Download Growth in Children With Congenital Heart Disease

Growth in Children With Congenital Heart Disease
WHAT’S KNOWN ON THIS SUBJECT: Children with congenital
heart disease (CHD) are at increased risk for poor growth.
Several factors may play a role in poor growth, including feeding
difficulties, increased caloric requirements, and the effects of
cardiac lesions on growth regulation.
WHAT THIS STUDY ADDS: In children with CHD, impaired growth
as measured by weight, length, and head circumference occurs
simultaneously rather than sequentially, supporting the theory
that altered growth regulation likely plays an important role in
the poor growth of children with CHD.
abstract
OBJECTIVE: We sought to describe growth in young children with
congenital heart disease (CHD) over time.
METHODS: We performed a retrospective matched cohort study, identifying children with CHD in a large primary care network in Pennsylvania, New Jersey, and Delaware and matching them 10:1 with control
subjects. The primary endpoint was the difference in mean World
Health Organization z score for cases and controls for weight-forage (WFAZ), length-for-age (LFAZ), weight-for-length (WFLZ), and head
circumference-for-age (HCFAZ) at traditional ages for preventive visits,
stratified by CHD category.
RESULTS: We evaluated 856 cases: 37 with single ventricle (SV) physiology, 52 requiring complex repair (CR), 159 requiring simple repair
(SR), and 608 requiring no repair. For children in the SV, CR, and SR
categories, large, simultaneous, and statistically significant (Student’s
t test P , .05) decreases in WFAZ and LFAZ appeared within the first
month of life, peaked near 4 months, and persisted through 24 or 36
months. There were fewer and smaller decreases in the no-repair
group between 2 and 18 months. HC data were available between 1
week and 24 months; at those ages, decreases in mean HCFAZ
generally paralleled decreases in WFAZ and LFAZ in the SV, CR, and
SR groups.
CONCLUSIONS: Children with CHD experience early, simultaneous
decreases in growth trajectory across weight, length, and head circumference. The simultaneous decrease suggests a role for altered growth
regulation in children with CHD. Pediatrics 2013;131:e236–e242
AUTHORS: Carrie Daymont, MD, MSCE,a,b Ashley Neal, MD,c
Aaron Prosnitz, MD,d and Meryl S. Cohen, MDe
aDepartment of Pediatrics and Child Health, University of
Manitoba, Winnipeg, Canada; bThe Manitoba Institute of Child
Health, Winnipeg, Canada; cBoston Children’s Hospital, Boston,
Massachusetts; dYale-New Haven Children’s Hospital, New Haven,
Connecticut; and eDivision of Cardiology, Department of
Pediatrics, The Children’s Hospital of Philadelphia, The Perelman
School of Medicine at the University of Pennsylvania,
Philadelphia, Pennsylvania
KEY WORDS
congenital heart disease, growth, nutrition, failure to thrive
ABBREVIATIONS
CHD—congenital heart disease
CR—complex repair
HC—head circumference
HCFAZ—head circumference-for-age z score
ICD-9—International Classification of Diseases, Ninth Revision
IGF-1—Insulin-like growth factor 1
LFAZ—length-for-age z score
NR—no repair
R-C—repair-combined
SR—simple repair
SV—single ventricle
WFLZ—weight-for-length z score
WHO—World Health Organization
WFAZ—weight-for-age z score
Dr Daymont participated in the conception and design of the
study, analyzed the data, drafted the manuscript, and approved
the final manuscript as submitted; Dr Neal participated in the
acquisition of data, critically revised the manuscript for
important intellectual content, and approved the final
manuscript as submitted; Dr Prosnitz participated in the
acquisition of data, critically revised the manuscript for
important intellectual content, and approved the final
manuscript as submitted; and Dr Cohen participated in the
conception and design of the study, contributed to the
interpretation of results, critically revised the manuscript for
important intellectual content, and approved the final
manuscript as submitted.
www.pediatrics.org/cgi/doi/10.1542/peds.2012-1157
doi:10.1542/peds.2012-1157
Accepted for publication Aug 20, 2012
Address correspondence to Carrie Daymont, MD MSCE, The
Manitoba Institute of Child Health, 655A-715 McDermot Ave,
Winnipeg, Manitoba, R3E 3P4, Canada. E-mail: [email protected]
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).
Copyright © 2013 by the American Academy of Pediatrics
FINANCIAL DISCLOSURE: The authors have indicated they have
no financial relationships relevant to this article to disclose.
