Seminars in Fetal & Neonatal Medicine (2008) 13, 248e255

available at www.sciencedirect.com

journal homepage: www.elsevier.com/locate/siny

Neonatal polycythemia and hyperviscosity

Shikha Sarkar, Ted S. Rosenkrantz*

Department of Pediatrics, Division of NeonatalePerinatal Medicine, University of Connecticut School of Medicine,

263 Farmington Avenue, Farmington, CT 06030, USA

KEYWORDS Summary Neonatal polycythemia and hyperviscosity are defined as a hematocrit 65% and
Hyperviscosity; a viscosity value >2 standard deviations greater than the norm. Although polycythemia can re-
Organ blood flow; flect normal fetal adaptation, it has been thought to be responsible for abnormalities in the
Partial exchange neonate. Polycythemia and hyperviscosity are associated with blood-flow changes in some or-
transfusion; gans, which alter their function. Partial exchange transfusion (PET) has been used to treat both
Polycythemia symptomatic and asymptomatic patients. At present, no data support the use of PET in asymp-
tomatic infants; the potential benefit in symptomatic infants depends on the symptoms. Stud-
ies of long-term neurodevelopmental status do not show any clear long-term benefits for PET.
Crystalloids are as effective as colloids in PET and have the advantage of being cheaper and
more readily available; also, they do not confer any risk of infection or anaphylaxis.
2008 Elsevier Ltd. All rights reserved.

Introduction The following is a review of the alterations in physiology

Polycythemia of the neonate was first mentioned in the Bible
(Genesis 25:25). In the 1970s, there were a number of case
reports and small series of infants with symptoms that were
thought to be secondary to an elevated hematocrit and blood
viscosity.1e3 This was followed by clinical studies of larger
populations of infants, with the emphasis on polycythemia
and cerebral function. In the 1980s, several investigators ex-
amined the relationship between polycythemia, hyperviscos-
ity, and organ system dysfunction, which helped delineate
the changes in organ function as a result of increases in he-
matocrit, viscosity, and arterial oxygen content.
* Corresponding author. Tel.: 1 860 679 3105; fax: 1 860 679
1403.
E-mail address: rosenkrant@nso1.uchc.edu (T.S. Rosenkrantz).
and organ function in newborn infants with polycythemia
and hyperviscosity, clinical correlations, and recommenda-
tions about potential therapies for these infants.
Incidence
The incidence of polycythemia and hyperviscosity at sea
level is 1e2%, whereas at 1600 ft (430 m) it has been shown
to be 5%.4 Infants who experience chronic or acute fetal
hypoxia have a higher incidence. Premature infants less
than 34 weeks gestation rarely have polycythemia or
hyperviscosity.
The measured values for hematocrit and viscosity are
affected by a number of factors. Capillary and peripheral
vein sources with poor flow overestimate the hematocrit.
Samples of blood from a free-flowing or central source will
yield a true value. They are also affected by the timing at
which it is drawn after birth. Finally, the hematocrit is

1744-165X/$ - see front matter 2008 Elsevier Ltd. All rights reserved.
doi:10.1016/j.siny.2008.02.003
Neonatal polycythemia and hyperviscosity 249

affected by the technique used for analysis, spun is higher

but more accurate than automated.

