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 csection

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 -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 crossmatched 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