Hemolytic disease of the newborn - Revision history

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Ostermayer: Created page with "Hemolytic disease of the fetus and newborn (HDFN), also known as '''erythroblastosis fetalis''', is a condition in which '''maternal alloantibodies cross the placenta and destroy fetal/neonatal red blood cells''', causing '''hemolytic anemia''' and '''unconjugated hyperbilirubinemia'''.Hemolytic Disease of the Fetus and Newborn. ''StatPearls''. NCBI. 2025. The spectrum ranges from mild self-limited jaundice (most ABO cases) to '''fatal hydrop..."

2026-03-18T01:00:01Z

Created page with "Hemolytic disease of the fetus and newborn (HDFN), also known as '''erythroblastosis fetalis''', is a condition in which '''maternal alloantibodies cross the placenta and destroy fetal/neonatal red blood cells''', causing '''hemolytic anemia''' and '''unconjugated hyperbilirubinemia'''.<ref name="StatPearls">Hemolytic Disease of the Fetus and Newborn. ''StatPearls''. NCBI. 2025.</ref> The spectrum ranges from mild self-limited jaundice (most ABO cases) to '''fatal hydrop..."

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Hemolytic disease of the fetus and newborn (HDFN), also known as '''erythroblastosis fetalis''', is a condition in which '''maternal alloantibodies cross the placenta and destroy fetal/neonatal red blood cells''', causing '''hemolytic anemia''' and '''unconjugated hyperbilirubinemia'''.<ref name="StatPearls">Hemolytic Disease of the Fetus and Newborn. ''StatPearls''. NCBI. 2025.</ref> The spectrum ranges from mild self-limited jaundice (most ABO cases) to '''fatal hydrops fetalis''' (severe Rh disease). The emergency physician encounters HDFN as '''early-onset neonatal jaundice''' (within the first 24 hours — always pathologic), '''severe anemia in a neonate''', or '''a readmission for rapidly rising bilirubin'''. Timely recognition is critical because '''untreated severe hyperbilirubinemia causes kernicterus'''.

==Background==
*'''ABO incompatibility''' is now the '''most common cause''' of HDFN in the Western world, following the success of anti-D (RhoGAM) prophylaxis in preventing Rh disease<ref name="PMC_HDN">Haemolytic disease of the newborn. ''Arch Dis Child Fetal Neonatal Ed''. 2007;92(2):F83-F88. PMC2675453.</ref>
*'''Rh (D) incompatibility''' remains the most severe form but is now uncommon with appropriate prevention
*Other minor blood group antigens ('''Kell, Duffy, Kidd, MNS''') cause approximately 10% of severe cases; '''anti-Kell''' deserves special attention<ref name="AMBOSS">Hemolytic disease of the fetus and newborn. ''AMBOSS''. 2024.</ref>

{| class="wikitable"
|-
! Feature !! '''ABO incompatibility''' !! '''Rh (D) incompatibility''' !! '''Anti-Kell'''
|-
| Frequency || '''Most common''' cause of HDFN || Now uncommon (with prophylaxis) || ~10% of severe cases
|-
| First pregnancy affected? || '''Yes''' (preexisting natural anti-A/B IgG) || Usually '''no''' (sensitization during first pregnancy; affects subsequent) || Yes (if prior transfusion) or subsequent pregnancies
|-
| Typical severity || '''Mild to moderate''' || '''Moderate to severe''' || '''Severe'''
|-
| Direct Coombs (DAT) || Weakly positive or '''negative''' || '''Strongly positive''' || Positive
|-
| Anemia severity || Usually mild || Can be severe → hydrops || '''Severe''' (suppresses erythropoiesis directly; anemia out of proportion to hemolysis)
|-
| Hydrops fetalis || Rare || '''Can occur''' || Can occur
|-
| Bilirubin rise || Moderate || '''Rapid and severe''' || May be '''less than expected''' despite severe anemia (suppressed RBC production)
|-
| Prevention || None available || '''Anti-D immunoglobulin (RhoGAM)''' || Avoid Kell-positive transfusions in women of childbearing age
|}

===Mechanism===
*Mother lacks an antigen present on fetal RBCs (inherited from father)
*Maternal immune system produces '''IgG antibodies''' against the fetal antigen
*IgG crosses the placenta → binds fetal RBCs → '''extravascular hemolysis''' (in fetal spleen/liver)
*Hemolysis → anemia + increased unconjugated bilirubin production
*In utero: bilirubin is cleared by the placenta, so the fetus is ''not'' jaundiced; however, severe anemia → high-output cardiac failure → '''hydrops fetalis'''
*After birth: the neonatal liver cannot conjugate the sudden bilirubin load → '''unconjugated hyperbilirubinemia''' → risk of '''[[Kernicterus|kernicterus]]'''

