05 polycythemia in the newborn

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DOI: 10.1542/neo.12-1-e202011;12;e20-e28NeoReviews

Juan I. Remon, Aarti Raghavan and Akhil MaheshwariPolycythemia in the Newborn

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Polycythemiain the NewbornJuan I. Remon, MD,*

Aarti Raghavan, MD,*

Akhil Maheshwari, MD*

Author Disclosure

Drs Remon, Raghavan,

and Maheshwari have

disclosed no financial

relationships relevant

to this article. This

commentary does not

contain a discussionof an unapproved/

investigative use of a

commercial

product/device.

AbstractNeonatal polycythemia, defined as a venous hematocrit 65% (0.65), is a common

problem in newborns. Infants born postterm or small for gestational age, infants of

diabetic mothers, recipient twins in twin-to-twin transfusion syndrome, and those

who have chromosomal abnormalities are at higher risk. Although the cause of

polycythemia is often multifactorial, most cases can be classified as having active

(increased fetal erythropoiesis) or passive (erythrocyte transfusion) polycythemia. By

increasing blood viscosity, polycythemia can impair microcirculatory flow in end

organs and can present with neurologic, cardiopulmonary, gastrointestinal, and

metabolic symptoms. In this article, we review the pathophysiology, clinical presen-

tation, diagnosis, and management of polycythemia in the newborn.

Objectives After completing this article, readers should be able to:

1. List the causes of polycythemia and hyperviscosity in the neonate.

2. Review the signs, symptoms, and diagnostic criteria for polycythemia and

hyperviscosity.

3. Discuss the treatment of polycythemia and hyperviscosity in the neonate.

IntroductionPolycythemia (or more accurately, erythrocythemia), an abnormal elevation of the circu-

lating red blood cell (RBC) mass, is seen frequently in newborns. Although neonatal

polycythemia usually represents a normal fetal adaptation to hypoxemia rather than a truehematopoietic defect, the abnormal increase in hematocrit increases the risk of hyper-

viscosity, microcirculatory hypoperfusion, and multisystem organ dysfunction. In this

article, we review the definition, pathophysiology, clinical presentation, and management

of polycythemia in the newborn.

DefinitionIn healthy term infants, the hematocrit and hemoglobin concentrations in venous blood

obtained at birth are 50.26.9% (0.50.07) (mean standard deviation) and

15.91.86 g/dL (15918.6 g/L), respectively. (1) Polycythemia is defined in newborns

as a venous hematocrit greater than 65% (0.65) or a hemoglobin value greater than

22 g/dL (220 g/L). (2)(3)(4) Based on this definition, the incidence of polycythemia in

healthy newborns has been reported to be 0.4% to 5%. (5)(6)(7) Increased incidence isseen in certain high-risk groups such as postterm neonates, small-for-gestational age

infants, infants of diabetic mothers, identical twins who share the same placenta and

develop twin-to-twin transfusion, and infants who have chromosomal abnormalities.

(7)(8)(9)

PathophysiologyAlthough the cause of polycythemia is often multifactorial, most patients can be classified

as having active (increased fetal erythropoiesis) or passive (erythrocyte transfusion) poly-

cythemia (Table 1). (5)(7)

*Department of Pediatrics, University of Illinois at Chicago, Chicago, IL.

Article hematology

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Increased fetal erythropoiesis is frequently seen in

conditions associated with hypoxia:

Placental insufficiency due to preeclampsia, primary

renovascular disease, chronic or recurrent placental

abruption, maternal cyanotic congenital heart disease,postdate pregnancy, maternal smoking, and maternal

heavy alcohol intake. (10)(11)(12) The severity of

hematopoietic dysfunction in these conditions appears

to be proportional to the degree of placental insuffi-

ciency and fetal growth restriction. (8) Whereas mild

placental dysfunction and consequent tissue hypoxia

are associated with increased erythropoietin concen-

trations and polycythemia, more severe placental vas-

culopathy may cause erythropoietin resistance and

anemia. (13)(14) Endocrine abnormalities associated with increased

fetal oxygen consumption, such as congenital thyro-toxicosis or maternal diabetes with poor glycemic