Definitions

Polycythemia and hyperviscosity are not synonymous

terms. Both values vary depending on the source of blood
(umbilical vein, peripheral vein, or capillary sample), age
of the infant at the time of measurement and the
methodology of processing the blood.5
Most researchers define neonatal polycythemia as a he-
matocrit 65% when obtained from a large, freely flowing
peripheral vein. Gross et al. defined hyperviscosity as
a value that was 2 standard deviations greater than the
mean6; Ramamurthy and Brans defined hyperviscosity as 3
standard deviations from the mean for blood obtained
from three different sites (peripheral vein, capillary, and
umbilical vein).5 This coincided with an umbilical venous
hematocrit value of 63%. Ramamurthy and Brans found
that the capillary values were higher than the peripheral Figure 1 The shaded area represents the viscosity of cord
vein values, which were higher than the umbilical vein blood, at shear rates from 2 to 212 s1, for 102 healthy, full-
values. term AGA infants (mean  2 standard deviations). Viscosity
Polycythemia occurs as a result of increased red cell for 18 symptomatic infants is plotted at shear rates of
mass, with a decreased, normal, or increased plasma 11 s1 and 106 s1. Hematocrit (Hct) values for each group
volume.7 The hematocrit peaks at 4e6 h of life, then drops are indicated. Note that the viscosity values increase with
slowly over the next 12e18 h and, by 24 h, it has become higher hematocrit values and with lower shear rates (from
similar to the value at birth; thereafter it stays relatively Ref. 6, with permission).
stable.8 These changes are caused by transudation of fluid
out of the intravascular space.
It is important to understand the physics of the flow of
fluids to understand how blood viscosity affects blood flow Hematocrit
in the newborn infant.9 Viscosity, as defined by Poiseuille,
is the ratio of shear stress to shear rate: The hematocrit has a logarithmic relationship with blood
0 4
viscosity at different shear rates. The most significant
p  p r p shear stress
hZ Z changes take place at the lowest shear rates and at
8lQ shear rate hematocrits that exceed 65% (see Fig. 1).
where h Z is blood viscosity (dynes/s per square centime-
ter or poise), (p  p0 ) Z pressure gradient across the blood Plasma proteins
vessel, r Z radius, l Z length of the blood vessel, and
Q Z blood flow. Plasma viscosity (1.0e1.5 centipoise (cP)) is similar to that
The shear stress represents the pressure gradient of water and could be considered a Newtonian fluid under
along the blood vessel expressed in dynes.10 The shear normal conditions. It does not contribute significantly to
rate represents the velocity between the two fluid planes the blood viscosity of the newborn. It may be a problem
divided by the distance between them, expressed as per in adults with hyperproteinemic states such as Walden-
second (s1). In homogeneous, or Newtonian fluids viscos- stroms macroglobulinemia.
ity remains constant even as shear stress and shear rate
change. Blood, being a suspension of particles, does not Red blood cell deformability
behave as a Newtonian fluid. The viscosity of blood
does not remain constant with variations in the shear RBCs contribute significantly to blood viscosity, both be-
stress and shear rate (Fig. 1). The shear rates in large cause they are the most prominent particle suspended in
vessels, such as the aorta, are greater (100e300 s1) the blood and because of their intrinsic properties. RBCs
than those observed in the arterioles (11e25 s1). Thus consist of a membrane surrounding an internal body of
the viscosity in the aorta would be lower than the fluid. RBCs in newborns have a greater degree of deform-
arterioles. ability than adult RBCs. The viscosity of internal fluid
increases with increasing cell age and also decreasing shear
Factors that affect blood viscosity rate.

