Neonatal polycythemia

Author:
Joseph A Garcia-Prats, MD
Section Editors:
Donald H Mahoney, Jr, MD
Leonard E Weisman, MD
Deputy Editor:
Carrie Armsby, MD, MPH

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review
process is complete.
Literature review current through: Dec 2016. | This topic last updated: Sep 19,
2016.

INTRODUCTION Neonatal polycythemia is characterized by a venous hematocrit

(hct) that greatly exceeds normal values for gestational and postnatal age. This
condition affects approximately 1 to 5 percent of newborns. Although many affected
infants are asymptomatic, the characteristic clinical features are thought to result from
hyperviscosity and/or the metabolic effects of an increased red blood cell mass.

DEFINITIONS

Normal newborn physiology Compared with older infants and children, term
newborns have an increased red cell mass caused by the fetal response of increased
hemoglobin production to a relatively hypoxic intrauterine environment and possibly
vasomotor instability and venous pooling in newborn immediately after birth. The mean
hematocrit (hct) and hemoglobin concentrations from capillary samples in healthy term
infants at birth are 617 standard deviations (SD) percent and 19.32.2
(SD) g/dL, respectively [1].

Polycythemia Polycythemia is defined as hct or hemoglobin concentration >2 SD

above the normal value for gestational and postnatal age [2]. Accordingly, a term infant
is considered to be polycythemic if the hct from a peripheral venous sample is >65
percent or the hemoglobin is >22 g/dL [3-6]. In clinical circumstances, the definition
typically is based upon the hct, rather than the hemoglobin concentration.

The diagnosis of polycythemia is based upon peripheral venous samples because of

the variability in measurements obtained from capillary samples. Hcts of blood from
venous samples may be as much as 15 percent lower than those obtained from
capillary samples. (See 'Laboratory testing' below.)

Hyperviscosity Polycythemia must be distinguished from hyperviscosity, which is

defined as a blood viscosity >12 centipoise, measured at a shear rate of 11.5 per
second; or >6 centipoise, measured at a shear rate of 106 per second [7]. Whole blood
viscosity can be affected by significant increases in any of the elements of whole blood
including red cells, white cells, platelets, plasma proteins, immunoglobulins or clotting
factors. In neonates, the focus is generally on red cell excess [8].
Blood viscosity and hct have a linear relationship when the hct is <60 percent [6,9].
This relationship becomes exponential when the hct exceeds 65 percent, such that a
small increase in hct is associated with a dramatic increase in viscosity. The
relationship is less predictable for intermediate values [6]. In one report, for example,
hyperviscosity was present in 23 percent of infants with hcts in the range of 60 to 64
percent [6].

Even for hct values >65 percent, the relationship between hct and hyperviscosity is
somewhat inconsistent. This was examined in a study of cord blood in 2461 infants of
>34 weeks gestation [10]. Hyperviscosity was defined as >2 SD above the mean for
viscosity at each week of gestation, and polycythemia as an hct >65 percent.
Hyperviscosity occurred in only 47.4 percent of infants with polycythemia.

INCIDENCE Polycythemia occurs in 1 to 2 percent of healthy newborns born at sea-

level and up to 5 percent of infants born at high altitude [1,4,5,11,12]. Other factors that
influence the hematocrit (hct) during the first day after birth include:

Time delay between birth and clamping of the umbilical cord The amount of
placental transfusion is increased when cord clamping is delayed [13].
(See "Management of normal labor and delivery", section on 'Cord clamping'.)
Site of blood sampling Hct values can vary substantially depending on the type
of blood sample obtained. Hct values are highest in capillary samples,
intermediate in peripheral venous samples, and lowest in samples drawn from the
umbilical vein [6]. In one study of newborns with peripheral venous hcts 65
percent, the mean values for capillary, peripheral venous, and umbilical venous
hcts were 75, 71, and 63 percent, respectively [14].
Age at the time of sampling Hcts increase from birth, reaching a maximum at
approximately two hours of age, then decrease to levels in cord blood by 18 hours
of age [14-16].
Method of hct measurement Values obtained from centrifuged samples are
higher than those using cell counters and correlate better with blood viscosity [17].

Hyperviscosity measured in venous samples occurred in only 3 to 5 percent of

polycythemic infants detected by routine capillary screening [5,9,18]. Using cord blood
samples, hyperviscosity occurred in approximately one-half of infants with
polycythemia [10]. No matter how one measures the occurrence rate, neonatal
hyperviscosity is still an uncommon clinical entity.

