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
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•
•
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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
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•
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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
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•
•
•
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 twintwin 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 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