Although a number of factors affect the viscosity of the White blood cells
blood, the hematocrit, i.e. the concentration of red blood
cells (RBCs), is the primary determinant in the newborn White blood cells (WBCs) are larger than RBCs; they are also
infant. less deformable. However, WBCs do not affect blood
250
viscosity unless their number significantly exceeds the
normal count, such as in congenital leukemia.
Fibrinogen
Fibrinogen contributes little to blood viscosity as it is
normally low in the newborn.
Platelets
Although the platelets are inflexible, under normal condi-
tions they do not contribute much to blood viscosity. They
can affect blood viscosity in adults with conditions such as
vaso-occlusive disease, as platelet aggregates will increase
blood viscosity in small or narrow vessels.
Blood pH
Blood viscosity increases with acidosis. At a blood pH < 7
fluid enters the RBCs and alters their shape. This phenom-
enon might play an important role in increasing the viscos-
ity in neonates with birth asphyxia.
Blood vessel size
In large blood vessels like the aorta, the blood flow and the
shear rate (100e300 s1) are high compared with the arteri-
oles (11e25 s1). Thus, the viscosity in the aorta is lower
than the arterioles. This does not apply to capillaries ranging
in diameter from 3 to 5 mm. Fahraeus and Lindqvist showed
that viscosity decreases with decreasing size of capillaries.
Figure 2 Blood viscosity in small capillaries (from Ref. 11,
with permission).
S. Sarkar, T.S. Rosenkrantz
This phenomenon, referred to as bolus flow, reflects high
hemodynamic efficiency.11 Thus, the hematocrit does not
affect blood viscosity at the capillary level (Fig. 2).
Clinical etiologies of polycythemia
and hyperviscosity
Erythropoiesis in the human fetus varies with the arterial
oxygen content (CaO2) of the blood delivered to the kidney.
Decreased oxygen delivery to the kidney results in increased
erythropoietin production and release by the fetal kidney.
Circulating erythropoietin stimulates the production of
RBCs. The endpoint is sufficient oxygen-carrying capacity
and delivery to keep the fetus well oxygenated. The three
common mechanisms of polycythemia are reviewed below.
Chronic fetal hypoxia
A host of fetal and intrauterine factors can lead to chronic
fetal hypoxia, and in turn result in increased fetal eryth-
ropoiesis, RBC mass, hematocrit, and blood viscosity. The
increase in RBC mass compensates for the low partial
pressure of oxygen (PaO2) of the fetus resulting in a normal
CaO2 and tissue oxygenation. Pregnancy-related conditions
associated with chronic fetal hypoxia include maternal dia-
betes, pregnancy-induced hypertension, fetal hyperthy-
roidism, and maternal smoking.
Maternal diabetes is associated with an increased risk of
intrauterine hypoxia. These neonates have a high preva-
lence of polycythemia, elevated erythropoietin levels, and
decreased iron and ferritin levels. Hod et al. showed an
increased prevalence of polycythemia in infants of diabetic
mothers (13.3%) versus controls (4.9%).12 However, hypoxia
and polycythemia can be prevented with good maternal
glycemic control. Fetal hyperthyroidism is associated with
increase in the fetal metabolic rate and results in chronic
hypoxia and polycythemia in the newborn. Maternal smok-
ing leads to increased levels of carbon monoxide, which
crosses the placenta and competes with oxygen for fetal
hemoglobin-binding sites.
Acute fetal hypoxia
Perinatal asphyxia and acute fetal hypoxia remain signifi-
cant causes of polycythemia. Acute intrauterine hypoxia
results in a shift of blood from the placental compartment
to the fetus.13 Philip et al. examined placental residual vol-
umes and neonatal outcomes.14 Fetal distress and low Ap-
gar scores were associated with low residual placental
volumes. There is a correlation between duration of hyp-
oxia and the volume of blood shifted into the fetal compart-
ment. The data also suggest that fetal vasodilatation
associated with acute fetal hypoxia is responsible for this
shift in blood volume.
Delayed cord clamping and stripping
of the umbilical cord
Stripping the umbilical cord towards the neonate leads to
a significant placental transfusion, polycythemia, increased
Neonatal polycythemia and hyperviscosity
blood volume, and increased RBC mass, especially if the
neonate is being held below the level of the placenta.
Saigal and Usher raised the first concern regarding delayed
cord clamping contributing to polycythemia in 1977.15 More
recent randomized studies have confirmed higher hema-
tocrits in both preterm and term infants with late cord
clamping as opposed to early cord clamping (30 s).16
Linderkamp et al. demonstrated a marked rise in the cord
blood viscosity of infants with delayed cord clamping.17
Polycythemia is often seen in BeckwitheWeiderman
syndrome and with trisomies 13, 18, and 21. The etiologies