PATHOPHYSIOLOGY Blood flow is determined by resistance to flow, which varies

directly with the viscosity of the blood and inversely with the fourth power of the radius
of the vessel through which the blood is passing. This is expressed by the equation
derived from Poiseuille's law:

R = 8hL / r(4)

Where R = resistance to blood flow, h = viscosity, L = length of the vessel, and r =

radius of the vessel. According to this relationship, a decrease in the radius of the
vessel affects resistance to flow more strongly than does an increase in viscosity.
Thus, an increase in viscosity will reduce blood flow only if the vessel radius remains
constant.

Hyperviscosity is thought to result in reduced blood flow to organs, leading to poor

tissue perfusion. However, studies in newborn lambs suggest that decreased cerebral
blood flow in polycythemia may be due in part to a vascular response to increased
arterial oxygen content related to the increased hemoglobin concentration, rather than
to hyperviscosity. When polycythemia was maintained in these lambs but the oxygen
delivery was reduced by infusing sodium nitrite, brain blood flow increased to baseline
values [19].

CAUSES The causes of polycythemia are multifactorial but are due to two major
mechanisms: passive (erythrocyte transfusion) and active (increased intrauterine
erythropoiesis). The table lists those conditions that have been associated with
polycythemia (table 1) [20].

Erythrocyte transfusion The most common cause of polycythemia in normal term

infants is delayed clamping of the umbilical cord, which results in increased transfer of
placental blood to the infant (erythrocyte transfusion) [21,22]. This can occur
intentionally or unintentionally (eg, at an unattended delivery) and may be exaggerated
if the baby is held at a level below the mother immediately following birth, before
clamping of the cord.

A 2013 meta-analysis of 15 trials involving 3911 mother-infant pairs found a

nonsignificant trend toward lower risk of polycythemia with early versus late clamping
of the cord (relative risk 0.39 [95% CI 0.12-1.27]) [13]. Hemoglobin levels were lower
among newborns in the early cord clamping group than in the late clamping group at 24
to 48 hours, but not at subsequent assessments. Fewer infants in the early cord
clamping group required phototherapy for jaundice than in the late cord clamping
group. There were no differences between early and late clamping in neonatal mortality
or long-term neurodevelopmental outcome.(See "Management of normal labor and
delivery", section on 'Cord clamping'.)

Intrapartum hypoxia has also been associated with increased placental transfusion.
Other associations include twin-to-twin transfusion, which occurs in 10 to 15 percent of
monochorionic twins, and maternal-fetal transfusion [23], which is less common.
(See "Twin-twin transfusion syndrome and twin anemia polycythemia sequence:
Pathogenesis and diagnosis".)

Increased intrauterine erythropoiesis Increased intrauterine erythropoiesis

usually results from placental insufficiency and chronic intrauterine hypoxia [12,18].
This typically is seen in infants who are small for gestational age or whose mothers
have preeclampsia or other hypertensive or vascular disorders. Polycythemia may
occur in pregnancies complicated by chronic maternal hypoxemia due to cardiac or
pulmonary disorders, drugs such as propranolol, smoking, high altitude, or postterm
delivery. (See "Postterm infant" and "Infants with fetal (intrauterine) growth
restriction" and "Preeclampsia: Clinical features and diagnosis".)
Polycythemia predominantly due to increased erythropoiesis can also occur in:

Infants of diabetic mothers (see "Infant of a diabetic mother")

Infants who are large for gestational age, including those with Beckwith-
Wiedemann syndrome (see "Large for gestational age newborn" and "Beckwith-
Wiedemann syndrome")
Other endocrine abnormalities, such as congenital adrenal hyperplasia [24],
hypothyroidism [25], or hyperthyroidism [26] (see "Genetics and clinical
presentation of classic congenital adrenal hyperplasia due to 21-hydroxylase
deficiency" and "Clinical features and detection of congenital
hypothyroidism" and "Evaluation and management of neonatal Graves' disease")
Chromosomal anomalies, such as trisomy 21, 18, and 13 [27] (see "Down
syndrome: Clinical features and diagnosis" and "Congenital cytogenetic
abnormalities", section on 'Trisomy 18 syndrome' and "Congenital cytogenetic
abnormalities", section on 'Trisomy 13 syndrome')

