Neonatal Anemia: DR - Santosh Reddy

Neonatal Anemia
Dr.Santosh Reddy
Definition
• Anemia, defined as hematocrit (Hct) or hemoglobin (Hb)
concentration < 2 SD below mean for age
• Anemia is defined as Hct <45% in a term infant.
• A hemoglobin value less than the normal range for birthweight and
postnatal age.
Physiological Anemia ?
HEMATOLOGIC PHYSIOLOGY OF THE
NEWBORN
Normal Physiologic anemia of infancy
1. In utero, the fetal aortic oxygen saturation is low at 45%, erythropoietin levels
are high, and RBC production is rapid. The fetal liver is the major site of
erythropoietin production.
2. After birth, the oxygen saturation is much higher at 95%, and hence,
erythropoietin is undetectable. Reticulocyte counts are low, and the hemoglobin
level falls.
3. Although hemoglobin levels fall, oxygen availability to tissues remains good.
This physiologic “anemia” is not a functional anemia.
4. At 8 to 12 weeks, hemoglobin levels reach their nadir, oxygen delivery to the
tissues decreases, renal erythropoietin production is stimulated, and RBC
production increases.
5. During this period of active erythropoiesis, iron stores are rapidly utilized. Iron is
available from degraded RBC. Iron stores are sufficient for 15 to 20 weeks in term
infants. After this time, the hemoglobin level decreases if iron is not supplied.
Anemia of prematurity
Anemia of prematurity is an exaggeration of the normal physiologic anemia

1. RBC mass and iron stores are decreased because of low birth weight;
however, hemoglobin concentrations are similar in preterm and term infants.
2. The hemoglobin nadir is reached earlier than in the term infant because of
the following:
• a. RBC survival is decreased in comparison with that in the term infant.
• b. Rapid rate of growth in premature babies than in term infants.
• c. Iatrogenic phlebotomy for laboratory tests.
• d. Vitamin E deficiency.
3. The hemoglobin nadir in premature babies is lower than in term
infants because erythropoietin is produced by the term infant at a
hemoglobin level of 10 to 11 g/dL but is produced by the premature
infant at a hemoglobin level of 7 to 9 g/dL.
4. Once the nadir is reached, RBC production is stimulated, and iron
stores are rapidly depleted because less iron is stored in the premature
infant than in the term infant.
ETIOLOGY OF ANEMIA IN THE NEONATE
A. Anemia due to blood loss

