anemia-physiological,hypoplastic,anemia of prematurity,hemorrhagic,polycythemia

1. ANEMIA,POLYCYTHEMIA IN A
NEWBORN
-Dr.Apoorva
Pediatrics pg

2. ANEMIA IN NEONATES

3. Physiologic Anemia Of Infancy
• In utero,due to high oxygen saturation(45%) in fetal
aorta,erythropoietin levels are high &hence,RBC
production is rapid.
• At one week postnatally, all RBC indices begin
declining to a minimum value reached at about 8-12
weeks of age (11g/dl)
– decreased RBC production
– plasma dilution associated with increasing blood volume
– shorter life span of neonatal RBCs (50-70 days)
– more fragile RBCs

4. • Switch from HbF to HbA (switch to HbA provides for
greater unloading of oxygen to tissues d/t lower
oxygen affinity of HbA relative to HbF.)
• Seldom produces symptoms.
• As the hemoglobin levels reach nadir,oxygen delivery
to tissues is impaired,erythropoietin stimulated,RBC
production increases.
• Iron stores rapidly utilized for this process.
Hence,iron has to be supplied.

5. Anemia of Prematurity
• Occurs in low birth weight infants.
• The nadir is lower and is reached sooner.
• Average nadir is 7-9 g/dL and is reached at 4-8 weeks of
age.
• Due to a combination of :
decreased RBC mass at birth,
increased iatrogenic losses from lab draws,
shorter RBC life span,
inadequate erythropoietin production,
low iron stores,
rapid rate of growth,
Vitamin E deficiency.

6. • Signs and Symptoms :
apnea
poor weight gain
pallor
decreased activity
Tachycardia.
• Iron administration does not alter nadir reached or its
rate of reduction.

7. 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

8. Hemorrhagic anemia
• Antepartum period
– Loss of placental integrity
• Abruption, previa, traumatic amniocentesis.
– Anomalies of the umbilical cord or placental vessels
• Velamentous insertion of the cord , communicating vessels, cord
hematoma, entanglement of the cord,vasa previa.
– 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

9. Hemorrhagic anemia
• Intrapartum period
– Fetomaternal hemorrhage
• Increased risk with ECV,ICV,breech delivery,placental
malformations
– 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

10. Hemorrhagic anemia
• Neonatal period
– Enclosed hemorrhage: suggests obstetric trauma or severe
perinatal hypoxia
• Hemorrhagic caput succedaneum, cephalhematoma, intracranial
hemorrhage, visceral hemorrhage
– Defects in hemostasis
• Congenital coagulation factor deficiency
• Consumption coagulopathy: DIC, sepsis
• Vitamin K dependent factor deficiency
• Thrombocytopenia: immune, or congenital with absent radii
– Iatrogenic blood loss due to blood draws

11. Hemolytic anemia
• Immune hemolysis:
Rh/ ABO /minor blood group incompatibility or
autoimmune hemolysis
• Nonimmune:
sepsis, TORCH infection
• Congenital erythrocyte defect
– G6PD, thalassemia, membrane defects (hereditary
spherocytosis,elliptocytosis)
• Systemic diseases: galactosemia, osteopetrosis
• Nutritional deficiency: vitamin E

12. Hypoplastic anemia
• Congenital
– Diamond-Blackfan syndrome, congenital leukemia,
sideroblastic anemia
• Acquired
– Infection: Rubella and parvovirus are the most
common
– Drug induced

13. Clinical presentation
• Determine the following factors :
– Age at presentation
– Associated clinical features
– Hemodynamic status of the infant
– Presence or absence of compensatory
reticulocytosis
– Family history,obstetric history

14. Presentation of hemorrhagic anemia
• Acute hemorrhagic anemia
– Pallor without jaundice,cyanosis unrelieved by
oxygen
– Tachypnoea
– Decreased perfusion progressing to hypovolemic
shock
– Acidosis
– Normocytic or normochromic RBC indices
– Reticulocytosis within 2-3 days of event

15. • Chronic
– Pallor
– Minimal signs of respiratory distress
– Microcytic or hypochromic RBC indices
– Compensatory reticulocytosis
– Enlarged liver d/t extramedullary erythropoiesis

16. Presentation of hemolytic anemia
• Jaundice is usually the first symptom
• Compensatory reticulocytosis
• Pallor
• Hepatosplenomegaly

17. Presentation of hypoplastic anemia
• Uncommon
• Presents after 48 hours of age
• Absence of jaundice
• Reticulocytopenia

18. Presentation of other forms
• Twin-twin transfusion
– Growth failure in the anemic twin
• 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

19. Diagnosis
• Initial studies
– Hemoglobin
– RBC indices
• Microcytic or hypochromic suggest chronic hemorrhage or
thalassemia
• Normocytic or normochromic suggest acute hemorrhage,
systemic disease, intrinsic RBC defect or hypoplastic
anemia
– Reticulocyte count
• elevation suggests chronic hemorrhage or hemolytic
anemia while low count is seen with hypoplastic anemia

20. Diagnosis
– Blood smear to look for
• spherocytes (hereditary spherocytosis,immune
hemolysis)
• elliptocytes (hereditary elliptocytosis)
• pyknocytes ,bite cells,heinz bodies(G6PD)
• Schistocytes,fragmented RBC’s (consumption
coagulopathy)
– Direct Coombs test: positive in isoimmune or
autoimmune hemolysis

21. Other diagnostic studies
• Blood type and Rh in isoimmune hemolysis
• Kleihauer-Betke test on maternal blood to look for
fetomaternal hemorrhage
• CXR for pulmonary hemorrhage
• Bone marrow aspiration for congenital hypoplastic or
aplastic anemia
• TORCH: IgM levels, urine for CMV
• DIC panel, platelets looking for consumption
• Occult hemorrhage: cranial or abdominal ultrasound
• Intrinsic RBC defects: enzyme studies, globin chain ratios,
membrane studies