CLINICAL FEATURES Most polycythemic infants have no clinical signs of the

condition [20]. In two large prospective studies of infants with polycythemia that
included matched controls, the majority of polycythemic infants were asymptomatic (74
to 90 percent) [28,29]. The most commonly identified symptoms compared with the
controls were gastrointestinal symptoms (poor feeding or vomiting) (17 percent),
hypoglycemia (12 percent), and cyanosis/apnea (<10 percent) [28]. Necrotizing
enterocolitis was reported in both study and control groups, but no statistically
significant difference was demonstrated. Other findings often attributed to
polycythemia, such as plethora, respiratory distress, tachycardia, hematuria, renal vein
thrombosis, priapism, gallstones, hypotonia, irritability, increased pulmonary vascular
resistance, abnormal cry, lethargy, jitteriness, and seizures, are a compilation from
retrospective studies [4] or small case series [14,30-32] with no control patients and,
therefore, may reflect observer bias.

Symptoms, when present, often begin by two hours after birth, after fluid shifts have
occurred and the hematocrit (hct) is at its peak [9]. Onset may be delayed to the
second or third day of life in some infants who develop an increased hct because of
excessive extracellular fluid loss. In this case, the volume depletion may exaggerate
the expression of an already increased red cell mass or, in extreme cases, it may be
the primary cause of the high hct. Infants with no symptoms by 48 to 72 hours of age
are likely to remain asymptomatic [15,33].

Symptoms usually attributed to this disorder are thought to be due to reduced tissue
perfusion or associated metabolic abnormalities. However, animal data raise some
questions as to whether this indeed is the pathophysiology [19]. These signs and
symptoms occur with many other neonatal disorders and may be associated with, but
not caused by, the polycythemia.

Cardiorespiratory effects Cardiorespiratory signs, such as cyanosis and

tachycardia, are uncommon, with reported occurrence of <15 percent of prospective
studies [28,29]. Respiratory symptoms, including tachypnea, develop in <5 percent of
patients [28,29].

Gastrointestinal disorders Gastrointestinal symptoms, which occur in as many as

17 percent of affected patients, include vomiting and poor feeding [28,29].

Hypoglycemia Hypoglycemia is a common metabolic problem in patients with

polycythemia. It occurs in 12 to 40 percent of cases [4,28,31,34]. The mechanism may
involve increased glucose utilization by the increased number of circulating red cells.
However, there are no data to support a causal relationship and hypoglycemia in these
infants may be related to the multifactorial causes of polycythemia (eg, polycythemia
commonly occurs in infants of diabetic mothers who are at risk for hypoglycemia due to
increased insulin production). (See "Infant of a diabetic mother", section on
'Hypoglycemia'.)

Hyperbilirubinemia At least one-third of infants with polycythemia develop

hyperbilirubinemia [4], most likely due to the breakdown of an increased number of
circulating red cells. This may occasionally lead to the development of gallstones [20].
The actual effect of polycythemia on hyperbilirubinemia is difficult to quantify, since
interventions for polycythemia, such as exchange transfusion and hydration, also
mitigate the hyperbilirubinemia. These treatment effects may explain why some studies
do not show an association between polycythemia and hyperbilirubinemia [28].

DIAGNOSIS

Which infants should be screened? The hematocrit (hct) should be measured in

infants who have signs or symptoms that may be due to polycythemia, including
cyanosis, tachypnea, and poor feeding and vomiting. We do not routinely measure the
hct in term infants who appear well (including those with growth restriction) because
asymptomatic newborns with polycythemia do not appear to benefit from treatment
[35].

Laboratory testing The hct is often first measured on a capillary blood sample,
usually taken from a warmed heel. If the capillary hct is >65 percent, testing should be
repeated on a sample of venous blood. The venous hct usually will be 5 to 15 percent
lower than the capillary hct. The diagnosis of polycythemia is made if the venous hct is
>65 percent.

As noted above, less than half of infants with polycythemia have hyperviscosity [14].
Conversely, some infants with hyperviscosity are not polycythemic. However,
measurement of viscosity is not widely available. Thus, hct remains the best laboratory
tool to consider initiating evaluation and intervention. (See 'Hyperviscosity' above.)

