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Organizational Principles to Guide and Dene the Child

Health Care System and/or Improve the Health of all Children

STATEMENT OF ENDORSEMENT

Neonatal Encephalopathy and Neurologic Outcome,


Second Edition
The American Academy of Pediatrics has endorsed the following publication: American College of Obstetricians and
Gynecologists. Executive summary: neonatal encephalopathy and neurologic outcome. Obstet Gynecol. 2014;123:896901
(executive summary follows on next page).

All statements of endorsement from the American Academy of Pediatrics automatically expire 5 years after publication unless reafrmed, revised, or retired at or
before that time.
www.pediatrics.org/cgi/doi/10.1542/peds.2014-0724
doi:10.1542/peds.2014-0724
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275).
Copyright 2014 by the American Academy of Pediatrics

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Neonatal Encephalopathy and Neurologic Outcome,


Second Edition
Report of the American College of Obstetricians and Gynecologists
Task Force on Neonatal Encephalopathy

Neonatal Encephalopathy and Neurologic Outcome, EXECUTIVE SUMMARY


Second Edition, was developed by the Task Force on
Neonatal Encephalopathy: Mary E. DAlton, MD, Chair, Gary In the rst edition of this report, the Task Force on Neonatal Encephalopathy
D.V. Hankins, MD, Vice Chair, Richard L. Berkowitz, MD, and Cerebral Palsy outlined criteria deemed essential to establish a causal
Jessica Bienstock, MD, MPH, Alessandro Ghidini, MD, Jay
Goldsmith, MD, Rosemary Higgins, MD, Thomas R. Moore, link between intrapartum hypoxic events and cerebral palsy. It is now known
MD, Renato Natale, MD, Karin B. Nelson, MD, Lu-Ann that there are multiple potential causal pathways that lead to cerebral palsy
Papile, MD, Donald Peebles, MD, Roberto Jose Romero,
MD, Diana Schendel, PhD, Catherine Yvonne Spong, MD,
in term infants (see Fig 1), and the signs and symptoms of neonatal en-
Richard N. Waldman, MD, Yvonne Wu, MD, MPH, and the cephalopathy may range from mild to severe, depending on the nature and
American College of Obstetricians and Gynecologists timing of the brain injury. Thus, for the current edition, the Task Force on
staff: Gerald F. Joseph Jr, MD, Debra Hawks, MPH, Alyssa
Politzer, MA, Chuck Emig, MA, and Kelly Thomas. Neonatal Encephalopathy determined that a broader perspective may be
more fruitful. This conclusion reects the sober recognition that knowl-
edge gaps still preclude a denitive test or set of markers that accurately
identies, with high sensitivity and specicity, an infant in whom
neonatal encephalopathy is attributable to an acute intrapartum
event. The information necessary for assessment of likelihood can
be derived from a comprehensive evaluation of all potential con-
tributing factors in cases of neonatal encephalopathy. This is the
broader perspective championed in the current report. If a compre-
hensive etiologic evaluation is not possible, the term hypoxicischemic
www.pediatrics.org/cgi/doi/10.1542/peds.2014-0724 encephalopathy should best be replaced by neonatal encephalopathy
doi:10.1542/peds.2014-0724 because neither hypoxia nor ischemia can be assumed to have been
PEDIATRICS (ISSN Numbers: Print, 0031-4005; Online, 1098-4275). the unique initiating causal mechanism. The title of this report has
Copyright 2014 by the American College of Obstetricians and been changed from Neonatal Encephalopathy and Cerebral Palsy:
Gynecologists, 409 12th Street, SW, PO Box 96920, Washington, DC Dening the Pathogenesis and Pathophysiology to Neonatal Enceph-
20090-6920. All rights reserved. No part of this publication may be
reproduced, stored in a retrieval system, or transmitted, in any alopathy and Neurologic Outcome to indicate that an array of develop-
form or by any means, electronic, mechanical, photocopying, re- mental outcomes may arise after neonatal encephalopathy in addition
cording, or otherwise, without prior written permission from the
publisher.
to cerebral palsy.
To determine the likelihood that an acute hypoxicischemia event
that occurred within close temporal proximity to labor and de-
livery contributed to neonatal encephalopathy, it is recommended
that a comprehensive multidimensional assessment be per-
formed of neonatal status and all potential contributing factors,
including maternal medical history, obstetric antecedents,
intrapartum factors (including fetal heart rate monitoring results
and issues relating to the delivery itself), and placental pathology.
A description of the items to be included in the assessment fol-
lows.

