Rh Incompatibility

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Chapter 221 Rh Incompatibility

INTRODUCTION

Description: Isoimmunization to any fetal blood group not possessed by the mother is possible. The most common example is the Rh (D) factor. What was once a common cause for intrauterine fetal death has largely been eradicated by prophylactic administration of immune globulin to those at risk.

Prevalence: Uncommon since the routine use of D immune globulin therapy.

Predominant Age: Reproductive.

Genetics: Mothers who are Rh (D) negative. (The genes for the CDE blood groups are inherited separately from the ABO groups and are located on the short arm of chromosome 1.)

ETIOLOGY AND PATHOGENESIS

Causes: Antibody formation against the D antigen.

Risk Factors: Any process that exposes the woman to blood carrying the D antigen including blood transfusion, miscarriage, ectopic or normal pregnancy, trauma, amniocentesis during pregnancy, and others.

CLINICAL CHARACTERISTICS

Signs and Symptoms

• Elevated serum titers of anti-D immunoglobulin (IgM)

• Fetal hydrops, erythroblastosis fetalis, hemolytic disease of the newborn

• Intrauterine fetal demise

DIAGNOSTIC APPROACH

Differential Diagnosis

• Other isoimmunizations (most frequently Lewis, Kell, or Duffy antigens)

• Iron-deficiency anemia (maternal)

• Hemoglobinopathy

Associated Conditions: Polyhydramnios.

Workup and Evaluation

Laboratory: Serum antibody titers (at first visit, 20 weeks, and approximately every 4 weeks thereafter), testing of baby’s father’s antibody status. Emerging data suggest that it may be possible to determine the Rh status of the fetus directly from fetal cells circulating in maternal blood.

Imaging: Ultrasonography is useful to establish gestational age and monitor amniotic fluid volume and fetal growth. Some studies have assessed the ability of ultrasonography to monitor the degree of fetal anemia, but this technique has not gained wide usage.

Special Tests: Amniocentesis or umbilical cord blood sampling if titers are elevated or there has been a prior affected pregnancy.

Diagnostic Procedures: Serum titers, amniocentesis, or umbilical cord blood sampling.

MANAGEMENT AND THERAPY

Nonpharmacologic

General Measures: Evaluation, increased surveillance.

Specific Measures: When antibody titers are ≤1 : 8, no intervention is required. When titers are ≥1 : 16 in albumin or 1 : 32 by an indirect Coombs test, amniocentesis or umbilical cord blood sampling should be considered. In severely affected fetuses, intrauterine transfusion may be required.

Diet: No specific dietary changes indicated.

Activity: No restriction.

Patient Education: American College of Obstetricians and Gynecologists Patient Education Pamphlet AP027 (The Rh Factor: How It Can Affect Your Pregnancy)

Drug(s) of Choice

None if isoimmunization has taken place. Prophylaxis (with Rh-positive father): D immune globulin—50 micrograns for miscarriage before 13 weeks of gestation or after chorionic villus sampling; 300 micrograns after amniocentesis or ectopic pregnancy; at 28 to 30 weeks of gestation in unsensitized patients or after normal delivery. (20 micrograns/1 mL of D-positive cells [2 mL of whole blood] infused or lost into the patient’s circulation.)

Contraindications: Patients who are already sensitized to the D antigen should not receive D immune globulin.

FOLLOW-UP

Patient Monitoring: Normal prenatal care with increased surveillance of fetal growth and health.

Prevention/Avoidance: All patients should have their Rh type established and be tested for isoimmunization (indirect Coombs test) at the first prenatal visit. Those who are Rh negative should receive D immune globulin after delivery, amniocentesis, fetal demise, miscarriage, ectopic pregnancy, or any other time exposure to Rh-positive cells may have occurred. Prophylactic administration between 28 and 30 weeks of gestation is also wise.

Possible Complications: Isoimmunization with subsequent immune damage to fetal red cells leading to lysis, anemia, hydrops, and fetal death.

Expected Outcome: With prophylaxis, the risk of isoimmunization is estimated to be 0.3%.

MISCELLANEOUS

ICD-9-CM Code: 656.1.

Bichler J, Schondorfer G, Pabst G, Andresen I. Pharmacokinetics of anti-D IgG in pregnant RhD-negative women. BJOG. 2003;110:39.

Geifman-Holtzman O, Grotegut CA, Gaughan JP. Diagnostic accuracy of noninvasive fetal Rh genotyping from maternal blood—A meta-analysis. Am J Obstet Gynecol. 2006;195:1163.

Mari G, Deter RL, Carpenter RL, et al. Noninvasive diagnosis by Doppler ultrasonography of fetal anemia due to maternal red-cell alloimmunization. Collaborative Group for Doppler Assessment of the Blood Velocity in Anemic Fetuses. N Engl J Med. 2000;342:9.

Queenan JT, Tomai TP, Ural SH, King JC. Deviation in amniotic fluid optical density at a wavelength of 450 nm in Rh-immunized pregnancies from 14 to 40 weeks’ gestation: a proposal for clinical management. Am J Obstet Gynecol. 1993;168:1370.

Ruma MS, Moise KJJr, Kim E, et al. Combined plasmapheresis and intravenous immune globulin for the treatment of severe maternal red cell alloimmunization. Am J Obstet Gynecol. 2007;196:138.e1.

Thornton JG, Page C, Foote G, et al. Efficacy and long term effects of antenatal prophylaxis with anti-D immunoglobulin. BMJ. 1989;298:1671.

Zimmerman R, Carpenter RJJr, Durig P, Mari G. Longitudinal measurement of peak systolic velocity in the fetal middle cerebral artery for monitoring pregnancies complicated by red cell alloimmunisation: a prospective multicentre trial with intention-to-treat. BJOG. 2002;109:746.

American College of Obstetricians and Gynecologists. Prevention of Rh D isoimmunization. ACOG Practice Bulletin 4. Washington, DC: ACOG, 1999.

American College of Obstetricians and Gynecologists. Management of alloimmunization during pregnancy. ACOG Practice Bulletin 75. Obstet Gynecol. 2006;108:457.

Bianchi DW, Avent ND, Costa JM, van der Schoot CE. Noninvasive prenatal diagnosis of fetal Rhesus D: ready for Prime(r) Time. Obstet Gynecol. 2005;106:841.

Bowman JM. The management of Rh-isoimmunization. Obstet Gynecol. 1978;52:1.

Contreras M. The prevention of Rh haemolytic disease of the fetus and newborn—General background. Br J Obstet Gynaecol. 1998;105:7.

Fairweather DV, Tacchi D, Coxon A, et al. Intrauterine transfusion in Rh-isoimmunization. BMJ. 1967;4:189.

Jabara S, Barnhart KT. Is Rh immune globulin needed in early first-trimester abortion? A review. Am J Obstet Gynecol. 2003;188:623.

Jones ML, Wray J, Wight J, et al. A review of the clinical effectiveness of routine antenatal anti-D prophylaxis for rhesus-negative women who are pregnant. BJOG. 2004;111:892.

Moise KJJr. Management of rhesus alloimmunization in pregnancy. Obstet Gynecol. 2002;100:600.

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