC surface antigen are present, although C and E factor incompatibilities of the Rh system may also occur. (See also Ch. 252.)

    Symptoms and Signs
    The most severely affected fetuses develop profound anemia in utero (erythroblastosis fetalis--see in Ch. 252) with intrauterine fetal death or are delivered with hydrops fetalis. The latter may be diagnosed before delivery on ultrasound, which shows scalp edema, cardiomegaly, hepatomegaly, pleural effusions, and ascites. Polyhydramnios may also be present. These newborns are extremely pale and may have severe generalized edema, including pleural effusions and ascites. Because of extramedullary hematopoiesis, the liver and spleen are enlarged. Heart failure may occur. Because of anemia and prematurity, asphyxia is more likely during labor and delivery, and cesarean section is usually indicated. Prematurity and asphyxia, along with hypoproteinemia, predispose these newborns to respiratory distress syndrome, the signs of which may be difficult to distinguish from those of heart failure. Less severely affected newborns may be anemic but do not have edema or other signs of hydrops; mildly affected infants may have little or no anemia at birth. Affected infants usually develop hyperbilirubinemia soon after delivery because of the continuing hemolytic effect of anti-Rh(D) antibodies that have crossed the placenta.

    Diagnosis and Prophylaxis
    The severity of the in utero hemolytic process can be evaluated by measuring the bilirubin in the amniotic fluid (measured as the optical density at 450 nm [OD 450] and corrected for gestational age) through sequential amniocenteses (see Table 252-2). For prophylaxis of the Rh-unsensitized woman, see Ch. 252.

    Before birth: Fetal blood can be sampled (for analysis of Hct, blood type, and direct Coombs' test) and transfusions of packed RBCs given to the severely affected fetus by cordocentesis in utero. Packed cells can also be given by intraperitoneal transfusion of type O Rh-negative RBCs, which should first be irradiated to kill lymphocytes that might otherwise cause graft-vs.-host disease. These procedures are performed with ultrasound guidance at a perinatal ICU.

    During labor: Fetal heart rate should be monitored; if signs of fetal distress occur or if the infant is severely affected, cesarean delivery is indicated. A newborn with hydrops fetalis or severe erythroblastosis fetalis without hydrops is critically ill and should be delivered at a perinatal ICU.

    After birth: In hydrops fetalis, profound anemia should be treated immediately with a partial exchange transfusion using packed Rh-negative RBCs. After the infant's condition stabilizes, a double volume exchange transfusion (ie, using twice the infant's calculated blood volume, which thereby removes 85% of the infant's blood, including circulating antibodies, sensitized RBCs, and accumulated bilirubin) should be performed with Rh-negative blood. Digoxin and diuretics for heart failure, alkali therapy for metabolic acidosis, and respiratory support for respiratory distress syndrome may be required.

    All newborns born to Rh-negative women should have cord blood examined immediately to determine the infant's blood type, and a direct Coombs' test should be performed. If the newborn is Rh-positive and the direct Coombs' test is positive, the newborn's Hct and reticulocyte count should be determined, and a blood smear should be checked for reticulocytes and nucleated RBCs. The bilirubin level in cord blood should be determined. A cord-blood Hct < 40% and a cord-blood bilirubin > 5 mg/dL (86 mol/L) indicate significant hemolysis.

    If the infant's condition is stable, an early exchange transfusion will remove sensitized RBCs and antibodies before hemolysis produces large amounts of bilirubin and may avert the eventual need for multiple exchange transfusions. If hemolysis is particularly severe, exchange transfusion for hyperbilirubinemia will almost certainly be required. Criteria suggesting the possible need for an early, but not emergency, exchange transfusion include an Hct < 40%, reticulocytes > 15%, and a cord bilirubin concentration > 5 mg/dL (> 86 mol/L) at birth; the most useful information is obtained by observing the rate at which serum bilirubin rises over several hours. If the level rises >= 1 mg/dL/h (>= 17 mol/L/h), the infant will likely need an exchange transfusion, although treatment with phototherapy may slow the rise in bilirubin, possibly avoiding the need for exchange transfusion.

    If an exchange transfusion is not indicated immediately, the infant can be followed with serial determinations of serum bilirubin and Hct. Exchange transfusion is indicated if bilirubin levels become markedly elevated (see hyperbilirubinemia under Premature Infant, above, and under Metabolic Problems in the Newborn, below) or significant anemia develops.

    Many affected Rh-positive newborns will not need an exchange transfusion; however, the Hct must be followed serially for several months, since severe anemia may develop because of slow ongoing hemolysis. Such infants may require a simple transfusion with packed type-specific Rh-negative RBCs rather than an exchange transfusion.

    ABO Blood Group Incompatibility
    In almost all cases of ABO incompatibility, the mother's blood type is O and the infant's is A or B. Anti-A sensitization is more common, but anti-B sensitization is likely to produce more severe hemolytic disease. Although the infant may develop anemia in utero, it is almost never severe enough to cause hydrops fetalis or intrauterine death. The major clinical problem is the development of significant hyperbilirubinemia after birth as a result of ongoing hemolysis.

