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Anemia & polycythemia in neonates
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- 3. Physiologic Anemia OfInfancy • 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 fromHbF 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 andSymptoms : apnea poor weight gain pallor decreased activity Tachycardia. • Iron administration does not alter nadir reached or its rate of reduction.
- 7. Pathophysiology • Anemia inthe 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 • Antepartumperiod – 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 • Intrapartumperiod – 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 • Neonatalperiod – 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 • Immunehemolysis: 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 • Determinethe 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 hemorrhagicanemia • 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 hemolyticanemia • Jaundice is usually the first symptom • Compensatory reticulocytosis • Pallor • Hepatosplenomegaly
- 17. Presentation of hypoplasticanemia • Uncommon • Presents after 48 hours of age • Absence of jaundice • Reticulocytopenia
- 18. Presentation of otherforms • 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 smearto 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 replacementtransfusion – 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 – Increasederythropoiesis without significant side effects
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- 26. • Polycythemia isincreased 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 occursin 2-4% of newborns – Half of these are symptomatic • Hyperviscosity occurs in 25% of infants with hematocrit 60-64%
- 28. Pathophysiology • Clinical signsresult 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 alterincidence • 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 • Enhancedfetal 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 • Symptomsare 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 venoushematocrit > 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 infantswith 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 • Serumglucose – 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 riskof 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
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