FUNDING: Dr Daymont’s time was supported by the Manitoba
Health Research Council and The Manitoba Institute of Child
Health.
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DAYMONT et al
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ARTICLE
Congenital heart disease (CHD) is the
most common congenital anomaly, affecting ∼8 in 1000 children.1 In addition
to the management of the specific heart
defect, practitioners are often challenged by issues related to the facilitation of normal growth and development
in this population. Growth status in
these vulnerable children may be associated with neurodevelopmental outcomes in addition to adult height and
weight.2–4 Risk factors for poor growth
are multifactorial and may include the
increased metabolic demands of congestive heart failure, poor oral-motor
skills, the physiologic impact of the
primary cardiac defect, and associated
genetic and noncardiac disease.5–7
The timing of growth differences may
provide insight into both the causes of
poor growth and critical periods for
possible intervention. Therefore, we
sought to evaluate longitudinal growth
in young children with CHD of variable
severity compared with the growth of
healthy peers.
METHODS
We performed a retrospective cohort
study comparing attained growth in
children with CHD to matched controls
without CHD as well as published references. We used electronic medical
record data from a large primary care
network. The records included data
from 33 practices in urban, suburban,
and semirural locations in Pennsylvania, New Jersey, and Delaware. Practices in the network started using the
electronic record between August 2001
and June 2006.
Patient Selection
We identified children born after January 1, 2000, and before January 31, 2009,
with International Classification of Diseases, Ninth Revision (ICD-9) codes for
structural CHD who had been seen in
a primary care practice and had at least
2 weight measurements before age 3
years in the electronic record. Each
chart was reviewed individually by at
least 1 author to confirm a true diagnosis of CHD. Children born prematurely
(before 37 weeks of gestation) and
those with ICD-9 codes for noncardiac
complex chronic conditions (as defined
by Feudtner et al,8 including “malignancy,
neuromuscular, respiratory, renal, gastrointestinal, immunodeficiency, and
metabolic, genetic, and other congenital anomalies”8), were excluded from
the analysis.
Cases were categorized into 1 of 4 categories of CHD: single-ventricle (SV)
physiology; 2-ventricle heart disease
requiring complex repair (CR), defined
as Risk Adjustment for Congenital Heart
Surgery 1 class 3 or higher; 2-ventricle
heart disease requiring simple repair
(SR), defined as Risk Adjustment for
Congenital Heart Surgery class 1 or 2;
and 2-ventricle heart disease requiring
no repair (NR).9 Cases were classified on
the basis of indicated or planned repair
at the last evaluable visit rather than
whether repair had occurred at the time
of the last evaluated visit. Chart review
was used to determine the age at repair.
Measures
All measurements for weight, length or
height, and head circumference (HC)
recorded before January 31, 2010, were
obtained from the electronic medical
record. Attained growth z scores for
each parameter (as well as weight-forlength were determined for the World
Health Organization (WHO) 2006 growth
standard by using data from the WHO
Anthro macro.10 Growth parameters
that were determined likely to be nonrepresentative of actual growth based
on the deviation of the recorded value
from inverse distance-weighted means
of the subject’s growth parameters
were excluded from analysis; values
that were extreme but consistent with
a subjects’ other growth parameters
were included.11–13
PEDIATRICS Volume 131, Number 1, January 2013
Evaluation of growth parameters in
a different cohort from the same primary care network indicated that the
distribution of growth parameters in
this regional population was not welldescribed by the WHO growth curves
or by the Centers of Disease Control
growth reference, as has been shown
in other populations.15–17 To identify a
population against which to compare
growth, each case was matched to 10
control subjects in the primary care
network database by year of birth (61
year), gender, race, and primary care
site. Site group (urban versus all others) was used to match when there
were insufficient controls in a site.
Some controls were excluded during
analysis because of insufficient growth
measurements at the evaluated ages.
Primary Analysis
The ages at which growth data were
available for each patient varied widely.
Therefore, we were unable to evaluate
each case’s growth compared with its
own controls at each age. Instead, we
evaluated growth at the ages of typical
preventive visits, comparing the mean
attained z score for cases and controls
for each of the four CHD classes separately. The birth age group consisted
only of measurements on the first day of
life, and the other age groups included
visits at the ages at which children were
most commonly seen for preventive visits in the network. We used a 1-week
range of ages for the 1- and 2-week visits;
a 2-week range for the 1-, 2-, and 4-month
visits; a 1-month range for the 6-, 9-, 12-,
15-, and 18-month visits, and a 2-month
range for the 24- and 36-month visits.
