Hemolytic Disease of the Newborn
Hemolytic Disease of the Newborn (HDN) is a blood-related disorder that occurs in a fetus or a newborn infant. This problem usually arises, when a mother has different blood type than her unborn baby, i.e. a condition known as “incompatibility”. Most common form of this incompatibility is ABO incompatibility, which is not very severe condition, and the least common form of the incompatibility is Rh incompatibility. Due to these differences in blood types, antibodies in the blood of mother attack the red blood cells of the developing baby resulting in the destruction of blood cells of the baby causing symptoms such as edema and newborn jaundice. HDN can be life threatening in some cases (MedLine Plus, nlm.nih.gov).
The management as well as diagnosis of pregnant woman with HDN can be done with the help of laboratory studies and radiographic monitoring. One or more of the following clinical conditions are present in HDN:
Bilirubin test is performed for bilirubinemia (Frazier, and Drzymkowski 122). Rapidly progressing hyperbilirubinemia that is severe, or hyperbilirubinemia that is prolonged,
Positive findings of maternal antenatal antibody,
Diagnosis of fetal hydrops, which is a condition of severe edema (McConnell 138), or anemia, and/or
Hemolysis on blood film diagnosis.
Hypoglycemia is commonly observed in the condition that occurs due to hyperinsulinism and islet cell hyperplasia. This problem is found to be secondary to the release of metabolic byproducts as, for example, glutathione from lysed red blood cells. Moreover, hypocalcemia, hyperkalemia, and/or hypokalemia commonly appear at the time and/or after exchange transfusion.
The seriousness of hematologic abnormalities shows the increased problem of hemolysis as well as the extent of hematopoiesis. Findings of complete blood count (CBC) can show following abnormalities:
Anemia: Laboratory measurements for anemia can be more accurate, if samples are taken from central arterial or venous portion rather than capillaries (Stanford Children’s Health, stanfordchildrens.org).
The reticulocyte count can be increased to as much as 40% in patients having no intrauterine intervention.
The nucleated RBC count can be increased and can falsely represent increased leukocyte count, thereby showing a condition of erythropoiesis.
Spherocytes (smaller and denser red blood cells) more commonly appear in the case of ABO incompatibility.
In severe cases of hemolytic disease, Echinocyte (red blood cells with abnormal cell membrane) and schistocytes (fragmented portion of red blood cells) can be seen showing the problem of disseminated intravascular coagulation.
Increased problems of polychromasia, anisocytosis, and cell fragmentation can also appear in laboratory findings.
Neutropenia, which is a condition that is found to be secondary to erythropoiesis. Neutrophilia can also be seen after intrauterine transfusion (Black, Vandy, and Maheshwari n.p.).
Thrombocytopenia: This condition is commonly observed after exchange or intrauterine transfusions as there is platelet-poor blood product and platelet production is suppressed.
Direct antibody test and direct Coombs test in the mother as well as affected newborn, and these tests show positive results. Indirect Coombs test show positive results in neonates having ABO incompatibility, but it has reduced predictive value for hemolysis (Hatfield 252). Usually, in newborn babies having hemolytic disease as a result of anti-C antibodies, direct antibody test may show negative results, but the diagnosis can be strengthened with indirect Coombs test.
IgG2 commonly appears in the serum of mother but it has reduced lytic activity resulting in the observation of reduced or no hemolysis with a positive result in direct antibody test. Whereas, substantial hemolysis is found to be related to negative direct antibody test result when IgG1 and IgG3 are leading antibodies, which are found in decreased concentration but have significant lytic activity, moving to neonatal circulation.
Treatment Procedures and Medicines Recommended
After diagnosis of HDN, it is important to treat the problem. Treatment procedures can be done in pregnancy and after birth. At the time of pregnancy, treatment of HDN may consist of (University of Rochester, urmc.rochester.edu):
Intrauterine transfusion of RBCs into the circulation of the baby (Frazier, and Drzymkowski 122). This procedure is performed by the placement of a needle through the uterus of the mother into the abdominal cavity of the fetus, or the procedure can be completed by direct insertion into the vein in the umbilical cord. In order to stop the movement of the baby, sedative medications can be used before the procedure. Moreover, the process of intrauterine transfusions can be repeated.