==Clinical features==
===Early-onset jaundice (the cardinal sign)===
*'''Jaundice within the first 24 hours of life is ALWAYS pathologic''' and HDFN must be considered<ref name="StatPearls"/>
*This distinguishes HDFN from physiologic jaundice (which appears after 24-48 hours)
*Bilirubin may rise rapidly: '''rate of rise >0.5 mg/dL/hour''' suggests significant hemolysis and warrants urgent intervention

===Spectrum of severity===
*'''Mild:''' jaundice only; no significant anemia; responds to phototherapy (most ABO cases)
*'''Moderate:''' significant jaundice + anemia; may require IVIG and/or exchange transfusion
*'''Severe:''' profound anemia, hepatosplenomegaly (from extramedullary hematopoiesis), edema, ascites → '''hydrops fetalis'''
*'''Fatal:''' stillbirth or neonatal death from severe anemia, heart failure, or kernicterus

===Examination findings===
*'''Jaundice''' (scleral icterus, yellow skin)
*'''Pallor''' (anemia — may mask cyanosis)
*'''Hepatosplenomegaly''' (extramedullary hematopoiesis; Rh disease more than ABO)
*'''Edema, ascites, pleural effusions''' (hydrops — severe cases)
*'''Petechiae''' (thrombocytopenia from marrow replacement or DIC)
*'''Lethargy, poor feeding, hypotonia''' (early bilirubin encephalopathy — see [[Kernicterus]])

===Late anemia (readmission risk)===
*Neonates treated for HDFN may develop '''late anemia''' at 2-8 weeks of age as maternal antibodies continue to hemolyze neonatal RBCs
*May present to the ED with pallor, poor feeding, tachycardia, respiratory distress
*'''Check hemoglobin in any HDFN infant readmitted for any reason'''

==Differential diagnosis==
===Neonatal jaundice within 24 hours===
*'''HDFN (ABO, Rh, minor antigens)''' — this page
*'''[[G6PD deficiency]]''' — most common enzyme deficiency causing neonatal hemolysis worldwide; often triggered by oxidative stress; Coombs-negative
*'''[[Hereditary spherocytosis]]''' — family history; spherocytes on smear; Coombs-negative; osmotic fragility increased
*'''[[Sepsis]]''' — ill-appearing; fever or hypothermia; WBC abnormalities
*'''Enclosed hemorrhage''' (cephalohematoma, subgaleal hemorrhage) — resorbing blood → bilirubin production; no hemolysis markers
*'''[[Crigler-Najjar syndrome]]''' — unconjugated hyperbilirubinemia without hemolysis (normal reticulocyte count, Coombs-negative, normal haptoglobin)
*'''Pyruvate kinase deficiency''' — rare; chronic hemolytic anemia; Coombs-negative

===Key distinguishing features of HDFN===
*'''Positive direct antiglobulin test (DAT/Coombs)''' — confirms antibody on neonatal RBCs (though may be weakly positive or negative in ABO disease)
*'''Blood type mismatch''' between mother and infant
*'''Elevated reticulocyte count''' (appropriate marrow response to hemolysis)
*'''Spherocytes''' on peripheral smear (especially in ABO incompatibility)

==Evaluation==
===ED workup===
*'''Fractionated bilirubin''' (total and direct): expect '''predominantly unconjugated'''
*'''Maternal and infant blood type and Rh:''' identifies the incompatibility
*'''Direct antiglobulin test (DAT/direct Coombs test):''' '''positive''' confirms antibody coating neonatal RBCs
**Strongly positive in Rh disease; may be weakly positive or negative in ABO disease (does '''not''' exclude ABO HDFN)
*'''CBC with reticulocyte count:''' anemia + '''elevated reticulocytes''' (expect >5-10%; may be markedly elevated)
*'''Peripheral blood smear:''' '''spherocytes''' (especially ABO); nucleated RBCs (erythroblastosis); polychromasia
*'''Haptoglobin, LDH:''' hemolysis markers (haptoglobin low, LDH elevated)
*'''Albumin level:''' low albumin reduces bilirubin binding capacity and lowers the threshold for kernicterus
*'''Blood glucose:''' neonates with hemolytic disease may be hypoglycemic