The analyses were limited to the first 36
months of life because of the relative
scarcity of measurements after that
age. When $1 value was available for
a subject in an age group, 1 value per
subject per age group was selected.
Visits designated as preventive visits
were retained preferentially, otherwise
selection was random.
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The primary endpoint was the difference in mean growth WHO z score for
weight-for-age (WFAZ), length-for-age
(LFAZ), weight-for-length (WFLZ), and
HC-for-age (HCFAZ) between cases and
controls in each group at each time
point. We evaluated the statistical significance of the differences by using
the Student’s t test with a threshold of
P = .05. Differences between CHD categories were evaluated by using linear
regression.
The proportion of subjects with a z score
#1.88 (corresponding to the third percentile) was also compared for cases
and controls. For this analysis, the SV,
CR, and SR groups were analyzed together as the repair-combined (R-C)
group to have sufficient sample size.
Statistical significance of the difference between cases and controls was
evaluated by using Fisher’s exact test
with a threshold of P = .05. Differences
between CHD categories were evaluated by using logistic regression.
Exploratory Analysis of Age and
Repair Status
Across CHD severity and growth parameters, the greatest difference between
cases and controls was seen near 4
months of age. An exploratory post hoc
analysis was designed to compare the
association of improvement in WFAZ
with age and with repair status in the R-C
group. All available measurements, including those taken at ages not traditionallyassociated withpreventivevisits,
were included in this analysis. Mixed
effects models were designed by using
the “xtmixed” command in Stata 11.2
to compare the change in slopes (Dz
score/time in years) of WFAZ before and
after a certain time point for cases and
controls clustered at the level of subject
nested within case group (a case and its
matched controls). We compared the
change in WFAZ slopes before and after
4 months of age for cases and controls
and then compared the change in WFAZ
slopes before and after the age at the
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cases’ second surgery (or first surgery
if only 1 surgery was done). Cases with
the first or second repair done after 365
days of life were excluded from this
analysis.
All analyses were performed by using
Stata 11.2. This project was approved by
the Institutional Review Board at the
Children’s Hospital of Philadelphia.
RESULTS
Identified Cases
There were 1862 potential cases initially
identified based on ICD-9 codes for CHD
(Fig 1). Three hundred twenty potential
cases were excluded because the subject did not have CHD; in most of these
cases, the ICD-9 code had been used to
indicate potential CHD that was not
confirmed with diagnostic testing. Ultimately, 64 116 visits from 856 cases
and 7674 controls were included in the
primary analysis (Supplemental Table
3). Characteristics of included cases
are described in Table 1 with primary
diagnostic categories in Table 2.
During data cleaning, 0.8% of weight,
2.5% of length, and 1.2% of HC measurements were excluded because they
FIGURE 1
Flow sheet describing exclusion of ineligible cases.
DAYMONT et al
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were likely to be nonrepresentative of
the subjects’ growth. A sensitivity analysis was performed including interpolated data to replace excluded values;
results were almost identical to that of
the primary analysis.
Growth in Controls
The means and SDs for WFAZ, LFAZ, LFAZ,
and HCAZ for controls were significantly
different from zero (P , .05) at many
ages for all 4 growth parameters (Fig
2). Z scores using Centers for Disease
Control growth curves were also significantly different from zero at many
ages.18 Therefore, our primary analysis
was performed as planned by using the
difference between case and control
mean WHO z scores at the various time
points as the primary endpoint.
Comparison of Means
At birth, WFA and LFA z scores for cases
in the SV, CR, and SR groups were all
lower than control z scores at birth, but
differences were relatively small and
were statistically significant (P , .05)
only for LFA in the SR group (Fig 2 and
Fig 3). For children with CHD requiring
repair, larger and statistically significant
ARTICLE
TABLE 1 Characteristics of Cases
Characteristic
SV
CR
SR
NR
n (cases)
n (controls)
Median age (d) at first repair
Male
Race
Asian
Black/African American
Native American
White
Other
37
344
4
23 (62%)
52
464
5
31 (60%)
159
1377
126
85 (53%)
608
5489
NA
260 (43%)
0 (0%)
12 (32%)
0 (0%)
24 (65%)
1 (3%)
2 (4%)
11 (21%)
0 (0%)
32 (62%)
7 (13%)
12 (8%)
43 (27%)
2 (1%)
92 (58%)
10 (6%)
15 (2%)
150 (25%)
1 (,1%)
367 (60%)
75 (12%)
Because gender and race were used as matching criteria, the proportions are the same in controls as for cases. NA, not
applicable.
differences appeared by 1 week of age.