Early delivery can be done, if there are chances of complications, i.e. if the lungs of the fetus are mature, labor and delivery can be started early in order to prevent worsening of the condition (Frazier, and Drzymkowski 122).
After birth of the baby, treatment procedures are as follows (University of Rochester, urmc.rochester.edu):
In case of severe anemia, blood transfusions can be done.
In case of low blood pressure, intravenous fluids are used.
In order to deal with the problem of respiratory distress, surfactant, oxygen, or a mechanical breathing machine can be used.
The process of exchange transfusion is used, so that the damaged blood of the baby could be replaced with fresh blood. Exchange transfusion is done by the process of giving and withdrawing blood in little quantities through an artery or vein. As a result of exchange transfusion, the RBC count increases and the levels of bilirubin decrease. However, if the bilirubin levels do not decrease, exchange transfusions can be repeated.
Recommended medicines for the treatment of HDN are as follows:
Intravenous immunoglobulin (IVIG), which act as immunomodulator can be used. IVIG is a solution developed from blood plasma containing antibodies, thereby helping the immune system of the body. Immunomodulators are helpful in normalizing the antibody levels in patients having primary defective antibody production. They can stop and treat some viral and bacterial infections and decrease the immune-mediated phagocytosis and hemolysis. With the help of IVIG, RBC breakdown is decreased and bilirubin levels are lowered. Use of IVIG can also reduce the need for exchange transfusions (de Alarcón, Werner, and Christensen 80). Doses in the range of 500 mg/kg to 1000 mg/kg are usually considered in the first few hours of birth of a newborn baby. However, efficacy of the doses and the treatment depends on the duration of treatment, timing of administration, and severity of the problem. It is important to consider that IVIG must not be mixed with normal saline.
Colony-stimulating factor can be used to correct the problem of anemia. These factors may include purified glycoprotein obtained from mammalian cells altered with coding of gene for human erythropoietin (EPO). In this case, sequence of amino acid is similar to the endogenous EPO. Biological activity of the substance is similar to the human urinary EPO, which can activate division as well as differentiation of committed erythroid progenitor cells and results in the activation of the release of reticulocytes to the blood stream from the bone marrow.
In order to prevent the problem of HDN, a drug known as Rh immunoglobulin (RhIg), also referred to as RhoGAM, can also be used, if the mother is Rh negative and has not been sensitized. RhIg is a specially engineered blood product that can stop the antibodies of an Rh negative mother to react with Rh positive cells. RhIg is usually administered during the 28th week of pregnancy. After the birth of the baby, the second dose is administered within 72 hours, if the baby is Rh positive, but the mother does not need another dose, if the baby is Rh negative (University of Rochester, urmc.rochester.edu).
Works Cited
Black, L. Vandy, and Akhil Maheshwari. "Disorders of the fetomaternal unit: hematologic manifestations in the fetus and neonate." Seminars in perinatology. Vol. 33. No. 1. WB Saunders, 2009.
de Alarcón, P., E. Werner, and R.D. Christensen. Neonatal Hematology: Pathogenesis, Diagnosis, and Management of Hematologic Problems. Cambridge University Press, 2013. Print.
Frazier, M.S., and J. Drzymkowski. Essentials of Human Diseases and Conditions. Elsevier - Health Sciences Division, 2015. Print.
Hatfield, N.T. Broadribb's Introductory Pediatric Nursing. Lippincott Williams & Wilkins, 2007. Print.
McConnell, T.H. The Nature of Disease: Pathology for the Health Professions. Lippincott Williams & Wilkins, 2007. Print.
MedLine Plus. "Hemolytic Disease of the Newborn". U.S. National Library of Medicine, 13 Jan. 2016. Web. 01 Feb. 2016 <https://www.nlm.nih.gov/medlineplus/ency/article/001298.htm>
Stanford Children’s Health. "Hemolytic Disease of the Newborn". Lucile Packard Children’s Hospital Stanford, n.d. Web. 01 Feb. 2016 < http://www.stanfordchildrens.org/en/topic/default?id=hemolytic-disease-of-the-newborn-90-P02368>