Exclusion of other disorders When a diagnosis of polycythemia is made, infants

should be evaluated for possible etiologies, including delayed clamping of the cord,
maternal factors, such as preeclampsia and diabetes, and the possibility of infant
factors, such as macrosomia and endocrine abnormalities including congenital adrenal
hyperplasia or thyroid abnormalities (table 1).
In addition, because symptoms attributed to polycythemia can occur in many neonatal
disorders, other possible causes of the symptoms should be investigated. These
include:

Respiratory disorders (eg, pneumonia). (See "Overview of neonatal respiratory

distress: Disorders of transition" and "Neonatal pneumonia".)
Cardiovascular abnormalities (eg, congenital heart disease, persistent pulmonary
hypertension). (See "Identifying newborns with critical congenital heart
disease" and "Persistent pulmonary hypertension of the newborn".)
Neurologic disorders (eg, intracranial hemorrhage, venous thrombosis,
intracranial anomalies, or metabolic abnormalities) (See "Clinical manifestations
and diagnosis of intraventricular hemorrhage in the newborn" and "Inborn errors of
metabolism: Epidemiology, pathogenesis, and clinical features".)
Dehydration - The possibility of dehydration can be evaluated by comparison of
birth weight and current weight; loss of >7 percent of birth weight during the first
five days of life may suggest dehydration (table 2). (See "Overview of the routine
management of the healthy newborn infant", section on 'Weight loss'.)

If the symptoms are not severe, these possibilities usually can be excluded by a
thorough physical examination and close observation. However, if these symptoms
worsen or persist, then a thorough review of the maternal labor and delivery course,
and metabolic screening tests of glucose and ionized calcium and a chest radiograph
are warranted.

MANAGEMENT

Overview of approach All polycythemic infants should be observed closely for

neurologic and cardiovascular symptoms and monitored for common complications,
such as hypoglycemia and hyperbilirubinemia. Once the clinician makes the diagnosis
of polycythemia, careful monitoring of blood glucose should be undertaken; if
hypoglycemia is discovered, adequate glucose supplementation should be given.
(See "Management and outcome of neonatal hypoglycemia".)

Serum bilirubin should be followed and hyperbilirubinemia should be treated

accordingly. (See "Treatment of unconjugated hyperbilirubinemia in term and late
preterm infants".)

The use of partial exchange transfusion (PET) is generally limited to patients with
severe polycythemia and/or marked symptoms. (See 'Partial exchange
transfusion' below.)

The management approach outlined below is based on largely on expert opinion.

Evidence supporting the long-term benefits of PET is generally lacking; weak
observational evidence suggests that there may some short-term benefits.

Asymptomatic infants Management of infants with polycythemia without symptoms

is usually guided by the hematocrit (hct) (algorithm 1) (in this context, plethora is not
considered a symptom):
 Infants who are asymptomatic and have a peripheral venous hct between 60 and
70 percent should be observed. Adequate hydration and glucose intake should be
ensured by monitoring oral intake, body weight, and urine output. Bilirubin and
blood glucose levels should be checked and monitored as needed. The venous
hct should be repeated in 12 to 24 hours, while monitoring closely for the
development of symptoms. If the hct remains <70 percent and the infant continues
to be asymptomatic, this approach is continued for 24 hours and the hct
rechecked.
If the hct is >70 percent, several different approaches are used:
Many centers (including the author's institution) manage such infants with
continued observation, with or without intravenous (IV) hydration.
Some groups perform PET in asymptomatic infants only if the venous hct is
>75 percent [36,37].
Some clinicians perform a PET for any infant with a venous hct >70 percent,
even if the infant is asymptomatic (this approach is less common) [38-40].

Symptomatic infants The optimal management of polycythemic infants with

symptoms (cyanosis/apnea, gastrointestinal symptoms [poor feeding or vomiting] or
hypoglycemia) has not been established and varies among centers (algorithm 1).

For infants with a peripheral venous hct >65 percent and symptoms that may be
attributed to hyperviscosity:

Our preferred method of management is to provide IV hydration and close

observation. The main reason for administering the IV fluids is to prevent
hypoglycemia, which is a common complication of polycythemia
(see 'Hypoglycemia' above). IV fluid is provided for the first 24 to 48 hours of age
at a rate of at least 100 mL/kg per day, including glucose at a rate of 6 to
8 mg/kg per min, while the infant is closely monitored. A PET may be performed
only if there is worsening of symptoms, such as persistent hypoglycemia, or
worsening cyanosis/apnea, or gastrointestinal symptoms. In addition, infants with
worsening symptoms should be evaluated for causes of the symptoms other than
polycythemia. (See 'Exclusion of other disorders' above.)
Other centers perform a PET to lower the hct in this setting [37]. When the
decision is made to perform PET, it should be done as soon as possible because
the neonatal hct and blood viscosity peaks between two and four hours after birth
[38]. (See 'Technique' below.)

