| Test | Implications of Results | Nursing Priorities |
|---|---|---|
| Cord blood type, group, and Coombs test | Sample of cord blood is collected at delivery to determine newborns blood type and group (Rh positive or negative). Coombs test is done, especially for those whose mothers have type O or Rh-negative blood, or for neonates who are considerably jaundiced. Direct Coombs test will determine if antibodies are present in the neonates blood. |
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| Phenylketonuria (PKU) | PKU is an autosomal recessive disease of protein synthesis in which the blood level of the amino acid phenylalanine becomes very high; the disorder results in mental retardation. If test is positive, retardation can be prevented through dietary control. Test is done with blood sample from neonates heel 2436 hours after having milk. Usually repeat screening recommended, especially if discharged early. |
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| Hypothyroidism | Mass neonatal screening for hypothyroidism is a cost-effective measure for preventing mental retardation caused by thyroid dysfunction. Sample of neonates blood is taken for analysis (may be done with PKU analysis). |
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| Galactosemia | Galactosemia is an autosomal recessive disease in which the inborn error of metabolism involves the bodys inability to convert galactose to glucose. Surplus of galactose causes liver and brain damage. May be done with blood sample for PKU. |
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| Sickle cell disease | Sickle cell is an autosomal recessive disorder occurring in certain ethnic groups, most commonly African American. Other ethnic origins may include: Mediterranean, Caribbean, Arabian, East Indian, and South and Central American. Disease is marked by crescent-shaped RBCs caused by defective hemoglobin. Severe, life-threatening attacks (crises) begin in childhood (fever and abdominal pain). Blood sample is taken after birth. |
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| Tay-Sachs disease | Tay-Sachs disease (TSD) is an autosomal recessive disease characterized by the absence of the enzyme hexosaminidase A (Hex-A). Especially common in people with eastern European (Ashkenazi) Jewish descent. Without Hex-A, a lipid GM2 ganglioside accumulates abnormally in cells, especially in the nerve cells of the brain. The destructive process begins in the fetus early in pregnancy, although the disease is not clinically apparent until the child is several months old. By the time a child with TSD is 3 or 4 years old, the nervous system is badly affected. Even with the best of care, all children with classical TSD die early in childhood, usually by age 5. |
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