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FIGURE 1
Prenatal and perinatal causal pathways to cerebral palsy in term infants. Distal risk factors exert a pathogenic effect on fetal brain development starting at
a time that is remote from the onset of irreversible brain injury. Examples include genetic abnormalities, environmental and sociodemographic factors, and
some placental abnormalities. Proximal risk factors exert pathogenic effects on fetal brain development at a time that closely predates or coincides with the
onset of irreversible brain injury. Examples include abruptio placentae, chorioamnionitis, and twintwin transfusion. There are multiple potential causal
pathways that lead to cerebral palsy in term infants, and the signs and symptoms of neonatal encephalopathy may range from mild to severe, depending
on the nature and timing of the brain injury. A. Intrapartum brain injury that is due to a proximal risk factor may lead to neonatal encephalopathy and
subsequent cerebral palsy. B. Intrapartum brain injury may be the result of both distal and proximal risk factors that predispose the fetus to brain injury
and cerebral palsy. C. Brain injury or anomaly may occur in the antepartum period as a result of distal and proximal risk factors. When brain injury or
anomaly occurs at a time that is remote from the delivery process, neonatal encephalopathy may or may not be seen after birth. D. Brain injury may
occur at multiple points during gestation. E. Proximal risk factor and brain injury may occur in the neonatal period following predisposing distal risk
factors. Abbreviations: DRF, distal risk factor; PRF, proximal risk factor.

I. CASE DEFINITION associated with contributing events in of cerebral palsy. However, most
close temporal proximity to labor and infants with low Apgar scores
Neonatal encephalopathy is a clinically
delivery. The goal of the assessment is will not develop cerebral palsy.
dened syndrome of disturbed neu-
to compile a constellation of markers 2. There are many potential causes
rologic function in the earliest days of
concerning neonatal status, contribut- for low Apgar scores. If the Apgar
life in an infant born at or beyond 35
ing events, and developmental outcome score at 5 minutes is greater
weeks of gestation, manifested by
to determine if they are consistent with than or equal to 7, it is unlikely
a subnormal level of consciousness or
acute hypoxiaischemia and may not that peripartum hypoxiaischemia
seizures, and often accompanied by dif-
be explained by other etiologies. Thus, played a major role in causing
culty with initiating and maintaining
when more of the elements from each neonatal encephalopathy.
respiration and depression of tone and of the item categories are met, it
reexes. This expanded clinical denition B. Fetal Umbilical Artery Acidemia
becomes increasingly more likely that
must be put into use based on measures peripartum or intrapartum hypoxia 1. Fetal umbilical artery pH less than
that can be reliably and accurately ischemia played a role in the patho- 7.0, or base decit greater than
implemented by trained staff. The rst genesis of neonatal encephalopathy. or equal to 12 mmol/L, or both,
mandatory step in an assessment of increases the probability that neo-
neonatal encephalopathy is to conrm natal encephalopathy, if present,
whether a specic infant meets the case II. NEONATAL SIGNS CONSISTENT had an intrapartum hypoxic com-
denition. WITH AN ACUTE PERIPARTUM OR ponent; lesser degrees of acidemia
In conrmed cases of neonatal en- INTRAPARTUM EVENT decrease that likelihood.
cephalopathy, the following assess- A. Apgar Score of Less Than 5 at 5 2. If the cord arterial gas pH levels
ment will determine the likelihood that Minutes and 10 Minutes are above 7.20, it is unlikely that
an acute peripartum or intrapartum 1. Low Apgar scores at 5 minutes intrapartum hypoxia played a
event was a contributor. This list is and 10 minutes clearly confer an role in causing neonatal en-
based on the premise that neonatal increased relative risk of cere- cephalopathy.
encephalopathy that is due to acute bral palsy. The degree of Apgar 3. Although the aforementioned
hypoxiaischemia will be accompanied abnormality at 5 minutes and 10 thresholds are commonly ac-
by abnormal neonatal signs and be minutes correlates with the risk cepted as indicative of pathologic