Peak differences for WFAZ occurred at
4 months of age in each category: 21.6
(SV), 21.5 (CR), 20.6 (SR), 20.2 (NR).
Peak differences for LFAZ were 21.4 at
4 months (SV), 21.3 at 2 months (CR),
20.6 at 2 months (SR), and 20.3 at 0.5
months (NR). Differences in growth
were smaller after 4 months of age but
persisted through age 36 months, ex-
TABLE 2 Diagnostic Categories of Cases
with CHD by Repair Category
CHD Diagnostic
Categories
SV CR SR
NR
Hypoplastic left heart
14
syndrome
Tricuspid atresia
5
Unspecified single ventricle
13
abnormality
Double-outlet right ventricle
1 4
Pulmonary valve abnormalities 4 2 13 84
Transposition of the great
21
arteries
Truncus arteriosus
3
Atrioventricular canal
9
Coronary abnormalities
3
Tetralogy of Fallot
5 24
Total anomalous pulmonary
1
1
venous return
Partial anomalous pulmonary
1
venous return
Aortic abnormalities
1 19
Aortic valve abnormalities
3
6 75
Pulmonic artery abnormalities
2
2
Patent ductus arteriosus
23 24
Atrial septal defect (including
17 54
patent foramen ovale)
Ventricular septal defect
40 360
Vascular ring
8
2
Mitral or tricuspid valve
6
abnormalities
Other
5
1
Total
37 52 159 608
cept WFAZ in the SR group. The decreases in mean WFAZ between cases
in the NR group and matched controls
were small compared with the decreases for children requiring repair
but were significant between 2 and 18
months.
There were substantial differences
between controls and cases requiring
repair in length as well as weight. Accordingly, decreases in WFLZ were
generally smaller than for WFAZ.
Few HC measurements were available
at birth and 36 months in the electronic
record, so only measurements between
1 week and 24 months were evaluated.
Even at those ages, HC was measured
less often than weight and length. Between 2 weeks and 24 months, the pattern of differences in HCFAZ between
cases and controlswas generally similar
to the pattern seen for weight and length
with a few important exceptions. There
was no difference in mean HCFAZ between cases and controls in the NR
group. There were also no differences in
HCFAZ between cases and controls in the
SV group at 9 months and older, but
a substantial decrease in HCFAZ persisted for cases in the CR and SR groups.
the combined repair group, cases were
significantly more likely than controls
to be less than the third percentile for
all growth parameters starting at 1
month of age and persisting through 24
months (WFAZ), 36 months (LFAZ), and 9
months (HCFAZ). In the NR group, differences in proportions for cases and
controls were statistically significant at
fewer ages. For WFAZ, differences in the
R-C group were significantly larger than
for the NR group at 1, 2, 4, and 6 months.
The odds ratios for being less than the
third percentile for cases versus controls were generally large in the postnatal period. At 2 months, the odds
ratios for the R-C group were 12.1
(WFAZ), 3.8 (LFAZ), and 20.9 (HCFAZ) and
for the NR group were 3.9 (WFAZ), 2.1
(LFAZ), and 2.5 (HCFAZ).
Exploratory Analysis of Age and
Repair Status
There were 25 973 visits from 180 cases
and 1643 controls included in the following analyses. The median age at
second repair (or first if only 1 was
performed) was 130 days (interquartile
range 46–213). Among cases in the R-C
group, increasing z scores were, temporally, more strongly associated with
age than with repair status. There was
a large, significant increase in slopes
(Dz score/time in years) for WHO weight
z score before and after 4 months (b =
4.2, 95% confidence interval 3.6–4.9).
The difference in slopes before and after repair was smaller (b = 2.1, 95%
confidence interval 1.7–2.5). This overall
pattern of findings was robust to sensitivity analyses excluding data from the
first month after surgery and using the
age at first surgery rather than second
surgery when .1 was performed.