22. Management
• Simple replacement transfusion
– Indications:
• acute hemorrhage
– Use 15-20 ml/kg O, RH- packed RBCs or blood cross-
matched to mother and adjust hct to 50%
– Give via UVC
– Draw diagnostic studies before transfusion
• ongoing deficit replacement
• maintenance of effective oxygen-carrying capacity
– Hct >35% in severe cardiopulmonary disease
– Hct >40% in mild-moderate cardiopulmonary disease,
apnea, symptomatic anemia, need for surgery

23. Management
• Exchange transfusion
– Indications
• Chronic hemolytic anemia
• Severe isoimmune hemolytic anemia
• Consumption coagulopathy
• Nutritional replacement: iron, folate, vitamin E

24. • Erythropoietin
– Increased erythropoiesis without significant side
effects

25. POLYCYTHEMIA
IN NEONATES

26. • Polycythemia is increased total RBC mass
– Central venous hematocrit > 65%
• Polycythemic hyperviscosity is increased
viscosity of the blood resulting from increased
numbers of RBCs
– Not all polycythemic infants have symptoms of
hyperviscosity

27. Incidence
• Polycythemia occurs in 2-4% of newborns
– Half of these are symptomatic
• Hyperviscosity occurs in 25% of infants with
hematocrit 60-64%

28. Pathophysiology
• Clinical signs result from regional effects of
hyperviscosity and from the formation of
microthrombi
– Tissue hypoxia
– Acidosis
– Hypoglycemia in the substrate
• Organs affected: CNS, kidneys, adrenals,
cardiopulmonary system, GI tract

29. What affects hyperviscosity?
• Hematocrit
– Increased hct is the most important single factor
– Results from increase in circulating RBCs or decreased
plasma volume (dehydration)
• Plasma viscosity
– Higher plasma proteins = increased viscosity
• Especially fibrinogen (typically low in neonates)
– Not usually an issue in neonates
• RBC aggregation
– Occurs in areas of low blood flow = venous
microcirculation
– Not a large factor in neonates
• Deformability of RBC membrane: usually normal

30. Conditions that alter incidence
• Altitude: increased RBC mass
• Neonatal age
– Physiologic increase in hematocrit due to fluid
shifts away from intravascular compartment with
maximum at 2-4 hours of age
• Obstetric factors: delayed cord clamping or
“stripping” of the umbilical cord
• High-risk delivery, especially if precipitous

31. Perinatal processes
• Enhanced fetal erythropoiesis usually related
to fetal hypoxia
– Placental insufficiency
• Maternal hypertension, abruption, post-dates, IUGR,
maternal smoking
– Endocrine disorders: due to increased oxygen
consumption
• IDM (>40% incidence), congenital thyrotoxicosis, CAH,
Beckwith-Wiedemann syndrome (hyperinsulinism)

32. DUE TO : Hypertransfusion
• Delayed cord clamping
• Should be done within 1 minute
• Gravity: positioning below the placenta will
increase placental transfusion
• Meds: oxytocin can increase contractions and
thus transfusion
• Decreased in c-section ( no contractions )
• Twin-twin transfusion
• Intrapartum asphyxia
• Enhances net umbilical flow toward the infant, while acidosis
increases capillary leak leading to reduced plasma volume

33. Clinical presentation
• Symptoms are non-specific!
• CNS: lethargy, hyperirritability, proximal muscle
hypotonia, vasomotor instability, vomiting,
seizures, cerebral infarction (rare)
• Cardiopulmonary: respiratory distress,
tachycardia, CHF, pulmonary hypertension
• GI: feeding intolerance, sometimes NEC
• GU: oliguria, ARF, renal vein thrombosis, priapism
• Metabolic: hypo-glycemia/-calcemia/-
magnesemia
• Heme: hyperbili, thrombocytopenia
• Skin: ruddiness

34. Diagnosis
• Central venous hematocrit > 65%
• ALWAYS draw a central venous sample if the
capillary hematocrit is > 65%
– Warmed capillary hematrocrit > 65% only
suggestive of polycythemia

35. Management
• Asymptomatic infants
– Expectant observation unless central venous hematocrit
>75% (consider partial exchange transfusion)
– Can do a trial of rehydration over 6-8 hr if dehydrated
• Give 130-150 ml/kg/d
– Check central hematocrit q6 hourly

36. Management
• Symptomatic infants with central hct > 65%
– Partial exchange transfusion is advisable but debatable
– For exchange can use normal saline, 5% albumin, or FFP
– Volume exchanged =
• (Weight (kg) x blood volume) x (hct - desired hct) / hct

37. Other investigations
• Serum glucose
– Hypoglycemia is common with polycythemia
• Serum bilirubin
– Increased bilirubin due to increased RBC turnover
• Serum sodium, BUN, urine specific gravity
– Usually high if baby is deyhdrated
• Blood gas to rule-out inadequate oxygenation as
cause of symptoms
• Platelets, as thyrombocytopenia can be present
• Serum calcium-hypocalcemia can be seen

38. Prognosis
• Increased risk of GI disorders and NEC with partial
exchange transfusion (PET)
• Older trials show decreased neurologic complications
from hyperviscosity with PET, but newer trials show
no real benefit
– PET is controversial!
• Infants with asymptomatic polycythemia have an
increased risk for neurologic sequelae
– Normocythemic controls with the same perinatal history
have a similarly increased risk

39. THANK YOU!