control. (13)(14) Thyrotoxicosis is presumed to in-

crease erythropoiesis through a direct effect on marrow

progenitor cells, increased erythropoietin expression,

and the indirect effects of intrauterine growth restric-

tion. (15)(16) In diabetic mothers who have poor

glycemic control, maternal hyperglycemia is proposed

to increase fetal erythropoiesis through fetal hyper-

insulinemia, tissue hypoxia, and increased erythro-

poietin concentrations. (17)(18) Although plasma lep-

tin concentrations are frequently elevated in infants

of diabetic mothers, the actual concentrations do not

correlate with the severity of polycythemia, and current

data do not support a causative role of leptin in this

process. (18) Genetic disorders, such as trisomy 13, trisomy 18,

trisomy 21, and Beckwith-Wiedemann syndrome. The

incidence of polycythemia in infants who have Down

syndrome is 15% to 33%. (19)(20)(21) Although the

cause of polycythemia in Down syndrome is not

known, high cord blood erythropoietin concentra-

tions in affected infants has led to the speculation that

intrauterine hypoxemia may play a role. (9) Among

neonates who have trisomy 13 and trisomy 18, the

prevalence of polycythemia has been estimated as 8%

and 17%, respectively. (22)

Erythrocyte transfusion polycythemia can result from

placental-fetal transfusion. Delayed cord clamping allows

for delivery of an increased blood volume to the infant.

When cord clamping is delayed more than 3 minutes

after birth, blood volume may increase by as much as

30%. (23) Hutton and Hassan (24) analyzed data from

seven randomized studies and showed that neonates in

the late-clamping group had a higher incidence of asymp-

tomatic polycythemia with a benign course (relative risk

(RR), 3.82; 95% confidence interval (CI), 1.11 to 13.21).

However, a more recent meta-analysis showed that delayed

cord clamping did not cause a clinically significant changein hematocrit at 1 and 4 hours of age. (25)

Placental-fetal transfusion is likely influenced by grav-

ity and the relative position of the delivered infant in

relation to the maternal introitus before cord clamping;

raising or lowering the baby by 15 to 20 cm or more with

the cord intact appears to influence placental transfusion.

(26) No randomized studies have examined this issue to

date. Placental transfusion is augmented in infants who

have perinatal asphyxia, which causes an active shift of

the blood volume from the placenta to the fetus. (27)

Oxytocin administration to the mother can also increase

the volume of placental transfusion to the newborn. (28)Twin-to-twin transfusion syndrome due to a vascular

communication occurs in approximately 10% of mono-

zygotic twin pregnancies. (29)

Polycythemia and HyperviscosityPolycythemia remains an area of interest due to its po-

tential effects on the viscosity of blood and its flow

properties in the microcirculation. (5)(7)(8) Viscosity is

a measure of the resistance of a fluid that is being de-

formed by either shear stress or tensile stress. (30) More

simply, viscosity refers to the thickness of a fluid and

is a measure of the fluids internal resistance to flow.

Table 1.

Conditions AssociatedWith Neonatal Polycythemia

Increased Fetal Erythropoiesis

Placental insufficiency due to preeclampsia, maternalchronic hypertension, chronic or recurrent placentalabruption, maternal cyanotic congenital heartdisease, postdate pregnancy, maternal smoking andheavy alcohol intake

Endocrine abnormalities such as congenitalthyrotoxicosis or maternal diabetes with poorglycemic control

Genetic disorders such as trisomy 13, trisomy 18,trisomy 21, and Beckwith-Wiedemann syndrome

Erythrocyte Transfusion

Placental-fetal transfusion with delayed cordclamping, relative positioning of the delivered infantin relation to the maternal introitus before cordclamping, perinatal asphyxia, oxytocin administration

Twin-to-twin transfusion syndrome

hematology polycythemia

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Hyperviscosity is arbitrarily defined as a viscosity mea-

surement of greater than 14.6 centipoise detected in a

viscometer at a shear rate of 11.5/sec. (5)(7)(30) Viscos-

ity rises linearly with increasing hematocrit until the

hematocrit reaches 60% (0.6) but increases exponentially

when hematocrit equals or exceeds 70% (0.7).

(5)(31)(32) Although the terms polycythemia and hy-

perviscosity are often used interchangeably, they are not

equivalent and show only modest concordance in clinical

cohorts. (5)(30) Furthermore, blood viscosity can also

rise with an increase in plasma proteins, platelets, leuko-

cytes, and endothelial factors. (30)(32)

Hyperviscosity occurs in polycythemia due to the

presence of an abnormally large number of circulating

erythrocytes; the plasma viscosity in the newborn is al-most always normal. (5)(7) According to Poiseuilles

law, flow velocities in the circulation are determined by

the resistance to flow, which varies with the viscosity of

the blood and inversely with the fourth power of the

radius of the blood vessel. This relationship can be ex-

pressed by the equation R8hL/r4, where R repre-

sents the resistance to blood flow,his the viscosity,Lis

the length of the vessel, and ris the radius of the vessel.

