It is possible for a newborn with this disease to have neutropenia and neonatal alloimmune thrombocytopenia as well. Hemolysis leads to elevated bilirubin levels. After delivery, bilirubin is no longer cleared (via the placenta) from the neonates blood and the symptoms of jaundice (yellowish skin and yellow discoloration of the whites of the eyes, or icterus) increase within 24 hours after birth. Like other forms of severe neonatal jaundice, there is the possibility of the neonate developing acute or chronic kernicterus, however the risk of kernicterus in HDN is higher because of the rapid and massive destruction of blood cells. It is important to note that isoimmunization is a risk factor for neurotoxicity and lowers the level at which kernicterus can occur. Untreated profound anemia can cause high-output heart failure, with pallor, enlarged liver and/or spleen, generalized swelling, and respiratory distress.HDN can be the cause of hydrops fetalis, an often-severe form of prenatal heart failure that causes fetal edema. Complications
Complications of HDN could include kernicterus, hepatosplenomegaly, inspissated (thickened or dried) bile syndrome and/or greenish staining of the teeth, hemolytic anemia and damage to the liver due to excess bilirubin. Conditions that may cause similar symptoms in the newborn period include: acquired hemolytic anemia, congenital toxoplasma, congenital syphilis infection, congenital obstruction of the bile duct, and cytomegalovirus (CMV) infection. High at birth or rapidly rising bilirubin
Prolonged hyperbilirubinemia
Bilirubin Induced Neurological Dysfunction
Cerebral Palsy
Kernicterus
Neutropenia
Thrombocytopenia
Hemolytic anemia – must not be treated with iron
Late onset anemia – must not be treated with iron. Can persist up to 12 weeks after birth.
It suppresses the bone marrow by inhibiting the erythroid progenitor cells.Anti-M also recommends antigen testing to rule out the presence of HDN as the direct coombs can come back negative in a severely affected infant.Kidd antigens are also present on the endothelial cells of the kidneys.One study states that it would be unwise to routinely dismiss anti-E as being of little clinical consequence. It also found that the most severe case of anti-E HDFN occurred with titers 1:2, concluding that titers are not reliable for the diagnosis of the anti-E type. Diagnosis
The diagnosis of HDN is based on history and laboratory findings:Blood tests done on the newborn baby

Biochemistry tests for jaundice including total and direct bilirubin levels. Complete blood count (CBC) which may show a decreased hemoglobin and hematocrit due to red blood cell destruction
Reticulocyte count which will usually be increased as the bone marrow makes new red blood cells to replace the ones that are being destroyed, and a peripheral blood smear to look at cell morphology. In the presence of significant hemolysis the smear will show schistocytes (fragmented red blood cells), reticulocytosis, and in severe cases Erythroblasts (also known as nucleated red blood cells). Positive direct Coombs test (might be negative after fetal interuterine blood transfusion)Blood tests done on the mother

Positive indirect Coombs testBlood tests done on the father (rarely needed)

Erythrocyte antigen status

Prevention
In cases of Rho(D) incompatibility, Rho(D) immunoglobulin is given to prevent sensitization. However, there is no comparable immunotherapy available for other blood group incompatibilities.Early pregnancy

IVIG – IVIG stands for Intravenous Immunoglobulin.