neonatal anemia kirsten e. crowley, md june 2005
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Neonatal Anemia
Kirsten E. Crowley, MDJune 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 -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
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