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fetal acidemia, there is a contin- undertaken optimally at 10 days B. Fetal Heart Rate Monitor Patterns
uum of increasing risk of neonatal of life (with an acceptable win- Consistent With an Acute Peripartum
encephalopathy with worsening dow between 7 days and 21 days or Intrapartum Event
acidemia. It is important to re- of life) will best delineate the full 1. A Category I or Category II fetal
member that even in the pres- extent of cerebral injury. heart rate tracing when asso-
ence of signicant acidemia, 4. Despite the advances in neuro- ciated with Apgar scores of 7
most newborns will be neurolog- imaging, the ability to precisely or higher at 5 minutes, normal
ically normal. The presence of time the occurrence (estimating umbilical cord arterial blood
metabolic acidemia does not de- within days rather than hours or ( 1 SD), or both is not con-
ne the timing of the onset of minutes) of a hypoxicischemic sistent with an acute hypoxic
a hypoxicischemic event. event is still limited. ischemic event.
C. Neuroimaging Evidence of Acute D. Presence of Multisystem Organ Fail- 2. There is a great distinction to be
Brain Injury Seen on Brain MRI or ure Consistent With HypoxicIschemic made between a patient who ini-
Magnetic Resonance Spectroscopy Encephalopathy tially presents with an abnormal
Consistent With HypoxiaIschemia fetal heart rate pattern and one
1. Multisystem organ failure can in-
1. MRI is the neuroimaging modal- clude renal injury, hepatic injury, who develops an abnormal fetal
ity that best denes the nature hematologic abnormalities, cardiac heart rate pattern during labor.
and extent of cerebral injury in dysfunction, metabolic derange- a. A category II fetal heart rate
neonatal encephalopathy. Cranial ments, and gastrointestinal injury, pattern lasting 60 minutes or
ultrasonography and computed or a combination of these. more that was identied on
tomography lack sensitivity for
2. Although the presence of organ initial presentation with per-
the evaluation of the nature and
dysfunction increases the risk sistently minimal or absent
extent of brain injury in the term
of hypoxicischemic encepha- variability and lacking accel-
encephalopathic infant.
lopathy in the setting of neona- erations, even in the absence
2. Distinct patterns of neuroimag- tal encephalopathy, the severity of decelerations, is sugges-
ing abnormalities are recognized of brain injury seen on neuro- tive of a previously compro-
in hypoxicischemic cerebral in- imaging does not always corre- mised or injured fetus. If fetal
jury in the infant born at or be- late with the degree of injury to well-being cannot be estab-
yond 35 weeks of gestation and other organ systems. lished by appropriate re-
have prognostic value for pre-
sponse to scalp stimulation
dicting later neurodevelopmental
III. TYPE AND TIMING OF or biophysical testing, the pa-
impairments. If the results of the
CONTRIBUTING FACTORS THAT ARE tient should be evaluated for
MRI or magnetic resonance spec-
CONSISTENT WITH AN ACUTE the method and timing of de-
troscopy, obtained after the rst
PERIPARTUM OR INTRAPARTUM livery. An emergency cesar-
24 hours of life, are interpreted
EVENT ean delivery may not benet
by a trained neuroradiologist
A. A Sentinel Hypoxic or Ischemic a fetus with previous severe
and no areas of injury are
noted, then it is unlikely that Event Occurring Immediately Be- compromise.
signicant peripartum or intra- fore or During Labor and Delivery b. The patient who presents
partum hypoxicischemic brain 1. A ruptured uterus with a Category I fetal heart
injury was a signicant factor in rate pattern that converts to
2. Severe abruptio placentae
neonatal encephalopathy. It is im- Category III as dened by the
3. Umbilical cord prolapse Eunice Kennedy Shriver Na-
portant to note that the full extent
of injury may not be evident on 4. Amniotic uid embolus with coin- tional Institute of Child Health
MRI until after the rst week of life. cident severe and prolonged ma- and Human Development guide-
ternal hypotension and hypoxemia lines is suggestive of a hypoxic
3. Early MRI obtained between 24
hours and 96 hours of life may 5. Maternal cardiovascular collapse ischemic event.
be more sensitive for the delin- 6. Fetal exsanguination from either c. Additional fetal heart rate pat-
eation of the timing of perinatal vasa previa or massive fetoma- terns that develop after a Cat-
cerebral injury, whereas an MRI ternal hemorrhage egory I fetal heart rate pattern