(33)(34) Because resistance is affected by viscosity as well

as the caliber of the blood vessel, the effects of poly-

cythemia on blood flow patterns are usually most pro-

nounced in the microcirculation. (34) In these smallvessels, non-newtonian mechanisms such as rouleaux

formation and increased erythrocyte-endothelial interac-

tion are also active and further contribute to the altered

flow. (32)

Polycythemia and hyperviscosity are associated with

decreased blood flow to the brain, heart, lung, intestines,

and carcass. (5)(7)(35)(36) Although renal blood flow is

not affected, renal plasma flow and glomerular filtration

rate are often diminished. (35) Hyperviscosity can also

reduce pulmonary blood flow that, in turn, can cause

systemic hypoxia. (36) In contrast to the effects of poly-

cythemia on the kidney and lungs, reduced cerebralblood flow in polycythemia likely represents a vascular

response to the increased arterial oxygen content (related

to increased hemoglobin concentrations) rather than

hyperviscosity. (7)(37) Changes in blood flow may also

alter the delivery of substrates (such as glucose) to organs

that are dependent on plasma flow. (7)(38)(39)

Clinical FindingsThe symptom complex associated with polycythemia is

frequently described by the term hyperviscosity syn-

drome, although it is important to remember that only

47% of infants who have polycythemia exhibit hypervis-

cosity, and only 24% of infants who have hyperviscosity

have a diagnosis of polycythemia. (6)(7)(40) Whereas

most patients who have polycythemia remain asymptom-

atic, characteristic clinical features may be recognized as

early as 1 to 2 hours after birth as the hematocrit peaks

with normal postnatal fluid shifts. (3) In some infants

who have high borderline hematocrits, symptoms may be

delayed until the second to third postnatal day, when

excessive depletion of the extracellular fluid may lead to

hemoconcentration and hyperviscosity. Infants who have

no symptoms by 48 to 72 hours of age are likely to

remain asymptomatic. (3)(41)

Clinical features associated with neonatal polycythe-

mia are generally nonspecific and include ruddy com-

plexion, irritability, jitteriness, tremors, feeding difficul-ties, lethargy, apnea, cyanosis, respiratory distress, and

seizures. (7) Neurologic symptoms occur in approxi-

mately 60% of affected patients. (5)(7)(42) The cause of

these symptoms is uncertain, but reduced cerebral blood

flow and altered tissue metabolism likely play important

roles. Neurologic signs may also be related to metabolic

changes such as hypoglycemia and hypocalcemia. Hypo-

glycemia is the most common metabolic derangement

and is observed in 12% to 40% of infants who have

polycythemia. Hypocalcemia is found in 1% to 11% of

neonates who have polycythemia, possibly related to

elevated concentrations of calcitonin gene-related pep-tide (CGRP) in affected infants. (43) The pathophysiol-

ogy of increased CGRP concentrations is not clear;

CGRP may play a role in the normal postnatal circulatory

adaptation to extrauterine life, and this process is pre-

sumed to be accentuated in infants who have polycythe-

mia. (44)

Polycythemia and hyperviscosity have been implicated

as pathogenic factors in necrotizing enterocolitis (NEC),

particularly in term or near-term neonates. (45)(46)(47)

(48)(49) Historically, polycythemia has been identified

in up to half of all term infants who have NEC.

(46)(47)(48) Although altered splanchnic perfusion iswidely considered to cause gut mucosal injury in affected

infants, recent data indicate that attempts to reduce the

hematocrit with partial exchange transfusions (PET) also

could contribute to the risk of NEC. (36)(42)(49)

Renal manifestations of polycythemia include de-

creased glomerular filtration rates, oliguria, hematuria,

proteinuria, and renal vein thrombosis. (5)(7) Thrombo-

ses can also be seen in other sites. Thrombocytopenia can

be seen in up to one third of all cases, presumably due to

platelet consumption in the microvasculature. (50)(51)

In neonates who have polycythemia due to increased

erythropoiesis, thrombocytopenia may also be related to




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progenitor steal, the diversion of hematopoietic pro-

genitors toward erythropoiesis at the expense of other

lineages. (8)(18) Overt disseminated intravascular coag-

ulation is rare. (51)