===Additional testing===
*'''Maternal antibody screen (indirect Coombs test):''' identifies circulating maternal antibodies; identifies non-D alloantibodies (Kell, Duffy, etc.)
*'''Antibody identification panel:''' if indirect Coombs is positive, to identify specific antibody
*'''Cord blood bilirubin''' (if obtained at delivery): >3.5 mg/dL suggests significant hemolysis<ref name="Medscape_HDN">Hemolytic Disease of the Newborn Treatment & Management. ''Medscape''. 2024.</ref>

===Interpreting the bilirubin===
*Use '''hour-specific bilirubin nomograms''' (Bhutani nomogram) — plot the bilirubin level against the infant's age in hours to determine risk zone<ref name="StatPearls"/>
*Neurotoxicity risk factors that '''lower the treatment threshold:''' prematurity (<38 weeks), isoimmune hemolytic disease (positive DAT), G6PD deficiency, asphyxia, sepsis, acidosis, hypoalbuminemia (<3 g/dL)

==Management==
===Phototherapy===
*'''Initiate immediately''' for any neonate with HDFN and bilirubin at or approaching the phototherapy threshold for age<ref name="StatPearls"/>
*'''Intensive phototherapy:''' high-irradiance blue LED light (460-490 nm); maximize skin surface exposure
*Phototherapy converts unconjugated bilirubin into water-soluble photoisomers excreted without hepatic conjugation
*Continue until bilirubin is well below the exchange transfusion threshold and declining
*Phototherapy indications specific to HDFN (more aggressive than non-hemolytic jaundice):
**Cord bilirubin >3.5 mg/dL: start immediately
**Bilirubin rising >0.5 mg/dL/hour despite phototherapy: escalate to intensive phototherapy and prepare for exchange transfusion

===Intravenous immunoglobulin (IVIG)===
*'''IVIG 0.5-1 g/kg IV''' if bilirubin is rising rapidly (>0.5 mg/dL/hour) despite intensive phototherapy, or if bilirubin is approaching exchange transfusion threshold<ref name="Medscape_HDN"/>
*Mechanism: blocks Fc receptors on neonatal reticuloendothelial cells → reduces antibody-mediated RBC destruction
*May '''avoid the need for exchange transfusion''' (NNT ~3-6)
*Can repeat once if needed
*'''Caution:''' rare but reported association with necrotizing enterocolitis (NEC) in late preterm/term infants

===Exchange transfusion===
*'''Definitive emergency treatment''' for severe HDFN with dangerously elevated bilirubin or signs of acute bilirubin encephalopathy<ref name="StatPearls"/>
*'''Double-volume exchange''' (twice the infant's blood volume, ~160-170 mL/kg)
*Removes: circulating unconjugated bilirubin, antibody-coated RBCs, and free maternal antibodies
*Replaces with: fresh donor RBCs that lack the offending antigen
*'''Blood selection:'''
**'''Rh disease:''' O-negative, Rh-negative, crossmatched against maternal serum
**'''ABO disease:''' O-type RBCs with AB plasma (or type-specific), Rh-compatible
**All blood should be '''irradiated and leukodepleted'''
*Indications:
**Cord hemoglobin <10 g/dL with hydrops<ref name="PMC_HDN"/>
**Bilirubin rising >0.5 mg/dL/hour despite intensive phototherapy + IVIG
**Bilirubin at or above the exchange transfusion threshold for age on nomogram
**Any signs of acute bilirubin encephalopathy (lethargy, opisthotonus, seizures)
*'''Give IV albumin 1 g/kg''' before exchange transfusion (binds free bilirubin, increases efficiency of exchange)

===Simple transfusion===
*For '''significant anemia''' (hemoglobin <7-10 g/dL depending on clinical status) without dangerously elevated bilirubin
*Also for '''late anemia''' on readmission (ongoing hemolysis after initial hospitalization)
*Use irradiated, leukodepleted, antigen-negative packed RBCs

===Supportive care===
*IV dextrose-containing fluids (prevent hypoglycemia; maintain hydration)
*Frequent bilirubin monitoring (every 4-6 hours during active hemolysis)
*Monitor hemoglobin serially (hemolysis is ongoing)
*Iron supplementation (after acute phase; hemolysis depletes iron stores)
*Folic acid supplementation
*'''Avoid medications that displace bilirubin from albumin:''' sulfonamides, ceftriaxone, salicylates

