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 Polycythemia is increased total RBC mass
• Central venous hematocrit > 65%
 Above 65% blood viscosity rises exponentially
 Polycythemic hyperviscosity is increased
viscosity of the blood resulting from
increased numbers of RBCs
• Not all polycythemic infants have symptoms of
hyperviscosity
 Polycythemia occurs in 2-4% of
newborns
• Half of these are symptomatic
 Hyperviscosity occurs in 25% of infants
with hematocrit 60-64%
• Hyperviscosity without polycythmia occurs in
1% (nonpolycythemic hyperviscosity)
 Clinical signs result from regional effects of
hyperviscosity and from the formation of
microthrombi
• Tissue hypoxia
• Acidosis
• Hypoglycemia
 Organs affected: CNS, kidneys, adrenals,
cardiopulmonary system, GI tract
 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
 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
 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)
 Delayed cord clamping
 Placental vessels contain 1/3 of the fetal blood volume,
half of which will be returned within 1 minute
 Gravity: positioning below the placenta will
increase placental transfusion
 Meds: oxytocin can increase contractions
and thus transfusion
 Decreased in c-section b/c no contractions
 Twin-twin transfusion
 Maternal-fetal transfusion
 Intrapartum asphyxia
 Enhances net umbilical flow toward the infant, while
acidosis increases capillary leak leading to reduced
plasma volume
 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
 Central venous hematocrit > 65%
 ALWAYS draw a central venous sample if
the capillary hematocrit is > 65%
• Warmed capillary hematrocrit > 65% only
suggestive of polycythemia
 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
 Usually at > 48 hours of age and weight loss > 8-10%
 Give 130-150 ml/kg/d
• Check central hematocrit q6 hours
 Normal peak is at 2-4 hours of age for acute polycythemia
 Symptomatic infants with central hct > 65%
• Partial exchange transfusion is advisable but
debatable
• For exchange can use normal saline, Plasmanate, 5%
albumin, or FFP
• Volume exchanged =
 (Weight (kg) x blood volume) x (hct - desired hct) / hct
 Blood volume is 80 ml/kg
• Exchange can be done via UVC that is not in the
liver, low UAC, or PIV
 Serum glucose
• Hypoglycemia is common with polycythemia
 Serum bilirubin
• Increased bili 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 b/c hypocalcemia can be
seen
 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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Polycythemia

  • 1.
  • 2.  Polycythemia is increased total RBC mass • Central venous hematocrit > 65%  Above 65% blood viscosity rises exponentially  Polycythemic hyperviscosity is increased viscosity of the blood resulting from increased numbers of RBCs • Not all polycythemic infants have symptoms of hyperviscosity
  • 3.  Polycythemia occurs in 2-4% of newborns • Half of these are symptomatic  Hyperviscosity occurs in 25% of infants with hematocrit 60-64% • Hyperviscosity without polycythmia occurs in 1% (nonpolycythemic hyperviscosity)
  • 4.  Clinical signs result from regional effects of hyperviscosity and from the formation of microthrombi • Tissue hypoxia • Acidosis • Hypoglycemia  Organs affected: CNS, kidneys, adrenals, cardiopulmonary system, GI tract
  • 5.  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
  • 6.  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
  • 7.  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)
  • 8.  Delayed cord clamping  Placental vessels contain 1/3 of the fetal blood volume, half of which will be returned within 1 minute  Gravity: positioning below the placenta will increase placental transfusion  Meds: oxytocin can increase contractions and thus transfusion  Decreased in c-section b/c no contractions  Twin-twin transfusion  Maternal-fetal transfusion  Intrapartum asphyxia  Enhances net umbilical flow toward the infant, while acidosis increases capillary leak leading to reduced plasma volume
  • 9.  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
  • 10.  Central venous hematocrit > 65%  ALWAYS draw a central venous sample if the capillary hematocrit is > 65% • Warmed capillary hematrocrit > 65% only suggestive of polycythemia
  • 11.  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  Usually at > 48 hours of age and weight loss > 8-10%  Give 130-150 ml/kg/d • Check central hematocrit q6 hours  Normal peak is at 2-4 hours of age for acute polycythemia
  • 12.  Symptomatic infants with central hct > 65% • Partial exchange transfusion is advisable but debatable • For exchange can use normal saline, Plasmanate, 5% albumin, or FFP • Volume exchanged =  (Weight (kg) x blood volume) x (hct - desired hct) / hct  Blood volume is 80 ml/kg • Exchange can be done via UVC that is not in the liver, low UAC, or PIV
  • 13.  Serum glucose • Hypoglycemia is common with polycythemia  Serum bilirubin • Increased bili 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 b/c hypocalcemia can be seen
  • 14.  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