DiagnosisThe diagnosis of polycythemia requires detection of a

venous hematocrit of at least 65% (0.65). (2)(3)(4)

This cut-off finds its origins in studies on blood viscosity

that show an exponential increase in viscosity above this

value. (3)(7) However, clinical evidence for this thresh-

old remains scant; studies have shown only modest

concordance between a hematocrit greater than 65%

(0.65) and actual demonstration of hyperviscosity. (7)

Although blood viscosity could be a useful guide fordeciding appropriate management strategies in affected

patients, hematocrits continue to be widely used surro-

gate markers of hyperviscosity due to limited availability

of tools for direct measurement of blood viscosity.

Detection of high hematocrits (55% [0.55]) in cord

blood could help predict the risk of polycythemia at

2 hours postnatal age, but such screening has not

gained acceptance because of the lack of data showing

that treatment of asymptomatic newborns who have

elevated hematocrits alters outcomes. (3) The possibility

of polycythemia should be considered in any infant ex-

hibiting signs of hyperviscosity. Detection of a highhematocrit in the first few hours after birth should trigger

a follow-up measurement in a few hours to identify any

further rise with normal postnatal fluid shifts. (3)

Close attention must be paid to the technique of

sample collection while interpreting the test results. Cap-

illary blood samples often show hematocrits that are 5%

to 15% higher than venous samples, and, therefore, high

hematocrit measurements in samples obtained by heel-

sticks should be confirmed in a free-flowing venous sam-

ple. (3)(52) The technique of sample analyses should

also be taken into account during serial evaluation of

results because microcentrifuge hematocrit may beslightly higher (due to trapped plasma of about 2%) than

that calculated from RBC volume and RBC count deter-

mined by hematology analyzer. (1)

Neonates who have polycythemia should be evaluated

for underlying causes such as intrauterine growth restric-

tion, maternal diabetes, or birth asphyxia. Because clini-

cal manifestations of hyperviscosity can overlap with

other conditions, alternative causes for the symptoms

should always be carefully excluded. Infants also should

be monitored for systemic complications of polycythe-

mia such as thromboses, NEC, hypoglycemia, hypocal-

cemia, hyperbilirubinemia, and thrombocytopenia.

TreatmentThe management of polycythemia is controversial be-

cause of the lack of evidence showing that aggressive

treatment improves long-term outcomes. Asymptomatic

infants whose central hematocrits are between 60%

(0.60) and 70% (0.70) can be monitored closely and

aggressively hydrated with adequate enteral intake or

administration of intravenous fluids. The hematocrit

should be reassessed in 12 to 24 hours, and plasma

glucose and bilirubin and cardiorespiratory status should

be monitored. If the hematocrit decreases or remains

stable and the patient remains asymptomatic, monitoring

can be continued for a further 24 to 48 hours. In asymp-

tomatic infants whose hematocrits are greater than 70%

(0.70), the treatment options are controversial. Al-though traditional treatment has been PET, studies show

a lack of difference in outcomes with continued hydra-

tion and expectant management versus aggressive man-

agement with PET. (36)(42) In the absence of a consen-

sus, the decision to perform PET is usually taken on a

case-by-case basis, with a careful analysis of risks and

potential benefits.

To perform PET, a precalculated volume of blood

(calculated to reduce the central hematocrit to 50%

[0.50] to 55% [0.55]) is replaced by an equivalent vol-

ume of normal saline, 5% albumin, commercially avail-

able solutions of human plasma protein fraction, or freshfrozen plasma. Colloid solutions do not offer any thera-

peutic advantages over normal saline and, at least in some

studies, have been associated with a higher incidence of

NEC. (53) Because of its lower cost, ready availability,

and absence of risk of transfusion-associated infection,

normal saline is generally accepted as the replacement

fluid of choice for PET in infants who have polycythemia.

(54)(55)

The total blood volume to be exchanged is deter-

mined as follows:

[Total blood volume (patients hematocrit desired hematocrit)]/(patients hematocrit)

where total blood volumethe patients weight in kilo-

grams multiplied by a presumed blood volume of

90 mL/kg. PET can be performed through a single

umbilical venous catheter using a pull-push technique

(withdrawal of blood alternated with replacement of

fluid through a single catheter) or by withdrawing blood

from an umbilical or peripheral arterial catheter and

administering replacement fluid simultaneously through

an umbilical or peripheral venous catheter. Regardless of

the sites used, small aliquots of 5 mL/kg or less should




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be used for removal or delivery, with each step carried

out over 2 to 3 minutes.

