Neonatal Anemia

Kirsten E. Crowley, MD
June 2005
Definitions
Anemia: Central venous hemoglobin < 13
g/dL or capillary hemoglobin < 14.5 g/dL in
infant > 34 weeks and 0-28 days old
Average value for central venous hemoglobin
at birth for > 34 weeks GA is 17 g/dL
Reticulocyte count in cord blood 3-7%
Average mean corpuscular volume 107 fL
Physiologic anemia of infancy
In healthy term infants, hemoglobin
levels begin to decline around the third
week of life
Reach a nadir of 11 g/dL at 8-12 weeks
Differences in premature infants
At birth they have slightly lower hemoglobin
levels, and higher MCV and retic counts
The nadir is lower and is reached sooner
Average nadir is 7-9 g/dL and is reached at 4-8
weeks of age
Related to a combination of decreased RBC mass
at birth, increased iatrogenic losses from lab
draws, shorter RBC life span, inadequate
erythropoietin production, and rapid body growth
Pathophysiology
Anemia in the newborn results from
three processes
Loss of RBCs: hemorrhagic anemia
Most common cause
Increased destruction: hemolytic anemia
Underproduction of RBCs: hypoplastic
anemia
Hemorrhagic anemia
Antepartum period (1/1000 live births)
Loss of placental integrity
Abruption, previa, traumatic amniocentesis
Anomalies of the umbilical cord or placental
vessels
Velamentous insertion of the cord in twins,
communicating vessels, cord hematoma, entanglement
of the cord
Twin-twin transfusion syndrome
Only in monozygotic multiple births
13-33% of twin pregnancies have TTTS
Difference in hemoglobin usually > 5 g/dL
Congestive heart disease common in anemic twin and
hyperviscosity common in plethoric twin
Hemorrhagic anemia
Intrapartum period
Fetomaternal hemorrhage (30-50% of
pregnancies)
Increased risk with preeclampsia-eclampsia, need for
instrumentation, and c-section
C-section: anemia increased in emergency c-
section
Traumatic rupture of the cord
Failure of placental transfusion due to cord
occlusion (nuchal or prolapsed cord)
Obstetric trauma causing occult visceral or
intracranial hemorrhage
Hemorrhagic anemia
Neonatal period
Enclosed hemorrhage: suggests obstetric trauma
or severe perinatal distress
Caput succedaneum, cephalhematoma, intracranial
hemorrhage, visceral hemorrhage
Defects in hemostasis
Congenital coagulation factor deficiency
Consumption coagulopathy: DIC, sepsis
Vitamin K dependent factor deficiency
Failure to give vit K causes bleeding at 3-4 days of age
Thrombocytopenia: immune, or congenital with absent
radii
Iatrogenic blood loss due to blood draws
Hemolytic anemia
Immune hemolysis: Rh incompatibility or
autoimmune hemolysis
Nonimmune: sepsis, TORCH infection
Congenital erythrocyte defect
G6PD, thalassemia, unstable hemoglobins,
membrane defects (hereditary spherocytosis,
elliptocytosis)
Systemic diseases: galactosemia,
osteopetrosis
Nutritional deficiency: vitamin E presents later
Hypoplastic anemia
Congenital
Diamond-Blackfan syndrome, congenital
leukemia, sideroblastic anemia
Acquired
Infection: Rubella and syphilis are the most
common
Aplastic crisis, aplastic anemia
Clinical presentation
Determine the following factors
Age at presentation
Associated clinical features
Hemodynamic status of the infant
Presence or absence of comensatory
reticulocytosis
Presentation of hemorrhagic anemia
Acute hemorrhagic anemia
Pallor without jaundice or cyanosis and
unrelieved by oxygen
Tachypnea or gasping respirations
Decreased perfusion progressing to
hypovolemic shock
Decreased central venous pressure
Normocytic or normochromic RBC indices
Reticulocytosis within 2-3 days of event
Presentation of hemorrhagic anemia
Chronic
Pallor without jaundice or cyanosis and unrelieved
by oxygen
Minimal signs of respiratory distress
Central venous pressure normal
Microcytic or hypochromic RBC indices
Compensatory reticulocytosis
Enlarge liver d/t extramedullary erythropoiesis
Hydrops fetalis or stillbirth may occur
Presentation of hemolytic anemia
Jaundice is usually the first symptom
Compensatory reticulocytosis
Pallor presents after 48 hours of age
Unconjugated hyperbilirubinemia of >
10-12 mg/dL
Tachypnea and hepatosplenomegaly
may be present
Presentation of hypoplastic anemia
Uncommon
Presents after 48 hours of age
Absence of jaundice
Reticulocytopenia

Presentation of other forms
Twin-twin transfusion
Growth failure in the anemic twin, often > 20%
Occult internal hemorrhage
Intracranial: bulging anterior fontanelle and
neurologic signs (altered mental status, apnea,
seizures)
Visceral hemorrhage: most often liver is damaged
and leads to abdominal mass
Pulmonary hemorrhage: radiographic opacification
of a hemithorax with bloody tracheal secretions
Diagnosis
Initial studies
Hemoglobin
RBC indices
Microcytic or hypochromic suggest fetomaternal or twin-
twin hemorrhage, or a-thalassemia
Normocytic or normochromic suggest acute hemorrhage,
systemic disease, intrinsic RBC defect, or hypoplastic
anemia
Reticulocyte count
elevation suggests antecedent hemorrhage or hemolytic
anemia while low count is seen with hypoplastic anemia
Diagnosis
Initial studies continued
Blood smear looking for
spherocytes (ABO incompatibility or hereditary
spherocytosis)
elliptocytes (hereditary elliptocytosis)
pyknocytes (G6PD)
schistocytes (consumption coagulopathy)
Direct Coombs test: positive in isoimmune
or autoimmune hemolysis
Other diagnostic studies
Blood type and Rh in isoimmune hemolysis
Kleihauer-Betke test on maternal blood looking for
fetomaternal hemorrhage
CXR for pulmonary hemorrhage
Bone marrow aspiration for congenital hypoplastic or
aplastic anemia
TORCH: bone films, IgM levels, serologies, urine for
CMV
DIC panel, platelets looking for consumption
Occult hemorrhage: placental exam, cranial or
abdominal ultrasound
Intrinsic RBC defects: enzyme studies, globin chain
ratios, membrane studies
Management
Simple replacement transfusion
Indications:
acute hemorrhage
Use 10-15 ml/kg O, RH- packed RBCs or blood cross-
matched to mom and adjust hct to 50%
Give via low UVC or central UVC if time permits
Draw diagnostic studies before transfusion
ongoing deficit replacement
maintenance of effective oxygen-carrying capacity
Hct < 35% in severe cardiopulmonary disease
Hct < 30% in mild-moderate cardiopulmonary disease,
apnea, symptomatic anemia, need for surgery
Hct < 21%

Management
Exchange transfusion
Indications
Chronic hemolytic anemia or hemorrhagic
anemia with increased central venous pressure
Severe isoimmune hemolytic anemia
Consumption coagulopathy
Nutritional replacement: iron, folate,
vitamin E
Prophylactic management
Erythropoietin
Increased erythropoiesis without significant
side effects
Decreases need for late transfusions
Will not compensate for anemia due to labs
Need to have restrictive policy for blood
sampling and micromethods in the lab
Nutritional supplementation: iron,
folate, vitamin E