are unknown.
Altered hemodynamics
Polycythemia and hyperviscosity are associated with alter-
ations in organ blood flow. In general, there is a decrease in
organ blood flow due to changes in red cell mass, CaO2,
and/or viscosity.
The brain
Polycythemia and blood hyperviscosity were presumed to
cause brain hypoxia and ischemia due to a reduction in the
brain blood flow resulting from sludging of RBC within small
blood vessels. A series of experiments performed between
1980 and 1995 has clarified the changes in brain blood flow,
oxygen delivery, and utilization of glucose. Rosenkrantz
and Oh used Doppler techniques to demonstrate a reduction
of brain blood flow in neonates with polycythemia that
returned to normal after partial exchange transfusion
(PET).18 To understand the factors responsible for the re-
duction in brain blood flow they performed further experi-
ments using newborn lambs. Data from these studies
revealed that the changes in the brain blood flow resulted
from an increase in the CaO2, a normal physiologic response
that correlated with an increase in the hematocrit.19
Therefore the decrease in cerebral blood flow in the new-
born with polycythemia is a physiologic response and does
not cause cerebral ischemia.
Heart and lungs
There is a decrease in cardiac output secondary to an increase
in the arterial oxygen content. Systemic oxygen transport,
delivery, consumption, and blood pressure are normal.20 Pul-
monary vascular resistance increases and pulmonary blood
flow decreases. This is thought to be due to changes in blood
viscosity. The decreased pulmonary blood flow can cause re-
spiratory distress and cyanosis. It can be reversed with a re-
duction in the hematocrit and blood viscosity.20
Kidneys
Renal function is compromised. Kotagal and Kleinman used
puppies to demonstrate that polycythemia, associated with
a decreased plasma volume, did not change renal blood
flow.21 However, the renal plasma flow, the glomerular filtra-
tion rate, urine output, and the urine sodium and potassium
excretion were greatly reduced. If the polycythemia is
251
accompanied by expanded blood volume, as with delayed
clamping of the umbilical cord, then the glomerular filtration
rate and urine output are normal.22 In summary, the renal
function is dependent on both hematocrit and blood volume.
Gastrointestinal tract
Nowicki et al. have demonstrated decreased intestinal
blood flow, oxygen extraction, and uptake in both the
unfed and fed state.23 Human studies have shown an ele-
vated bile concentration in serum and a low lipase and tryp-
sin activity in the duodenum on the first day of life.24
Partial exchange transfusion did normalize the bile and li-
pase levels but increased the risk of necrotizing enterocoli-
tis (NEC), especially if the fluid used for PET was fresh
frozen plasma (FFP).25
Metabolic
Neonates with polycythemia are at risk for hypoglycemia.
It is unclear if this is due to decreased gluconeogenesis or
increased utilization. Glucose is present in the plasma
fraction of the blood. As many infants with polycythemia
have a reduced plasma volume, the whole blood glucose
concentration might be significantly reduced even when
the plasma concentration is normal. Studies in poly-
cythemic newborn lambs demonstrated that at low to
normal plasma glucose concentration values, cerebral
glucose delivery and uptake was less than normal.26
These experiments also proved that it is the cerebral glu-
cose delivery, not the glucose concentration, that is the
limiting factor in cerebral glucose uptake. Black et al.
found that concurrent hypoglycemia placed polycythemic
infants at the highest risk of poor neurologic function.27
The finding of decreased cerebral glucose delivery and
uptake associated with normoglycemia in the lamb model
leads to the speculation that this might be one reason for
the neurologic sequelae observed in human polycythemic
neonates.
Clinical features
Polycythemia and hyperviscosity can affect multiple organ
systems and the affected neonate can present with a variety
of symptoms. The neonate appears ruddy or reddish
(rubeosis) with sluggish capillary refill and poor peripheral
perfusion. The most common clinical features associated
with polycythemia include lethargy, tachypnea, tremulous-
ness, irritability, jaundice, poor feeding, and vomiting.
Some of these features can be attributed to the associated
metabolic problems such as hypoglycemia (Table 1).28,29
Central nervous system
Polycythemia and hyperviscosity are associated with both
short- and long-term effects on the central nervous system.
Some of the immediate symptoms include lethargy, irrita-
bility, tremulousness, and e rarely e seizures. Several
studies have looked at the long-term neurologic outcomes.
A study of 20 infants by Goldberg et al. made no distinction
between symptomatic and asymptomatic infants and
252 S. Sarkar, T.S. Rosenkrantz

