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[1] A red cell exchange transfusion is usually given to treat severe hyperbilirubinemia or anemia in babies with hemolytic disease of the newborn. It removes neonatal red cells coated with maternal antibody and reduces the level of bilirubin. A ‘double volume exchange’ (160–200 ml/kg) removes around 90% of neonatal red cells and 50% of ...
Anemia of prematurity (AOP) refers to a form of anemia affecting preterm infants [1] with decreased hematocrit. [2] AOP is a normochromic, normocytic hypoproliferative anemia. The primary mechanism of AOP is a decrease in erythropoietin (EPO), a red blood cell growth factor.
If the anemia is severe, it can be treated with a blood transfusion, however this is rarely needed. On the other hand, neonates have underdeveloped livers that are unable to process large amounts of bilirubin and a poorly developed blood–brain barrier that is unable to block bilirubin from entering the brain.
This test tells whether there are antibodies in the maternal plasma. If positive, the antibody is identified and given a titer. Titers of 1:4 or higher is considered critical for Kell (compared to 1:16 for most other antibodies) and is considered to confer a high risk of fetal anemia. [17]
Neonatal isoerythrolysis (NI), also known as hemolytic icterus or hemolytic anemia, [1] is a disease most commonly seen in kittens and foals, but has also been reported in puppies. It occurs when the mother has antibodies against the blood type of the newborn. A 7 day old foal with neonatal isoerythrolysis.
Anemia of prematurity is a form of anemia affecting preterm infants [25] with decreased hematocrit. [26] Aplastic anemia: D60-D61: 866: Aplastic anemia is a condition where bone marrow does not produce sufficient new cells to replenish blood cells. [27] Autoimmune hemolytic anemia: D59.0-D59.1
Unlike hemolytic disease of the fetus and newborn, NAIT occurs during the first pregnancy in up to 50% of cases, [1] and the affected fetuses may develop severe thrombocytopenia (<50,000 μL −1) very early during pregnancy (as early as 20 weeks gestation, consistent with the development of platelet antigens, [1] and the majority of the time ...
Family history of jaundice and anemia, family history of neonatal or early infant death due to liver disease, maternal illness suggestive of viral infection (fever, rash or lymphadenopathy), maternal drugs (e.g. sulphonamides, anti-malarials causing red blood cell destruction in G6PD deficiency) are suggestive of pathological jaundice in neonates.