==Disposition==
*'''All neonates with confirmed HDFN and significant hyperbilirubinemia: admit'''
**NICU if exchange transfusion anticipated, hydrops present, or signs of encephalopathy
**Well-baby unit with continuous phototherapy if mild-moderate disease
*'''Readmission for late anemia:''' admit if symptomatic anemia; transfuse as needed; discharge with close hematology/pediatric follow-up and planned hemoglobin checks at 1-2 week intervals
*'''Discharge criteria after acute HDFN:'''
**Bilirubin declining and below phototherapy threshold
**Hemoglobin stable and adequate
**Feeding well
**'''Arrange follow-up hemoglobin check within 48-72 hours''' (and again at 1-2 weeks) — late anemia is common and frequently missed
*'''Prevention counseling (Rh disease):'''
**Ensure Rh-negative mothers receive '''anti-D immunoglobulin (RhoGAM)''' at 28 weeks gestation and within 72 hours of delivery of an Rh-positive infant
**Also indicated after miscarriage, ectopic pregnancy, amniocentesis, abdominal trauma, or any event that may cause fetomaternal hemorrhage

==See Also==
*[[Neonatal jaundice]]
*[[Kernicterus]]
*[[Neonatal hepatitis]]
*[[Crigler-Najjar syndrome]]
*[[Gilbert syndrome]]
*[[G6PD deficiency]]
*[[Hereditary spherocytosis]]
*[[Hydrops fetalis]]

==External Links==
*[https://www.ncbi.nlm.nih.gov/books/NBK557423/ StatPearls — Hemolytic Disease of the Fetus and Newborn]
*[https://pmc.ncbi.nlm.nih.gov/articles/PMC2675453/ Arch Dis Child — Haemolytic disease of the newborn (2007)]
*[https://emedicine.medscape.com/article/974349-treatment Medscape — Hemolytic Disease of the Newborn Treatment & Management]
*[https://medlineplus.gov/ency/article/001298.htm MedlinePlus — Hemolytic disease of the newborn]

==References==
<references/>

[[Category:Pediatrics]]
[[Category:Heme/Onc]]

← Older revision		Revision as of 09:32, 22 March 2026
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	*The emergency physician encounters HDFN as early-onset neonatal jaundice (within the first 24 hours — always pathologic), severe anemia in a neonate, or a readmission for rapidly rising bilirubin.		*The emergency physician encounters HDFN as early-onset neonatal jaundice (within the first 24 hours — always pathologic), severe anemia in a neonate, or a readmission for rapidly rising bilirubin.
	*Timely recognition is critical because untreated severe hyperbilirubinemia causes kernicterus.		*Timely recognition is critical because untreated severe hyperbilirubinemia causes kernicterus.
	* ABO incompatibility is now the ~~'''~~most common cause~~'''~~ of HDFN in the Western world, following the success of anti-D (RhoGAM) prophylaxis in preventing Rh disease<ref name="PMC_HDN">Haemolytic disease of the newborn. ''Arch Dis Child Fetal Neonatal Ed''. 2007;92(2):F83-F88. PMC2675453.</ref>		* ABO incompatibility is now the most common cause of HDFN in the Western world, following the success of anti-D (RhoGAM) prophylaxis in preventing Rh disease<ref name="PMC_HDN">Haemolytic disease of the newborn. ''Arch Dis Child Fetal Neonatal Ed''. 2007;92(2):F83-F88. PMC2675453.</ref>
	* Rh (D) incompatibility remains the most severe form but is now uncommon with appropriate prevention		* Rh (D) incompatibility remains the most severe form but is now uncommon with appropriate prevention
	*Other minor blood group antigens (~~'''~~Kell, Duffy, Kidd, MNS~~'''~~) cause approximately 10% of severe cases; ~~'''~~anti-Kell~~'''~~ deserves special attention<ref name="AMBOSS">Hemolytic disease of the fetus and newborn. ''AMBOSS''. 2024.</ref>		*Other minor blood group antigens (Kell, Duffy, Kidd, MNS) cause approximately 10% of severe cases; anti-Kell deserves special attention<ref name="AMBOSS">Hemolytic disease of the fetus and newborn. ''AMBOSS''. 2024.</ref>