Table 1 Frequency of clinical symptoms observed in association with polycythemia and hyperviscosity (from Ref. 29, with
permission)
Clinical symptoms Gross et al.6 Ramamurthy and Brans5 Black et al.27 Goldberg et al.29
(n Z 18) (%) (n Z 54) (%) (n Z 111) (%) (n Z 20) (%)
Cyanosis 89 17 7 Nr
Plethora 83 63 Nr Nr
Tremulousness/jitteriness 67 13 Nr Nr
Abnormal EEG 33 Nr Nr Nr
Seizures 28 0 0 Nr
Respiratory distress 44 4 10 15
Cardiomegaly 17 Nr Nr 85
Lethargy/poor feeding Nr 50 55
Hyperbilirubinemia 50 6 Nr 5
Abnormal blood smear 50 Nr Nr Nr
Thrombocytopenia 39 Nr Nr 25
Hypoglycemia 33 Nr 27 40
Hypocalcemia 6 Nr Nr 0
, Greater incidence compared with the control group; EEG, electroencephalogram; Nr, not reported or examined.

divided them into three groups: polycythemic infants who Cardiopulmonary

were treated with PET, polycythemic infants who were
observed, and controls.30 The Bayley Scales of Infant Devel-
opment; MilanieComparetti Postural Reflex Examination;
and medical, neurological, and physical examinations
were performed on all three groups. Neurological abnor-
malities were found in all three groups: polycythemia
treated (67%), polycythemia observed (50%), and controls
(17%). There was also a higher incidence of spastic diplegia
in the two polycythemic groups.30
Van der Elst et al. made no distinction between
symptomatic and asymptomatic infants in the 49 infants
included in their study.10 There was no difference between
the observed group and the group who underwent PET in
the Brazelton neonatal assessment scale (BNBAS) and
Prechtl scores at 10 days.
A study by Ratrisawadi et al. of 105 asymptomatic
infants had 38% follow up at 2 years. An abnormal devel-
opmental quotient was defined as less than 100 on the
Gasel development test and was present in 11/25 treated
with PET and 4/15 in controls.31 Global developmental
delay at 1.5e2 years was found in infants with
polycythemia.
Bada et al. studied 28 asymptomatic infants who un-
derwent PET32; the infants were assessed at 24 months or
greater. PET did not affect long-term neurodevelopmental
outcome. The researchers used multivariate analysis, which
revealed that other perinatal risk factors, such as fetal dis-
tress, asphyxia, hypoglycemia, maternal pre-eclampsia,
and race, were responsible for the long-term neurodevelop-
mental sequelae in these infants, not the polycythemia.
They concluded that the intrauterine events are the cause
of both polycythemia and the developmental delays.
Black et al. investigated a sample size of 93 term
polycythemic infants, making no distinction between symp-
tomatic and asymptomatic infants.33 They followed these
infants until 2 years of age and identified a group who
had mental delay (this term was not further defined).
They found no neurologic benefit in patients who had
received PET.
There is no evidence of lasting cardiopulmonary complica-
tions from neonatal polycythemia. Cyanosis, tachypnea,
cardiomegaly, pulmonary vascular congestion, pleural effu-
sions, and pulmonary hypertension are due to elevated
pulmonary vascular resistance and increased intrapulmo-
nary shunting secondary to increased blood viscosity.32 Mur-
phy et al. demonstrated elevated right ventricular pre-
ejection to right ventricular ejection time ratios in 19
asymptomatic polycythemic infants. They also showed that
the peak rate of left ventricular emptying was lower in
a group of polycythemic infants than in age-matched con-
trols. These infants also had evidence of decreased stroke
volume and cardiac output leading to the clinical manifesta-
tions of cyanosis, tachycardia, murmurs, and signs of con-
gestive heart failure.34 Most investigators have reported
complete resolution of respiratory symptoms with PET.
Gastrointestinal
Multiple studies have reported on infants with polycythe-
mia and poor feeding and vomiting35; some suggest an asso-
ciation between neonatal polycythemia and NEC.36 Most of
these infants had other risk factors for NEC, such as intra-
uterine growth retardation, birth asphyxia, or both. In
a randomized study, Black et al. observed that 6% of the un-
treated polycythemic infants exhibited gastrointestinal
symptoms, whereas 51% of those who received PET ex-