Several randomized studies have evaluated the efficacy

of PET in patients who have polycythemia (Table 2).

Malan and de V Heese (n49), (56) Goldberg and

colleagues (n20), (57) Black and coworkers (n94),

(58) and Ratrisawadi and associates (n42) (59) ran-

domly assigned infants to receive either PET using

plasma or supportive care. Bada and colleagues (n28)

(60) compared PET using a commercially available

human plasma protein solution with supportive care.

Kumar and Ramji (61) randomized 45 infants to periph-

eral PET using normal saline or to routine medical

management. None of these six studies documented abeneficial effect of PET on neurodevelopmental out-

come. Dempsey and Barrington (42) systematically re-

viewed five of these studies to investigate whether

PET was associated with improved short- and long-term

outcomes in neonates who had polycythemia. They doc-

umented no improvement in long-term neurologic out-

come (mental developmental index, incidence of devel-

opmental delay, and incidence of neurologic diagnoses)

after PET in symptomatic or asymptomatic infants.

There was also no evidence of improvement in early

neurobehavioral assessment scores (Brazelton neonatal

behavioral assessment scale). PET could have been asso-ciated with an earlier improvement in symptoms, but the

data were insufficient to calculate the size of the effect.

Ozek and coworkers (36) reviewed six randomized

trials to determine the effect of PET on primary out-

comes of mortality and neurodevelopmental outcomes at

2 years and at school age. Secondary outcomes included

seizures, cerebral infarction, NEC (Bell stage 2 or greater),

hypoglycemia, hyperbilirubinemia, and thrombocytope-

nia. Only one study reported data on mortality, and no

significant increase was noted with PET (RR, 5.23; 95%

CI, 0.66, 41.26). Four studies reported neurodevelop-

mental outcomes at 18 months or older, and no signifi-cant delay was reported in the PET group (typical RR,

1.45; 95% CI, 0.83 to 2.54 including all studies and

typical RR, 1.35; 95% CI, 0.68 to 2.69 when only

randomized, controlled trials were included). How-

ever, these results were based on data limited by poor

follow-up and did not account for patients who were lost

to follow-up. The authors performed a worst case/best

case scenario post hoc analysis, which showed a signifi-

cant skewing toward or away from the association of

PET with poor neurodevelopmental outcomes and was

considered to reflect the wide distribution of data points

rather than actual outcomes. The authors concluded that

there is no significant benefit of PET in asymptomatic

patients or those who have mild symptoms.

Patients who have polycythemia and show signs or

symptoms that may be related to hyperviscosity are fre-

quently treated with PET, even though the practice is

not supported by high-quality evidence. The arguments

in favor of PET are based on the pathophysiology of

hyperviscosity syndrome because most of the symptoms

are presumed to be related to altered microcirculatory

perfusion and tissue hypoxia. (5)(7) By replacing some of

the circulating RBC mass with a crystalloid solution,

PET is believed to reduce blood viscosity and improve

end-organ perfusion. However, no randomized clinical

studies demonstrate a clear benefit of PET in the treat-ment of symptomatic polycythemia. The groups led by

Bada, (60) Ratrisawadi, (59) and Kumar (61) random-

ized only asymptomatic polycythemic infants, while

those led by Black, (58) Goldberg, (57) and Malan (56)

made no distinction between symptomatic and asymp-

tomatic newborns. In nonrandomized clinical reports,

PET has been shown to lower pulmonary vascular resis-

tance, improve cerebral blood flow velocity, (63)(64)

and possibly normalize cerebral hemodynamics and im-

prove the clinical status of infants who have polycythe-

mia. (65) However, the long-term benefits of PET re-

main unclear.Concerns remain about potential adverse events fol-

lowing PET. PET was associated with an increased risk

of NEC in the systematic reviews performed by both

Dempsey (42) (RR, 8.68; 95% CI, 1.06 to 71.1) and

Ozek (36) (two studies: typical RR, 11.18; 95% CI, 1.49,

83.64 and typical risk difference, 0.14; 95% CI, 0.05,

0.22). Malan and de V Heese (56) reported that 1 of

their 24 patients in the exchanged group developed NEC

within the first 24 hours after PET compared with none

of the control patients. Black and associates (58) re-

corded NEC in 8 of their 43 infants in the PET group

compared with none of the 50 control infants. PET alsodid not alter the frequency of hypoglycemia (two studies)

or thrombocytopenia (one study). (36) Given the risks of

PET for polycythemia in the newborn and the lack of

evidence indicating clear benefit, we are generally reluc-

tant to use PET in asymptomatic infants. We do offer

PET for treatment of infants who have symptoms that

could be ascribed to hyperviscosity, but this decision is

taken cautiously, with a careful review of all risk factors.