	{\| class="wikitable"		{\| class="wikitable"
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	===Mechanism===		===Mechanism===
	*Mother lacks an antigen present on fetal RBCs (inherited from father)		*Mother lacks an antigen present on fetal RBCs (inherited from father)
	*Maternal immune system produces ~~'''~~IgG antibodies~~'''~~ against the fetal antigen		*Maternal immune system produces IgG antibodies against the fetal antigen
	*IgG crosses the placenta → binds fetal RBCs → ~~'''~~extravascular hemolysis~~'''~~ (in fetal spleen/liver)		*IgG crosses the placenta → binds fetal RBCs → extravascular hemolysis (in fetal spleen/liver)
	*Hemolysis → anemia + increased unconjugated bilirubin production		*Hemolysis → anemia + increased unconjugated bilirubin production
	*In utero: bilirubin is cleared by the placenta, so the fetus is ''not'' jaundiced; however, severe anemia → high-output cardiac failure → ~~'''~~hydrops fetalis~~'''~~		*In utero: bilirubin is cleared by the placenta, so the fetus is ''not'' jaundiced; however, severe anemia → high-output cardiac failure → hydrops fetalis
	*After birth: the neonatal liver cannot conjugate the sudden bilirubin load → ~~'''~~unconjugated hyperbilirubinemia~~'''~~ → risk of ~~'''~~[[Kernicterus\|kernicterus]]~~'''~~		*After birth: the neonatal liver cannot conjugate the sudden bilirubin load → unconjugated hyperbilirubinemia → risk of [[Kernicterus\|kernicterus]]

	==Clinical features==		==Clinical features==
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	*'''Jaundice within the first 24 hours of life is ALWAYS pathologic''' and HDFN must be considered<ref name="StatPearls"/>		*'''Jaundice within the first 24 hours of life is ALWAYS pathologic''' and HDFN must be considered<ref name="StatPearls"/>
	*This distinguishes HDFN from physiologic jaundice (which appears after 24-48 hours)		*This distinguishes HDFN from physiologic jaundice (which appears after 24-48 hours)
	*Bilirubin may rise rapidly: ~~'''~~rate of rise >0.5 mg/dL/hour~~'''~~ suggests significant hemolysis and warrants urgent intervention		*Bilirubin may rise rapidly: rate of rise >0.5 mg/dL/hour suggests significant hemolysis and warrants urgent intervention

	===Spectrum of severity===		===Spectrum of severity===
	* Mild: jaundice only; no significant anemia; responds to phototherapy (most ABO cases)		* Mild: jaundice only; no significant anemia; responds to phototherapy (most ABO cases)
	* Moderate: significant jaundice + anemia; may require IVIG and/or exchange transfusion		* Moderate: significant jaundice + anemia; may require IVIG and/or exchange transfusion
	* Severe: profound anemia, hepatosplenomegaly (from extramedullary hematopoiesis), edema, ascites → ~~'''~~hydrops fetalis~~'''~~		* Severe: profound anemia, hepatosplenomegaly (from extramedullary hematopoiesis), edema, ascites → hydrops fetalis
	* Fatal: stillbirth or neonatal death from severe anemia, heart failure, or kernicterus		* Fatal: stillbirth or neonatal death from severe anemia, heart failure, or kernicterus

