Get access

Clinically significant hemolytic disease of the newborn secondary to passive transfer of anti-D from maternal RhIG

Authors

  • Daniel N. Cohen,

    1. Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center and Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
    Search for more papers by this author
  • Mary S. Johnson,

    1. Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center and Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
    Search for more papers by this author
  • Wayne H. Liang,

    1. Department of Pediatrics, Vanderbilt University Medical Center and Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
    Search for more papers by this author
  • Heather L. McDaniel,

    1. Department of Pediatrics, Vanderbilt University Medical Center and Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
    2. Division of Hematology and Oncology, Vanderbilt University Medical Center and Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
    Search for more papers by this author
  • Pampee P. Young

    Corresponding author
    1. Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center and Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
    2. Department of Medicine, Vanderbilt University Medical Center and Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee
    • Address reprint requests to: Pampee Young, MCN CC2217, 21st Avenue South, Nashville, TN 37232-2561; e-mail: pampee.young@vanderbilt.edu.

    Search for more papers by this author

Abstract

Background

RhIG is used worldwide to reduce the incidence of alloimmunization to D during pregnancy. We report a case of clinically significant neonatal hemolysis mediated by maternally administered RhIG.

Case Report

A 25-year-old, O–, primigravid mother with a negative antenatal antibody screen delivered a 6-lb 4-oz, blood group A, D+ baby girl at 36.5 weeks' gestation. Prenatal care included a dose of intramuscular RhIG at 28 weeks' gestation. At delivery, the newborn was markedly jaundiced with a total bilirubin of 6.3 mg/dL, which reached more than 20 mg/dL after 6 days. The newborn's lactate dehydrogenase (LDH) was 485 U/L (normal, <226 U/L) and further laboratory studies revealed reticulocytosis (17.2%; normal range, 0.36%-1.9%) and a hemoglobin (Hb) of 14.3 g/dL (normal for age range, 13.4-19.8 g/dL) that decreased to 11.5 g/dL (normal for age range, 13.5-22.6 g/dL) by Day-of-life 7. Although the maternal antibody screen was negative, the newborn's direct antiglobulin test (DAT) was positive for immunoglobulin (Ig)G, with an anti-D identified by elution studies. The possibility of hemolytic disease of the newborn (HDN) due to anti-A was considered, but ultimately ruled out by the absence of anti-A1 in the eluate. The newborn's hyperbilirubinemia was adequately managed with phototherapy. Analysis of the mother's plasma 10 days postpartum revealed an anti-D titer of 8. Two months after birth, the child's laboratory studies, DAT, antibody screen, and peripheral smear were unremarkable.

Conclusion

In the context of neonatal anemia, elevated LDH, and reticulocytosis, a positive IgG DAT with anti-D identified in the eluate suggests RhIG-mediated HDN. This appears to be a rarely reported event.

Ancillary