Partial exchange transfusion Isovolumetric PET reduces the hct without causing
hypovolemia. There is some evidence that PET has beneficial short-term effects on
measures of perfusion. However, PET does not appear to affect long-term outcome in
infants with polycythemia. (See 'Outcome' below.)

Short-term effects In clinical studies, PET has been found to have beneficial
effects on physiologic measures related to viscosity (eg, cerebral blood flow, cardiac
index, and oxygen transport) [7,35,41-45]; however, PET has not been demonstrated
to alter the symptoms associated with polycythemia [38].
Long-term effects Based on the available evidence, PET does not appear to
improve long-term outcomes. Several small clinical trials and two meta-analyses have
found that long-term neurodevelopmental outcomes are similar among infants
managed with and without PET [28-31,35,46-48]. In addition, the risk of gastrointestinal
injury may be increased with PET [47,48]. (See 'Complications' below
and 'Outcome' below.)

It is important to note, however, that in most studies evaluating PET, the intervention
was usually performed after six hours of life, so the effect of earlier intervention is
unknown.

Technique PET can be performed in several ways. One approach is to remove

blood from an umbilical venous or arterial catheter and infuse normal saline into a
peripheral vein [49,50]. The exchange volume (in mL) is calculated using the following
formula:

Exchange volume = [(observed hct desired hct) x blood volume] observed hct

Where hct = hematocrit, and blood volume is calculated at 80 to 100 mL/kg body
weight. Higher volumes are associated with lower gestational ages and/or delayed cord
clamping. The desired hct is usually set at 55 percent.

In general, the exchange volume is 15 to 20 mL/kg body weight. Blood can be removed
and saline infused continuously (isovolumetric technique, the best approach in unstable
infants) or the process can be accomplished using serial aliquots of 10 to 15 mL/kg.

Complications The risk of necrotizing enterocolitis (NEC) may be increased in

infants treated with PET for polycythemia [47,48]. In a small trial, NEC developed in 8
of 43 patients with hyperviscosity who underwent the procedure and in none of the
controls [51]. Treated infants also had significantly more gastrointestinal symptoms (eg,
abdominal distension, bloody stools, and emesis). Contrasting results were reported in
a retrospective analysis of 185 polycythemic term infants treated with PET, in which no
evidence of severe gastrointestinal injury was detected [52]. The contrasting findings
might be explained by differences between the PET techniques used in the two
studies: in the second study, the umbilical vein was used to withdraw the allotted
volume of blood to be exchanged, and the replacement volume was administered via
peripheral vein. Because this study did not test and select patients for hyperviscosity,
the population studied was probably at lower risk for complications. The study is also
limited by its retrospective nature and lack of a control group. (See "Clinical features
and diagnosis of necrotizing enterocolitis in newborns".)

OUTCOME Whether neonatal polycythemia or its treatment affect long-term

outcome is uncertain. The available evidence suggests that the clinical outcome may
depend more upon associated conditions, such as hypoglycemia, or on the underlying
disorder (eg, placental insufficiency), than on polycythemia itself. As previously
discussed, partial exchange transfusion (PET) does not appear to improve long-term
outcomes [47,48]. (See 'Long-term effects' above.)
Studies evaluating the effects of polycythemia and hyperviscosity on long-term
neurodevelopmental outcomes have produced conflicting results. Some studies have
found associations between hyperviscosity and neurologic sequelae (including motor
and speech delays, intellectual disability, and lower academic achievement)
[28,29,31,46]; while others have not found an association [30,35].

A study evaluating three-year outcomes of 111 newborns with hyperviscosity (of whom
42 received PET) compared with 110 controls found that infants with hyperviscosity
had more motor and neurologic abnormalities (38 versus 11 percent) than controls did.
These findings did not differ according to treatment [29]. Maternal preeclampsia and
neonatal hypoglycemia were more common in the hyperviscosity group than in the
control group. In addition, many infants in both groups were lost to follow-up, including
approximately one-third of the patients with hyperviscosity.

A similar study compared neurodevelopmental outcomes of 93 infants with

hyperviscosity, half of whom were randomly assigned to receive PET, with 93 controls
[28]. Hyperviscosity was associated with delays in speech and fine motor development
at one and two years of age, and persistent effects on intelligence quotient (IQ) scores
and academic achievement also were seen in the patients available for follow-up at
seven years of age (53 percent of the original cohort) [46]. Among the infants with
hyperviscosity, treatment with PET was not associated with effects on any of these
neurodevelopmental outcomes, except for neurologic diagnoses and fine motor
abnormalities at two years of age; no differences were noted at seven years.