• is characterized by a normal bilirubin level (unless the hemorrhage is
retained).
• If blood loss is recent (e.g., at delivery), the hematocrit (Hct) and
reticulocyte count may be normal, and the infant hypovolemic. The
Hct will fall later because of hemodilution.
• If the bleeding is chronic, the Hct will be low, the reticulocyte count
up, and the baby normovolemic
1.Obstetric causes of blood loss
1. Incision of the placenta at the time of cesarean section
2. Rupture of anomalous vessels (e.g., vasa previa, velamentous
insertion of the cord, or rupture of communicating vessels in a
multilobed placenta)
3. Hematoma of the cord caused by varices or aneurysm
4. Rupture of the cord (more common in short cords and in dysmature
cords)
5. Abruptio placentae f. Placenta previa (uncommon to have fetal
blood loss)
2.Occult blood loss
1. Fetomaternal bleeding
2. Fetoplacental bleeding
3. Twin-to-twin transfusion
3.Bleeding in the neonatal period
1. Intracranial bleeding (Prematurity, Traumatic assisted delivery , Underlying coagulation
disorder)
2. Massive cephalohematoma, subgaleal hemorrhage, or hemorrhagic caput succedaneum
3. Retroperitoneal bleeding
4. Ruptured liver or spleen
5. Adrenal or renal hemorrhage
6. Gastrointestinal bleeding (maternal blood swallowed from delivery or breast should be
ruled out by the Apt test)
i. Necrotizing enterocolitis (NEC)
ii. Nasogastric catheter
7. Bleeding from the umbilicus
i. Slipped ligature or cord clamp
ii. Loss from an indwelling umbilical artery or venous catheter
B. Hemolysis
• manifested by a decreased Hct, an increased reticulocyte count, and
an increased bilirubin level.
1. Immune hemolysis
• Rh incompatibility
• ABO incompatibility
• Minor blood group incompatibility (e.g., c, E, Kell, Duffy)
• Maternal disease (e.g., lupus), autoimmune hemolytic disease (Direct Coomb’s Test [DCT]
will be positive in the mother and newborn) or drugs
2. Hereditary RBC disorders
• RBC membrane (spherocytosis, elliptocytosis, or stomatocytosis)
• Metabolic defects—glucose-6-phosphate dehydrogenase (G6PD)
• Hemoglobinopathies
i. α- and γ-thalassemia syndromes
ii. α- and γ-chain structural abnormalities
3. Acquired hemolysis
• Infection—bacterial or viral
• Disseminated intravascular coagulation
Diminished RBC production
manifested by a decreased Hct, decreased reticulocyte count, and
normal bilirubin level.
1. Physiologic anemia or anemia of prematurity
2. Diamond–Blackfan syndrome
3. Congenital leukemia (very rare)
4. Infections, especially rubella and parvovirus.
5. Osteopetrosis, leading to inadequate erythropoiesis, presents in
infancy
DIAGNOSTIC APPROACH TO ANEMIA IN THE
NEWBORN
• History :
A. The family history should include questions about anemia, jaundice, gallstones,
and splenectomy.
B. The obstetric history should be evaluated for severe abdominal pain (abruptio) or
intrapartum blood loss.
C. The physical examination may reveal an associated abnormality and provide clues
to the origin of the anemia.
1. Acute blood loss leads to shock, with cyanosis, poor perfusion, and acidosis.
2. Chronic blood loss produces pallor, but the infant may look well and exhibit only
mild symptoms of respiratory distress or irritability.
3. Chronic hemolysis is associated with pallor, jaundice, and hepatosplenomegaly.
Laboratory Evaluation
• Complete blood cell count
• Reticulocyte count
• Peripheral blood smear
• Coomb’s test and bilirubin level
• Apt test on gastrointestinal blood of uncertain origin
• Ultrasound of the abdomen and head
• Parental testing
• Studies for infection
• Bone marrow (rarely used except in cases of bone marrow failure from
hypoplasia or tumor)
THERAPY
• A. Transfusion
• a. Infants with significant respiratory disease or congenital heart disease
(e.g., large left-to-right shunt) may need their Hct maintained above 40%.
Transfusion with adult RBCs provides the added benefit of lowered
hemoglobin oxygen affinity, which augments oxygen delivery to tissues.Blood
should be fresh (3 to 7 days old) to ensure adequate 2,3-DPG levels.
• b. Infants with ABO incompatibility who do not have an exchange transfusion
may have protracted hemolysis and may require a transfusion several weeks
after birth.
• c.Growing premature infants may manifest a need for transfusion by
exhibiting poor weight gain, apnea, tachypnea, or poor feeding.
Blood products and methods of transfusion
• a. Packed RBCs. We generally transfuse 15 to 20 mL/kg. The blood has to
be used within 35 days of donation, while for exchange transfusion it
needs to be used within less than 5 days from donation.
• b. Whole blood is rarely used these days.
• c. Partial exchange with high Hct-packed RBCs may be required for
severely anemic infants,
Prophylaxis
Premature infants (preventing the anemia of prematurity).
1. Delayed cord clamping
2. Iron supplementation in the preterm infant introduced between 4
and 6 weeks improves iron stores, and lowers the risk of iron
deficiency anemia after the first 6 months of life.
3. Erythropoiesis-stimulating agents. Recombinant human
erythropoietin (rh-EPO) or Darbepoietin has been evaluated as a
promising measure in ameliorating anemia of prematurity
Thank You

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Neonatal Anemia

Anemia of prematurity is an exaggeration of the normal physiologic anemia

A. Anemia due to blood loss

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