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Hemolytic Disease of the Newborn

Hemolytic disease of the fetus and new given birth to is a problem in which red skin cells of of the fetus or neonate are damaged by the antibodies made by the mother. This condition occurs when Rh negative woman becomes pregnant with RH positive baby. When Rh positive baby's bloodstream enters into the mothers circulation scheduled to injury or during dilivery the mother becomes sensitized and produces anti-D antibodies. These antibodies are IgG type in order to mix the plasenta easily. Then antibodies enters into the fetus blood flow and damages the fetus red blood skin cells and the fetus becomes anemic, gradully the fetus will perish. Within the other side if the mom do not sensitized before in case she is pregnant for the very first time and if there is no any injury, the fetus bloodstream enters into the mother's blood flow during dilivery an ailment known as feto-maternal hemorrage (FMH) and the mom becomes sensitized. Could be the first child develop well since there is no antibodies that enters into the baby's flow.

In subsequent pregnancy, IgG antibodies mix the plasenta and ends up with red blood cell distruction by macrophages in the fetal liver and spleen. In the event the RBC destruction goes on, the fetus becomes ever more anemic. Fetal liver organ and spleen enlarge as erythropoiesis boosts in an effort to compensate for the RBC destructions. Erythroblasts are released in to the fetal blood flow (Erythroblastosisfetalis). If this condition is left untreated, cardiac failure can occur accompanied by hydropusfetalis, or edema and liquid build up in fetal peritoneal and pleural cavities.

Hemolytic disease of the fetus and new blessed is usually scheduled to Rh, ABO and other slight bloodstream group sysytem incompatibilities. Rh incompatibility triggers the most unfortunate conditions and it occurs when Rh negative mother become pregnant Rh positive baby. Also ABO incompatiblity causes HDFN. It's quite common but light type. This occurs when mother's ABo bloodstream group will not compatible with the fetus especially when bloodstream group O mom posesses, B or Belly fetus. Group O mother has anti-A and Anti-B antibodies which are Generally IgG type. Then this IgG type antibodies cross the placenta and damages the fetus red bloodstream cells. Nonetheless it is not sever as Rh antibodies.

ABO incompatibility often affects the first motherhood as a result of occurrence of non-RBC activated ABO Stomach muscles. HDFN can be also induced by other blood group system incompatibilities like kell system (anti-k), Kidd, Lewis, Duffy, MN, P and others. Anti-K 1 antibodies causes from light to severe disease. It causes the second most typical form of severe HDFN

Sign and symptoms of HDFN

Clinical demonstration of HDN varies from slight jaundice and anemia to hydrops fetalis. Because the placenta clears bilirubin, only risk to the fetus is anemia. Extramedullary hematopoiesis (scheduled to anemia) ends in hepatosplenomegaly. Dangers during labor and delivery include asphyxia and splenic rupture.

Postnatal problems include:

  • Asphyxia, Pulmonary hypertension
  • Pallor (credited to anemia) Edema (hydrops, due to low serum albumin)
  • Respiratory distress
  • Coagulopathies ( " platelets & clotting factors)
  • Jaundice, Kernicterus (from hyperbilirubinemia)
  • Hypoglycemia (anticipated to hyperinsulinemnia from islet cell hyperplasia)

Laboratory Findings differ with seriousness of HDFN you need to include:

  • Anemia
  • Hyperbilirubinemia
  • Reticulocytosis (6 to 40%)
  •  ' nucleated RBC matter (>10/100 WBCs)
  • Thrombocytopenia
  • Leucopenia
  • Positive Direct Antiglobulin Test
  • Hypoalbuminemia
  • Smear: polychromasia, anisocytosis,

Assessment of HDFN

Pre-natal prognosis: Testing of each pregnant women

  • ABO and Rh typing
  • Antibody screening
  • Antibody identification
  • Antibody titration
  • Pregnant women
  • Rh positive mother
  • Rh negative With anti-D
  • Rh negative No anti-D
  • No problem
  • Antibody Titer
  • Repeat the titer every 2-4 weeks until delivery
  • Repeat screening for anti-D
  • Every 2-4 weeks until delivery

Father testing

Testing of father's blood group system with mother's blood type is important to ascertain genotype of the infant. The father's blood vessels should be analyzed for ABO, Rh and other significant antigens to anticipate the opportunity the fetus has of being Rh positive and influenced by HDFN.

Molecular Genotyping

  • Rh type of mother, father, and fetus
  • Fetal bloodstream typing by using fetal DNA from amniocentesis or cell-free, fetal-derived DNA present in maternal plasma
  • Heterozygosity or homozygosity of the daddy for RHD allele

Post partum tests: Collect cord bloodstream and test

Fetal bloodstream (or umbilical cord blood)

  • ABO and Rh typing of the infant
  • Antihuman globulin test (DAT)
  • Antibody identification
  • Full blood count
  • Liver and renal function tests
  • Blood morphology examination

Maternal blood

Acid elution strategy of Kleihauer-Betke test to confirm if the fetal red blood vessels cells pass into the mother blood flow.

Indirect Coombs test for IgG antibodies that cause HDFN

Treatment of the fetus experiencing hemolytic disease

Intrauterine bloodstream transfusion

This is done by positioning a needle through the mother's uterus and in to the abs cavity of the fetus or directly into the vein in the umbilical cable.

  • Intraperitoneal transfusion - blood vessels transfused into fetal abdomen
  • Intravascular transfusion - blood vessels transfused into fetal umbilical vein

Exchange transfusion

For infants who develop hyperbilirubinemia and/or anemia due to HDFN, exchange transfusion is usually completed.

Exchange transfusion is removal of smaller amounts of bloodstream from the neonate and replace with donor blood until a one or two-volume exchange is accomplished.

Helps to:

  • To replace normal red cells(modification of anemia)
  • Remove awareness of bilirubin
  • Remove imperfect free antibodies
  • Remove fetal red cells coated with maternal antibody
  • Provides the newborn is with suitable donor red cells.

Phototherapy (light treatment)

is the procedure of using ultraviolet light to get rid of bilirubin in the bloodstream. These light waves are soaked up by the baby's epidermis and blood and change the indirect bilirubin into immediate bilirubin, that can be easily excreted by the newborn.

Prevention of hemolytic disease of the fetus and newborn:

Prophylaxis of the mother with Rh immunoglobulin

RhIG remains the treating choice for preventing HDFN. Rh D-negative moms given a drug called Rh immunoglobulin (RhIg), also called RhoGAM. That is a specially developed bloodstream product that can prevent Rh negative mother's antibodies from being able to react to Rh positive cells.

This anti-D Ig is given at about 28 weeks gestation, which is about the time when fetal RBCs learn to point out the D antigen, and moms receive another medication dosage at about 34 weeks, a few weeks before labor begins during which the risk of feto-maternal hemorrhage is high. A final dosage of anti-D Ig is given following the baby has been provided within 72 time.

The future

A quantity of new strategies look appealing for the future

Down-regulation of the immune system in sensitized patients with Healing vaccine reduces or can stop the production of anti-D antibodies by the sensitized women that are pregnant.

Molecular typing of Rh (RHD and RHCE), Kell (K & k), Duffy (Fya & Fyb), and Kidd (Jka & Jkb) loci. In prenatal trials programs, molecular typing can determine the Rh type of the mother, father, and fetus and may be achieved if the mom has anti-D or another antibody known to cause HDFN.

Fetal bloodstream typing can be done using free fetal DNA from skin cells obtained by amniocentesis or by screening cell-free, fetal-derived DNA present in maternal plasma.

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