Comparison of Proportion Below
the Third Percentile
DISCUSSION
There was no difference in the proportion of cases and controls with
growth parameters below the third
percentile (z score #1.88) at birth in
either the R-C or NR categories (Fig 4). In
Within weeks of birth, children with
CHD show large, early, statistically significant deficits in weight, length, and
HC trajectory compared with matched
controls without CHD from the same
PEDIATRICS Volume 131, Number 1, January 2013
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FIGURE 2
Means and 95% confidence intervals at typical ages for preventive visits for WHO z scores for cases and controls. Means are plotted when data were available for
at least 6 cases. Statistically significant differences (P , .05 using Student’s t test) are marked with a small plus.
primary care network. The largest differences in weight occurred at 4 months
of age. Full catch-up growth was not seen
by 36 months for children with CHD requiring repair. Children with CHD requiring repair were much more likely
to be below the third percentile for
weight, length, and HC in early infancy.
The magnitude and timing of differences
for WFAZ and LFAZ for cases in the SV
group were similar to those published
by Williams et al in 2011, and the
magnitude of differences in WFAZ at 1
year for cases in the CR and SR groups
was similar to those described by
Knirsch et al.19,20
A small increase in the risk of poor
growth is seen even in the population of
patients with CHD that does not require
surgery (NR group). The majority of
subjects in this group had ventricular
septal defects, which may be hemodynamically significant early in life even if
they later self-resolve.
FIGURE 3
Median weight for cases requiring CR and matched controls plotted on WHO growth curve. Values for
male and female subjects are combined by converting female z scores to the equivalent weight for male
subjects and plotting on the male growth curve. All time points demonstrated statistically significant
(P , .05) differences between case and control groups at $1 month.
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DAYMONT et al
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The strengths of our study include
comparison of growth of cases with
a control population rather than solely
with published references, the relatively large sample size, and the confirmation of diagnoses with chart
review rather than reliance solely on
billing codes. Analysis of cases using z
scores without comparison with peers
would have mischaracterized the differences between these children with
CHD and healthy children. For example,
at 6 months of age, 5.8% of cases, and
0.5% of controls in the C-R group had
microcephaly (HC less than third percentile). Therefore, cases were 11.6
times as likely as controls to have microcephaly. If we had compared them
only to the WHO standards, the expected proportion of underweight would
have been 3%, and it would have appeared that cases were only 1.9 times
as likely as healthy children to have
microcephaly, dramatically underestimating the difference between
children with CHD and healthy children
from the same population. Extensive
efforts were also made to identify
ARTICLE
to other factors, such as genetic abnormalities, decreased growth factors, and
hormonal changes. When caloric intake
is inadequate to meet demands, effects
are generally seen in weight before
length and finally HC. In this population,
no lag was seen between the decreased
growth trajectory for cases in WFAZ, LFAZ,
and HCFAZ. This simultaneous change in
trajectory supports the idea that impaired growth in children with CHD requiring repair is mediated at least in
part by factors unrelated to nutrition.
FIGURE 4
Proportion of controls versus cases below the third percentile for weight (WFA), length (LFA), and HC
(HCA) for age. The R-C includes subjects from the SV, CR, and SR categories. Statistically significant
differences (P , .05 using Fisher’s exact test) are marked with a small red plus.