    Laboratory studies are similar to those for Rh disease. The direct Coombs' test is usually weakly positive but may occasionally be negative, which does not rule out ABO incompatibility if other diagnostic criteria are met. Usually anti-A or anti-B antibodies can be found in the infant's serum (by positive indirect Coombs' test) or after antibody elution from the infant's RBCs. Also, many microspherocytes in the infant's blood and reticulocytosis suggest ABO incompatibility. Surveillance and treatment are identical to those for Rh incompatibility.

    Rare Blood Group Incompatibilities
    Many rare blood group incompatibilities have been documented (eg, Kell, Duffy). Although uncommon, they may be severe, and because hemolysis is involved, they produce anemia and hyperbilirubinemia in the pattern of Rh or ABO incompatibility. Since diagnosis of these incompatibilities may be time consuming, many advise routine screening of the mother's blood during pregnancy for rare or atypical antibodies. Treatment is similar to that for Rh incompatibility; blood used for exchange transfusion must lack the sensitizing antigen.

    Anemia Due to Congenital Spherocytosis
    (See also Anemias Caused by Excessive Hemolysis in Ch. 127.)

    Hemolysis in infants born with congenital spherocytosis often causes significant hyperbilirubinemia and possibly anemia. Significant splenomegaly usually does not occur in newborns. Spherocytes are seen on the blood smear, and the RBCs have increased osmotic fragility. This disorder may be inherited as a dominant trait. However, in many cases, family history is negative for spherocytosis. Early hyperbilirubinemia, if severe, is treated by exchange transfusion. Splenectomy may be required later to control chronic hemolytic anemia.

    Nonspherocytic Hemolytic Anemias
    Occasionally, newborns develop hemolytic anemia secondary to RBC enzymatic defects, such as pyruvate kinase deficiency or G6PD deficiency (see Anemias Caused by Alterations of Red Cell Membranes in Ch. 127). Heinz bodies in erythrocytes of an infant with hemolytic anemia suggest these disorders, and specific tests for enzyme activity can be performed. A definitive diagnosis in the newborn may be difficult. The course of the hemolytic anemia should be observed over time; amounts of blood large enough to diagnose specific RBC enzymatic defects will be easier to obtain when the infant is older.

    Hemolytic Anemia Due to Infections
    Hemolysis occurs with many congenital infections (eg, toxoplasmosis, rubella, cytomegalovirus, herpes simplex, and syphilis) and in infections due to hemolytic bacteria (eg, Escherichia coli or -hemolytic streptococci). Sepsis or UTI may cause early or severe hyperbilirubinemia.
  4. by   ResearchRN
    Go to google.com and search hemolytic newborn disease. You will find a wealth of information.
  5. by   cactus wren
    Now, remember,I`m an adult ICU nurse, but, as I fogily think back.......RH factor problems was solved once they came up with Rhogam (?sp) was invented in the 60`s.You might try looking for Rhogam at drug site.Before that when a rh- mom had her 2nd. baby (first baby did fine, but shared blood with mom, and set up allergic type response in mom), mom`s blood would fight off +rh in babes blood. Sometimes,if these babes actually came to term, they needed total blood replacement. Had kits for that, don`t think I ever saw on used as i got into nursing about time rhogam came out.This reaction could also be fatal to both mom and babe. Rarely seen today, except sometimes in mom`s who had ab, and wasn`t tested for Rh factor of fetus and she was rh-.
  6. by   cactus wren
    WOW Sunnygirl.....Glad to see my old brain does retain some stuff I haven`t used in a long,long time........Good post....
    Originally posted by ResearchRN
    Go to google.com and search hemolytic newborn disease. You will find a wealth of information.
    I gotta agree here. Really, a search for the words "Newborn Hemolytic Disease" on any search engine will turn up more info than we could ever give you.

    Allright, so I decided I'll be nice and give you a little hint... you'll want to look up ABO Incompatibilities too.

    But yoo'll have to sift through the info all by your lonesome.....

  9. by   kcsunshyn8
    Thank you all very much! Now that is one less thing I have to worry about tomorrow before my Chemistry Test! Wish me luck!
  10. by   NicuGal
    We still see this sometimes even if the mom got Rhogam. Sometimes the mom's miscarry and don't get Rhogam and then the next pregnancy has problems.

    We rarely have to do exchange transfusions on these kids. I have seen a few with hcts as low as 15! It is a very interesting topic
  11. by   Vsummer1
    Here is am interesting sidebar to this discussion... if Mom was given Rhogam prior to 1992 have her checked for Hep C. Rhogam is a human blood product, and transmission of Hep C has been document from this immunoglobulin shot. There was an excellent study done in Ireland on this (pretty sure it was the Irish, haven't read the study in about 3 years). How do I know? I am AB-, husband was + and I got Rhogam -- and Hep C. That was my ONLY risk factor. BTW, I did the interferon/ribaviron for 48 wks and am PCR negative x 2 years. And that is also why I had to quit RN school and why I am just now returning to it.