Anemia & polycythemia in neonates
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Transcript of Anemia & polycythemia in neonates
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ANEMIA,POLYCYTHEMIA IN A NEWBORN
-Dr.ApoorvaPediatrics pg
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ANEMIA IN NEONATES
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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
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• 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.
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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.
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• Signs and Symptoms :apneapoor weight gainpallordecreased activityTachycardia.
• Iron administration does not alter nadir reached or its rate of reduction.
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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
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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
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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
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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
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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
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Hypoplastic anemia
• Congenital – Diamond-Blackfan syndrome, congenital leukemia,
sideroblastic anemia• Acquired– Infection: Rubella and parvovirus are the most
common– Drug induced
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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
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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
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• Chronic– Pallor– Minimal signs of respiratory distress– Microcytic or hypochromic RBC indices– Compensatory reticulocytosis– Enlarged liver d/t extramedullary erythropoiesis
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Presentation of hemolytic anemia
• Jaundice is usually the first symptom• Compensatory reticulocytosis• Pallor• Hepatosplenomegaly
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Presentation of hypoplastic anemia
• Uncommon• Presents after 48 hours of age• Absence of jaundice• Reticulocytopenia
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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
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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
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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
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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
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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
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Management
• Exchange transfusion– Indications• Chronic hemolytic anemia• Severe isoimmune hemolytic anemia• Consumption coagulopathy
• Nutritional replacement: iron, folate, vitamin E
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• Erythropoietin– Increased erythropoiesis without significant side
effects
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POLYCYTHEMIA IN NEONATES
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• 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
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Incidence
• Polycythemia occurs in 2-4% of newborns– Half of these are symptomatic
• Hyperviscosity occurs in 25% of infants with hematocrit 60-64%
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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
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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
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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
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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)
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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
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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
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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
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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
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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
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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
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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
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THANK YOU!