Routine use of PET in neonatal polycythemia is not

supported by current evidence, and further study is

needed to identify patients who would be more likely to

benefit from aggressive correction of polycythemia.




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Table

2.

ClinicalTrialsofPartialExchangeTra

nsfusioninNeonatalP

olycythemia

Study

Randomization/

SampleSize

Hematocrit(Hct)

atEnrollment

ModeofExchange/

Repla

cementfluid

OutcomeMeasuremen

ts

Studiesincludedinthemeta-analysisbyOzeketal(36)

Studiesincludedinthemeta-analysisbyDempseyandBarrington(42)

Malanand

deVHeese

(56)

Notclearlys

tated;

n49

Hct>65%

(0.6

5)

UVC

FFP

Brazeltonneonatalscale

Prechtlneurologic

assessmentat

10days

Neurodevelopmental

assessmentat

8months

Goldbergetal

(57)

Notclearlys

tated;

n20

Hct>64%

(0.6

4)

andhyperviscosity

UVC

FFP

Brazeltonneonatalscale

at8hours,

24hours,

72hours,and

2weeks

BSIDandneurologic

assessmentat

8months

Blacketal(58)

Randomized;

n93

Antecubitalvenous

Hct>65%

(0.6

5)

andhyperviscosity

UVC

FFP

Neonatalsigns

BSIDandneurologic

assessmentat1and

2years

Cognitivetestingat

7years

Badaetal(60)

Notclearlys

tated;

n28

Radialartery

Hct>65%

(0.6

5)

Routenotstated;

Pla

smaprotein

solution

CerebralarteryDoppler

measurement

BSIDorcognitive

testingat30months

Ratrisawadietal

(59)

Randomized;

n105

Centralvenous

Hct>65%

(0.6

5)

Routenotstated

GaselDevelopmentat

1.5

to2years

Hakansonetal

(62)*

Notclearlys

tated;

n24

Hyperviscosity

(undefined)

Notclearlystated;

FFP

BSIDat8months

Kumarand

Ramji(61)

Randomized;

n22

Peripheralvenous

Hct>70%

(0.7

0)

Peripheral;Normal

saline

Neurologicdeficitsat

3,

6,

9,

12,

18month

s

FFP

fresh

frozenp

lasma,

BSID

Bay

ley

Scale

ofInfantDeve

lopment,UVCum

bilica

lvenous

line,

*a

bstracton

ly




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American Board of Pediatrics Neonatal-Perinatal

Medicine Content Specifications

Know the causes of neonatal polycythemia.

Know the clinical manifestations,

management, and outcomes of neonatal

polycythemia.

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NeoReviews Quiz

6. Polycythemia represents an abnormal elevation of the circulating red blood cell mass, which increases therisk of hyperviscosity, microcirculatory hypoperfusion, and multisystem organ dysfunction. Of the following,the hematocrit threshold that best defines polycythemia is:

A. 55% (0.50).B. 60% (0.60).C. 65% (0.65).D. 70% (0.70).E. 75% (0.75).

7. Polycythemia in neonates is often associated with metabolic complications. Of the following, the mostcommon metabolic abnormality associated with polycythemia in neonates is:

A. Hyperchloremia.B. Hyperkalemia.C. Hypernatremia.D. Hypocalcemia.E. Hypoglycemia.

8. The treatment of polycythemia includes partial exchange transfusion in which a precalculated volume ofblood is replaced by an equivalent volume of fluid. Of the following, the mostaccepted choice of fluid forpartial exchange transfusion is:

A. Albumin solution.B. Fresh frozen plasma.C. Lactated Ringer solution.D. Normal saline.

E. Plasma protein fraction.




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DOI: 10.1542/neo.12-1-e202011;12;e20-e28NeoReviews

Juan I. Remon, Aarti Raghavan and Akhil MaheshwariPolycythemia in the Newborn

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