erroneous values without eliminating
values from subjects with growth at the
extremes of the distribution. The limitations of our study include its reliance
on a single network, its retrospective
nature, the lack of HC data at birth and
in the neonatal period, lower case
numbers for specific categories of disease complexity, and the variability in
timing of growth measurements. We
also did not have sufficient information
to determine whether some patients
were cyanotic before repair, which
likely has a large impact on growth.7,21
HC become apparent, particularly in
the SV and CR groups, is a significant
limitation to our study. Review of 3
published studies evaluating HC at
birth in children with CHD does not
reveal a consistent answer.22–25
A postnatal decrease in HC growth velocity in children with CHD would indicate a restriction of brain growth
during the critical developmental period of infancy and may have lifelong
effects on neurodevelopment.2,3 It is
important to determine whether this
decrease in HC growth in children with
CHD is confirmed in other studies and
whether it is modifiable by nutritional
or other treatments. The lack of HC
values at birth and our subsequent
inability to determine more precisely
the time point at which differences in
It is important to identify the etiology of
poor growth in CHD in order to guide
attempts to improve growth. Inadequate caloric intake certainly plays
a role in poor growth for at least some
children with CHD.19 Children with CHD
frequently have feeding difficulties,6
and many have increased metabolic
demands as a result of their cardiac
defect.26 These higher demands are often most profound in the first 6 months
of life as pulmonary vascular resistance
decreases. However, decreased growth
in children with CHD may also be related
One previous study found no association between prerepair weight ,10th
percentile and neurodevelopmental outcomes among children with CHD. However, the sample size of 101 subjects may
not have been sufficient to identify an
association if one were present, and the
study did not formally assess HC.20
PEDIATRICS Volume 131, Number 1, January 2013
Dinleyici et al identified decreases in
insulin-like growth factor 1 (IGF-1), an
important anabolic hormone affecting
childhood growth, in children with
CHD, particularly those who are cyanotic.21 Another recent study identified
increases in IGF-1 and its carrier protein
insulin-like growth factor binding
protein-3 after surgical repair in children with acyanotic CHD.27 Although
the authors postulate that these
increases are related to improved
postoperative nutrition, the increase in
growth factors may be more directly
related to the repair, which often
results in resolution of congestive
heart failure with improved cardiovascular physiology. However, our exploratory analysis of time at repair did
not suggest a strong independent association between repair and growth
velocity in the overall population. Rather,
a consistent improvement of growth velocity at ∼4 months was seen. Prospective evaluation will be crucial to
confirm this finding and to determine if
it is related to diet, such as the addition
of solid foods at ∼4 months of age, or
primarily mediated by growth factors
or other physiologic changes.
CONCLUSIONS
Children with complex CHD have large,
early, and sustained decreases in
growth trajectory compared with their
peers. The simultaneous change in all
3 parameters seen in this analysis
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supports the role of factors beyond
calorie balance in the growth of children
with CHD. However, the extent to which
the poor growth seen in children with
CHD is caused by potentially modifiable
factors, such as the amount and type of
nutrition support, medical treatment of
CHD, and timing of surgical repair, is
unclear. Additional observational studies
would provide information to allow appropriate design of randomized controlled trials. Such studies would ideally
beprospective evaluationsof populations
in other centers and include longitudinal
evaluations of body growth, head growth,
and neurodevelopment. Study designs
involving data on nutritional support,
metabolic rate and demands, CHD treatment, degree of CHF and cyanosis, as well
as biochemical markers associated with
growth, including hormones and inflammatory markers, would add greatly
to our understanding of the growth and
development of children with CHD.
10. WHO Anthro for personal computers, version 3, 2009: Software for assessing growth
and development of the world’s children.
Geneva: World Health Organization; 2009.
Available at: www.who.int/childgrowth/
software/en. Accessed August 27, 2010
11. Shepard D. A two-dimensional interpolation
function for irregularly-spaced data. ACM ’68:
Proceedings of the 1968 23rd ACM National
Conference. New York, NY: ACM Press; 1968:
517–524. Available at: http://portal.acm.org/
citation.cfm?doid=800186.810616. Accessed
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R, Herbst K. Data cleaning: detecting, diagnosing, and editing data abnormalities.
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Available at: www.census.gov/srd/papers/pdf/
rr9805.pdf. Accessed November 11, 2011
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Ong KK. Monitoring head size and growth
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e242
DAYMONT et al
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Growth in Children With Congenital Heart Disease
Carrie Daymont, Ashley Neal, Aaron Prosnitz and Meryl S. Cohen
Pediatrics; originally published online December 10, 2012;
DOI: 10.1542/peds.2012-1157
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PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly
publication, it has been published continuously since 1948. PEDIATRICS is owned, published,
and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk
Grove Village, Illinois, 60007. Copyright © 2012 by the American Academy of Pediatrics. All
rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.
Downloaded from by guest on May 2, 2017
Growth in Children With Congenital Heart Disease
Carrie Daymont, Ashley Neal, Aaron Prosnitz and Meryl S. Cohen
Pediatrics; originally published online December 10, 2012;
DOI: 10.1542/peds.2012-1157
The online version of this article, along with updated information and services, is
located on the World Wide Web at:
/content/early/2012/12/05/peds.2012-1157
PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly
publication, it has been published continuously since 1948. PEDIATRICS is owned,
published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point
Boulevard, Elk Grove Village, Illinois, 60007. Copyright © 2012 by the American Academy
of Pediatrics. All rights reserved. Print ISSN: 0031-4005. Online ISSN: 1098-4275.
Downloaded from by guest on May 2, 2017