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	===Late anemia (readmission risk)===		===Late anemia (readmission risk)===
	*Neonates treated for HDFN may develop ~~'''~~late anemia~~'''~~ at 2-8 weeks of age as maternal antibodies continue to hemolyze neonatal RBCs		*Neonates treated for HDFN may develop late anemia at 2-8 weeks of age as maternal antibodies continue to hemolyze neonatal RBCs
	*May present to the ED with pallor, poor feeding, tachycardia, respiratory distress		*May present to the ED with pallor, poor feeding, tachycardia, respiratory distress
	* Check hemoglobin in any HDFN infant readmitted for any reason		* Check hemoglobin in any HDFN infant readmitted for any reason
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	==Evaluation==		==Evaluation==
	===ED workup===		===ED workup===
	* Fractionated bilirubin (total and direct): expect ~~'''~~predominantly unconjugated~~'''~~		* Fractionated bilirubin (total and direct): expect predominantly unconjugated
	* Maternal and infant blood type and Rh: identifies the incompatibility		* Maternal and infant blood type and Rh: identifies the incompatibility
	* Direct antiglobulin test (DAT/direct Coombs test): ~~'''~~positive~~'''~~ confirms antibody coating neonatal RBCs		* Direct antiglobulin test (DAT/direct Coombs test): positive confirms antibody coating neonatal RBCs
	**Strongly positive in Rh disease; may be weakly positive or negative in ABO disease (does ~~'''~~not~~'''~~ exclude ABO HDFN)		**Strongly positive in Rh disease; may be weakly positive or negative in ABO disease (does not exclude ABO HDFN)
	* CBC with reticulocyte count: anemia + ~~'''~~elevated reticulocytes~~'''~~ (expect >5-10%; may be markedly elevated)		* CBC with reticulocyte count: anemia + elevated reticulocytes (expect >5-10%; may be markedly elevated)
	* Peripheral blood smear: ~~'''~~spherocytes~~'''~~ (especially ABO); nucleated RBCs (erythroblastosis); polychromasia		* Peripheral blood smear: spherocytes (especially ABO); nucleated RBCs (erythroblastosis); polychromasia
	* Haptoglobin, LDH: hemolysis markers (haptoglobin low, LDH elevated)		* Haptoglobin, LDH: hemolysis markers (haptoglobin low, LDH elevated)
	* Albumin level: low albumin reduces bilirubin binding capacity and lowers the threshold for kernicterus		* Albumin level: low albumin reduces bilirubin binding capacity and lowers the threshold for kernicterus
Line 96:		Line 96:
	===Interpreting the bilirubin===		===Interpreting the bilirubin===
	*Use '''hour-specific bilirubin nomograms''' (Bhutani nomogram) — plot the bilirubin level against the infant's age in hours to determine risk zone<ref name="StatPearls"/>		*Use '''hour-specific bilirubin nomograms''' (Bhutani nomogram) — plot the bilirubin level against the infant's age in hours to determine risk zone<ref name="StatPearls"/>
	*Neurotoxicity risk factors that ~~'''~~lower the treatment threshold:~~'''~~ prematurity (<38 weeks), isoimmune hemolytic disease (positive DAT), G6PD deficiency, asphyxia, sepsis, acidosis, hypoalbuminemia (<3 g/dL)		*Neurotoxicity risk factors that lower the treatment threshold: prematurity (<38 weeks), isoimmune hemolytic disease (positive DAT), G6PD deficiency, asphyxia, sepsis, acidosis, hypoalbuminemia (<3 g/dL)

	==Management==		==Management==
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	* IVIG 0.5-1 g/kg IV if bilirubin is rising rapidly (>0.5 mg/dL/hour) despite intensive phototherapy, or if bilirubin is approaching exchange transfusion threshold<ref name="Medscape_HDN"/>		* IVIG 0.5-1 g/kg IV if bilirubin is rising rapidly (>0.5 mg/dL/hour) despite intensive phototherapy, or if bilirubin is approaching exchange transfusion threshold<ref name="Medscape_HDN"/>
	*Mechanism: blocks Fc receptors on neonatal reticuloendothelial cells → reduces antibody-mediated RBC destruction		*Mechanism: blocks Fc receptors on neonatal reticuloendothelial cells → reduces antibody-mediated RBC destruction
	*May ~~'''~~avoid the need for exchange transfusion~~'''~~ (NNT ~3-6)		*May avoid the need for exchange transfusion (NNT ~3-6)
	*Can repeat once if needed		*Can repeat once if needed
	* Caution: rare but reported association with necrotizing enterocolitis (NEC) in late preterm/term infants		* Caution: rare but reported association with necrotizing enterocolitis (NEC) in late preterm/term infants
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	** Rh disease: O-negative, Rh-negative, crossmatched against maternal serum		** Rh disease: O-negative, Rh-negative, crossmatched against maternal serum
	** ABO disease: O-type RBCs with AB plasma (or type-specific), Rh-compatible		** ABO disease: O-type RBCs with AB plasma (or type-specific), Rh-compatible
	**All blood should be ~~'''~~irradiated and leukodepleted~~'''~~		**All blood should be irradiated and leukodepleted
	*Indications:		*Indications:
	**Cord hemoglobin <10 g/dL with hydrops<ref name="PMC_HDN"/>		**Cord hemoglobin <10 g/dL with hydrops<ref name="PMC_HDN"/>
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	===Simple transfusion===		===Simple transfusion===
	*For '''significant anemia''' (hemoglobin <7-10 g/dL depending on clinical status) without dangerously elevated bilirubin		*For '''significant anemia''' (hemoglobin <7-10 g/dL depending on clinical status) without dangerously elevated bilirubin
	*Also for ~~'''~~late anemia~~'''~~ on readmission (ongoing hemolysis after initial hospitalization)		*Also for late anemia on readmission (ongoing hemolysis after initial hospitalization)
	*Use irradiated, leukodepleted, antigen-negative packed RBCs		*Use irradiated, leukodepleted, antigen-negative packed RBCs