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HDFN: ABO Incompatibility
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ABO Incompatability
Hemolytic disease of the newborn (and fetus)
What's the deal?
Caused by the destruction of neonatal RBCs by maternal IgG Abs
What's the deal?
Primarily involves the major blood groups: Rh, A, B, AB, O.
Tell me more.
We won't worry about Rh disease today. Just know it's due to maternal exposure to the major D antigen in Rh- mothers. It can cause hydrops fetalis.
Mechanism of Disease
- At approximately 3-6 months of age we begin to make A and/or B antibodies to antigens (found in food and bacteria).
- Because of this, ABO hemolytic disease can occur in the first pregnancy.
- Usually mild. Most common and severe in infants of African descent and mothers who are typo O blood.
- Antibodies stick to and destroy fetal or neonate RBCs.
How does it appear?
Generally, kids do great.
- Treatments, when needed, consist mostly of phototherapy with some going on to IVIG or exchange transfusion.
- Typically, ABO incompatibility is less severe than Rh(D) incompatibility. Hydrops fetalis is rare and less than 0.1% of infants with evidence of hemolysis require exchange tranfusions.
Clinical Presentation
Mild to Moderate Disease: Manifests as hyperbilirubinemia within the first 24 hours of life. Possibly signs of anemia (lethargy and tachycardia).
Hydrops fetalis: Life threatening anemia with skin edema, pleural/pericardial effusion/ascites (most often due to Rh(D) or minor blood type HDFN.--> May present as shock.
Clinical Presentation
Minor Blood Types
Minor Blood Types
There are 33 total blood group systems with over 300 antigens. Some examples of other, minor blood groups are Duffy, MNS, P, Kell, and more.
Kell is included in Rh(D) with increased risk of hydrops fetalis.
Diagnosis
Most importantly: Demonstration of incompatible blood types between the infant and mother (Rh vs type O).
Evidence of hemolysis: peripheral blood smear showing low RBCs, reticulocytosis, macrocytosis, and polychromasia.
Confirmed via either direct or indirect antigloblin testing (DAT/IAT)
Diagnosis
DAT vs IAT
Direct (Coombs) vs Indirect Antiglobulin Test
- Infant RBCs are suspended in serum containing Abs to IgG.
- In ABO incompatibility, a DAT does not exclude HDFN (60% sensitive). Infant A&B antigens are less well developed and further apart than in adults and older children.
- If DAT negative--> IAT. Use infant serum and donor RBCs.
DAT vs IAT
Diff Dxs
- Erythrocyte Membrane Defects: Hereditary spherocytosis vs ellitocytosis vs stomatocytosis etc
- Eryhtrocyte enzyme defects- G6PD (Heinz Bodies) vs pyruvate kinase deficiencies
- Liver Defects: Gilbert's Syndrome, Crigler-Nijar, Dubin-Johnson, Rotor, etc.
Differential
Management
"An Ounce of Prevention"
Management
- Prenatal:
- Maternal screening
- Prenatal monitoring--> fetal RBC transfusions
- RhoGAM
- Postnatal:
- Excellent physical exam
- Regular vital checks for signs of anemia
- High suspicion and sending of cord blood
Cord Blood
What do we do with it?
- Blood type
- Coombs testing
- Hematocrit, reticulocyte count, and bilirubin
- Cross match for subsequent transfusion
Anemia
- Hydrops--> O-neg emergent transfusion and early exchange transfusion
- Symptomatic but stable--> Simple Transfusion vs Exchange Transfusion (if elevated bilirubin also)
- Administration of IVIG
Anemia
Hyperbilirubinemia
Hyper-
bilirubinemia
- Phototherapy
- Hydration (2/2 phototherapy, increased urination)
- Exchange transfusion (consult normogram)
- IVIG-- Theoretically blocks antibody receptors on RBCs. High risk only, and inconclusive data.
- Breastfeeding!