By contrast, in a study of 71 infants with neonatal polycythemia identified by routine

screening, of whom 46 were available for follow-up at an average age of 30 months,
neurodevelopmental outcomes were similar among infants with symptomatic
hyperviscosity, asymptomatic hyperviscosity, and asymptomatic infants with normal
viscosity [35]. Another study reported normal neurologic and developmental
achievement at 8 months and at two years of age among 49 infants with polycythemia
and hyperviscosity treated with and without PET [30].

There are important limitations to these studies that preclude a clear understanding of
the effects of polycythemia, or a firm answer on the clinical benefits of PET. Most
reports include patients with polycythemia detected by routine screening who also had
documented hyperviscosity. Thus, the results may not apply to infants with
polycythemia alone or those in whom polycythemia was detected because they were
symptomatic. Most studies did not control for preexisting confounders such as maternal
diabetes, smoking, or intrauterine growth retardation, so the observed differences in
neurodevelopmental outcomes may not be caused by the polycythemia. In studies
evaluating PET, the intervention was usually performed after six hours of life, so the
effect of earlier intervention is unknown.

SUMMARY AND RECOMMENDATIONS

Polycythemia is defined as hematocrit (hct) >2 standard deviations above the

normal value for gestational and postnatal age. A term infant is considered to be
polycythemic if the hct from a peripheral venous sample is >65 percent. There is
considerable variability in measurements obtained from capillary samples; if the
capillary hct is >65 percent, testing should be repeated on a sample of venous
blood. (See 'Definitions' above and 'Laboratory testing' above.)
Hyperviscosity occurs in approximately 50 percent of infants with polycythemia,
and the risk of hyperviscosity increases sharply as the hct increases above 65
percent. Polycythemia is associated with reduced blood flow to organs, but it is
unclear whether this is due to the hyperviscosity or to the increased arterial
oxygen content related to the polycythemia. (See 'Hyperviscosity' above
and 'Pathophysiology' above.)
The most common association of polycythemia in normal term infants is delayed
clamping of the umbilical cord, which results in increased transfer of placental
blood to the infant. Other associations include twin-to-twin transfusion, placental
insufficiency, maternal hypoxemia or diabetes, and infant risk factors including
macrosomia and endocrine abnormalities (table 1). (See 'Causes' above.)
The majority of infants (74 to 90 percent) with polycythemia are asymptomatic. In
other infants, symptoms associated with polycythemia may
include cyanosis/apnea, vomiting, or poor feeding. The primary laboratory
abnormality associated with polycythemia is hypoglycemia. Symptoms, when
present, often begin by two hours after birth, but may be delayed to the second or
third day of life in some infants. (See 'Clinical features' above.)
All polycythemic infants should be observed closely for hydration status and
monitored for common complications, such as hypoglycemia and
hyperbilirubinemia. (See 'Management' above.)
For infants with asymptomatic polycythemia, management is based on the
venous hct (algorithm 1):
We suggest that asymptomatic infants with a peripheral venous hct between
60 and 70 percent not undergo PET (Grade 2C). Adequate hydration and
glucose intake should be ensured by monitoring oral intake, body weight, and
urine output. The venous hct should be repeated in 12 to 24 hours, while
monitoring closely for the development of symptoms.
Asymptomatic infants with a hct >70 percent can be treated with supportive
care such as intravenous hydration, or (less often) with PET.
For infants with symptomatic polycythemia, we suggest supportive treatment
with intravenous hydration and glucose rather than partial exchange transfusion
(PET) (Grade 2C). In addition, management includes close monitoring of urine
output and pursuit of other possible reasons for the symptoms. PET is a
reasonable alternative treatment based on limited data on short-term beneficial
effects; however, the available evidence suggests that PET does not improve
long-term neurodevelopmental outcome, and that PET may be associated with
possible risks (eg, necrotizing enterocolitis). (See 'Symptomatic infants' above
and 'Partial exchange transfusion' above.)
Whether neonatal polycythemia or its treatment affect long-term outcome is
uncertain. The available evidence suggests that the clinical outcome may depend
more upon associated conditions, such as hypoglycemia, or on the underlying
 disorder (eg, placental insufficiency), than on polycythemia itself.
(See 'Outcome' above.)
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