hibited serious gastrointestinal symptoms, including NEC.
This study suggested that the most important risk factor
for developing NEC is PET, not polycythemia itself. Those
receiving FFP during PET were at highest risk.25 Martinez-
Tallo et al. studied a group of polycythemic term infants
and showed little or no association between polycythemia
and NEC.37 Boehm et al. showed evidence of delayed post-
natal development of lipase and trypsin activity and also al-
tered enterohepatic circulation, which might explain the
feeding intolerance observed in these infants.24
Neonatal polycythemia and hyperviscosity
Renal
Neonates present with a decreased urine output and reduced
excretion of sodium and potassium.21 In polycythemic infants
with normal blood volume, these renal changes are thought
to be due to decreased plasma volume, renal plasma flow,
and the glomerular filtration rate.22 PET will improve renal
function in these infants. Urine analysis sometimes shows
proteinuria and elevated levels of urinary N-acetyl-b-D-
glucosaminidase, which signify renal tubular damage.38
Endocrine and metabolic
The two common metabolic abnormalities encountered in
these infants are hypoglycemia and hypocalcemia. Hypo-
glycemia occurs in 12e40% of infants, after correcting for
factors such as intrauterine growth restriction (IUGR).31 Al-
though there has been speculation about the mechanism,
decreased production versus increased uptake, there is no
definite consensus.39
Saggese et al. postulated that hypocalcemia was the
result of increased levels of calcitonin gene-related peptide
(CGRP).40 In a clinical study of 43 polycythemic infants and
20 controls, CGRP values were significantly elevated in the
polycythemic group, both at birth and at 16e36 h after
birth. Lower levels of 1,25-cholecalciferol and 24,25-chole-
calciferol were found in polycythemic infants when com-
pared with controls. Alkalay et al. proposed that the
hyperviscosity interfered with the ability of the kidneys to
convert 25-hydroxyvitamin D to its active dihydroxyl
metabolites.41
Treatment
Therapy for polycythemia and hyperviscosity is fraught with
controversy. The recommended therapy for symptomatic
infants is hemodilution by PET. Before considering PET the
infant should be evaluated for other causes of the observed
problems. PET has been shown to decrease pulmonary
vascular resistance, increase cerebral blood flow,18 correct
hypoglycemia, and improve renal function. It does not cor-
rect neurologic abnormalities in the newborn period or pre-
vent long-term neurologic dysfunction. Complications of
PET are thought to be similar to a single or double volume
exchange transfusion.
The goal of PET is to reduce the infants hematocrit and
viscosity while maintaining circulatory volume. The follow-
ing formula is used to calculate the volume of blood that
requires to be exchanged:
PETZcirculating blood volume
observed hematocrit  desired hematocrit
 sue damage.
observed hematocrit
Term infant intravascular volume Z 80e90 mL/kg
Desired hematocrit Z 50e55%
The Committee of the Fetus and Newborn of the American
Academy of Pediatrics (AAP) issued the following statement
253
regarding the treatment of neonatal polycythemia with
PET, especially in those without symptoms. The statement re-
flects the uncertainty regarding this modality of treatment42:
The accepted treatment of polycythemia is PET. How-
ever, there is no evidence that exchange transfusion
affects long-term outcome. Universal screening for poly-
cythemia fails to meet the methodology and treatment
criteria and also, possibly the natural criterion.
Despite this ambivalent statement, the standard of care in
many neonatal intensive care units continues to be PET for
symptomatic infants with hematocrits >65% and asymp-
tomatic infants with hematocrits >70%.43
Dempsey and Barrington performed a systematic review
evaluating short- and long-term outcomes following PET in
polycythemic infants.44 Their objective was to determine
whether PET is associated with improved short- and long-
term outcomes. The outcome measures included the
following:
 The proportion of infants with neurological diagnosis,
developmental delay, and or motor delay at 18 months
or older.
