Morning Report

Kelly Follett, MD, PGY2

The Case

AGA F born to 34 yo G4P1021 @ 39 0/7 via emergent c/s

Mom had decreased fetal movement so came in for NST which was non-reassuring and noted prolonged brady to 60s

APGARS 2, 8. Passed to NICU at 1 min and received several breaths PPV, perked up and transferred back to WBN.

Maternal History

Rubella immune, RPR NR, HIV negative, Hep B negative, GBS negative, and GC/Chlamydia negative FH: No hx of bleeding problems, SIDS, congenital defects, or genetic syndromes. SH: Infant will live at home with Mom and 10 yo brother. Mom and Dad no longer together, but he is present and involved. Denies any ETOH, tobacco, drug use during pregnancy. No maternal meds during pregnancy.

Physical Exam
WEIGHT 3475 kg (85%), OFC 34.5 (75%), LENGTH 49 cm (50%) T 37, HR 190, RR 20

GEN: NAD, pale HEENT: AFOSF, + RR, no cleft CV: RRR, no murmurs, CRT <3 sec, 2+ distal pulses RESP: CTAB, no increased WOB ABD: s/nd/nt, no HSM EXT: WWP, no clicks/clunks GU: Patent anus, normal female genitalia BACK: No cleft NEURO: Strong cry, good tone, moro/grasp/suck intact

Differential

Labs
Mom A+/-; Baby B+/+ WBC 23, Hgb 6, Hct 19.5, MCV 105, Platelets 255, I/T 0.08 Reticulocytes 22.7 Bili 7.1, LL 9

Hospital Course
Heme/Onc consult Transfused pRBC 15 cc/kg

4h post-transfusion Hct 41

Required phototherapy

Hematology
Maternal Kleihauer-Betke Stain + (fetal blood in mother) Blood smear: hypochromic, microcytic anemia; scant spherocytes but you would expect more in ABO incompatibility Fetal maternal hemorrhage vs alpha thalassemia with ABO incompatibility playing a role

Alloimmune Hemolytic Disease of the Newborn

Maternal IgG destroying baby RBC

Types

Rh D-

Rh D+

Rh

White > Hispanic/Black > Asians Major D antigen most common culprit, but there are 44 other Rh antigens associated with hemolytic disease Moms are sensitized due to previous exposure to Rh antigen

Transfusion with Rh+ RBC Pregnancy with Rh+ infant

Clinically, can range from mild, self-limited disease to severe, life-threatening anemia (hydrops fetalis) Hyperbilirubinemia usually occurs within first 24h Incidence has decreased with antenatal Rh(D) immune globulin prophylaxis = Rhogam

Types

A /B

ABO hemolytic disease

Black >> White/Hispanic/Asian People naturally make A and/or B antibodies to the antigens they do not possess thus it can occur with the first pregnancy. Clinical disease less severe than Rh

Hydrops and significant hemolysis are rare

Hyperbilirubinemia usually occurs within first 24h Kell, Duffy, etc.

Minor blood groups

Diagnosis
Coombs test Peripheral smear

Decreased RBC Reticulocytosis Polychromasia Spherocytosis

In

ABO but not usually Rh

References
American Academy of Pediatrics Subcommittee on Hyperbilirubinemia. Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics 2004; 114:297. Chvez GF, Mulinare J, Edmonds LD. Epidemiology of Rh hemolytic disease of the newborn in the United States. JAMA 1991; 265:3270. McDonnell M, Hannam S, Devane SP. Hydrops fetalis due to ABO incompatibility. Arch Dis Child Fetal Neonatal Ed 1998; 78:F220.