 Short-term neurological and behavioral assessment scores.
 Short-term resolution of clinical symptoms attributed
to polycythemia.
 Adverse effects.
The five randomized, controlled trials that the authors in-
cluded in their meta-analysis were: Van der Elst et al.,10
Goldberg et al.,30 Ratrisawadi et al.,31 Bada et al.,32 and
Black et al.33 The main results from the meta-analysis sug-
gested that there is no evidence for an improvement in
long-term neurological outcome (mental developmental in-
dex, incidence of mental delay, and incidence of neurologi-
cal diagnoses) after PET in symptomatic or asymptomatic
infants. Also, there was no evidence of improvement in early
neurobehavioral assessment (BNBAS). Partial exchange
transfusion might be associated with an early improvement
in some of the clinical symptoms associated with polycythe-
mia and hyperviscosity but the data were insufficient to de-
rive any conclusions. The incidence of NEC was increased,
but this was more often associated with the use of FFP as
the exchange fluid. The long-term outcome is most likely to
be related to the underlying cause of polycythemia.
Schimmel et al. made the following recommendations
based on the above studies45:
 In an asymptomatic polycythemic infant with presumed
normal or increased blood volume: monitoring is
sufficient.
 In symptomatic patients with a hematocrit >65%: PET
with normal saline should be used to reduce ongoing tis-
 In patients with reduced blood or plasma status, e.g.
IUGR infants: treatment should be with early feeding
or plasma expansion with intravenous fluids.
 Consider PET in asymptomatic polycythemic infants
with presumed normal plasma and blood volume only
if repeated measurements reveal a venous hematocrit
>75%.
254
Partial exchange transfusion: Fluid type
The other area of controversy regarding PET is the type of
fluid that should be used to perform the procedure:
crystalloid versus colloid. Systematic reviews of the liter-
ature were performed by De Waal et al. and Dempsey and
Barrington.46,47 The objective of both these reviews was to
determine whether crystalloid solutions were as effective
as colloid solutions when PET is performed in neonates
with polycythemia. The De Waal et al. review included six
relevant randomized controlled trials with a total of 235 in-
fants.46 The Dempsey and Barrington review included four
controlled, randomized studies, with a total of 200 pa-
tients.47 There was considerable overlap between these
two reviews and the conclusions were similar. Four studies
were included in both reviews. These were the studies by
Deorari et al.,48 Rothmaier et al.,49 Wong et al.,50 and
Krishnan and Rahim.51 The fluids used included plasma, sa-
line, Ringers lactate, 5% albumin, and FFP. The conclusion
of both reviews was that crystalloid solutions are as effec-
tive as colloid solutions for PET. Crystalloid solutions have
the additional benefits of lack of transmission of blood-
borne diseases and anaphylaxis, rapid and easy availability,
and the fact that they are less expensive. Crystalloid solu-
tions should therefore become standard for PET.
Summary
Polycythemia and hyperviscosity are common in the new-
born. Some of the clinical findings in such infants are
attributable to the increased hematocrit and blood viscos-
ity, and PET might improve these problems. However, PET
does not appear to prevent or reverse neurologic abnor-
malities found in this population.
Practice points
 Diagnosis of polycythemia is affected by sampling
site, timing, and the technique used for analysis.
 Polycythemia, hyperviscosity, and their associated
complications are the end results of acute or
chronic intrauterine hypoxia.
 PET is the recommended treatment for symptom-
atic infants.
 There are no clear, long-term neurological bene-
fits from PET.
 Crystalloids are as effective as colloids and have
the advantages of being cheaper, easily available,
and not conferring risk of infections or
anaphylaxis.
Research agenda
 To decide which infants should be treated.
 To determine optimal treatment.
 To search for interventions to improve short- and
long-term outcomes.
S. Sarkar, T.S. Rosenkrantz
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