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on presentation, which may agement and evaluation of the D. No Evidence of Other Proximal or
suggest intrapartum timing timing of cerebral injury, and Distal Factors That Could Be Con-
of a hypoxicischemic event, a second at day 10 of life or tributing Factors
include tachycardia with re- laterwill assist with full de- In the presence of other signicant risk
current decelerations and per- lineation of the nature and ex- factorssuch as abnormal fetal growth,
sistent minimal variability with tent of cerebral injury. maternal infection, fetomaternal hemor-
recurrent decelerations. 4. There are several well-dened rhage, neonatal sepsis, and chronic
C. Timing and Type of Brain Injury Pat- patterns of brain injury and placental lesionsan acute intrapartum
terns Based on Imaging Studies Con- their evolution on MRI that are event as the sole underlying pathogene-
sistent With an Etiology of an Acute typical of hypoxicischemic ce- sis of neonatal encephalopathy becomes
Peripartum or Intrapartum Event rebral injury in the newborn, in- much less likely.
1. Cranial ultrasonography lacks cluding deep nuclear gray matter
sensitivity for the common forms or watershed cortical injury. If IV. DEVELOPMENTAL OUTCOME IS
of brain injury in the encepha- a different pattern of brain injury SPASTIC QUADRIPLEGIA OR
lopathic newborn. However, if or evolution of injury exists on DYSKINETIC CEREBRAL PALSY
echodensity or echogenicity is de- MRI, then alternative diagnoses
A. Other subtypes of cerebral palsy
tected on cranial ultrasonography, should be actively pursued (eg,
are less likely to be associated with
as it may be the only neuroimag- metabolic and genetic investiga-
acute intrapartum hypoxicischemic
ing modality able to be obtained tions).
events.
in a very unstable infant, it is ob- 5. Certain patterns of brain injury
B. Other developmental abnormalities
servable 48 hours or longer after seen on MRIsuch as focal arte-
may occur, but they are not specic
an ischemic cerebral injury. Com- rial infarction, venous infarction,
to acute intrapartum hypoxicischemic
puted tomography lacks sensitiv- isolated intraparenchymal or in-
encephalopathy and may arise from
ity for brain injury in the newborn traventricular hemorrhage, por-
a variety of other causes.
and will often not reveal abnor- encephaly, or atypical patterns
malities in the rst 2448 hours of metabolic encephalopathies
after an injury. suggest that peripartum hypoxia NEUROIMAGING ADVANCES OVER
2. MRI and magnetic resonance ischemia did not play a role in THE PAST DECADE
spectroscopy are the most sen- causing neonatal encephalopathy. With the wider use of MRI, the recog-
sitive neuroimaging modalities to 6. Accurate interpretation of neu- nition of different patterns of injury has
assist with the timing of cerebral roimaging is important, and become established. Two main patterns
injury. MRIcombining conventional, ongoing education in the in- often are distinguished on MRI: 1) the
diffusion, and spectroscopy terpretation and reporting of basalgangliathalamus pattern and 2)
between 24 hours and 96 hours neonatal neuroimaging is en- the watershed or border zone pre-
of life provides the most useful couraged. If there is limited dominant pattern. In the interpretation
guide on the potential timing of a expertise in neonatal neurora- of the literature on MRI in neonatal
cerebral insult. diology and inconsistencies in encephalopathy, there are two major
3. Diffusion abnormalities are most the clinical prole of the in- weaknesses: 1) the exact timing of the
prominent between 24 hours and fant, an expert opinion should insult is generally not known and,
96 hours of life. With conven- be sought for the interpreta- more importantly, 2) there are little to
tional qualitative MRI, cerebral tion of the neuroimaging. no data on the neuropathological cor-
abnormalities will become most 7. In the presence of cerebral injury relate of the MRI pattern.
evident after 7 days from a cere- that is diagnostically consis- MRI studies have dened that the vast
bral injury. Two MRI or magnetic tent with a hypoxicischemic majority of cases of cerebral injury that
resonance spectroscopy scans pattern of injury, neuroimaging are seen in term-born infants with
the rst between 24 hours and cannot determine the etiology neonatal encephalopathy are acute. In
96 hours of life with emphasis of the hypoxia-ischemia, such comparison, epidemiologic studies have
on the evaluation of diffusion as placental insufciency or in- suggested that 70% of causation is re-
and spectroscopic abnormali- terruption of umbilical cord lated to chronic antenatal factors. This
ties to assist in clinical man- blood ow. apparent contradiction reects the fact

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that the MRI studies relate imaging imaging ndings. These studies should provided for performing a root cause
ndings in the rst 23 weeks of life include careful evaluation of the placenta. analysis as part of this process. Fur-
and demonstrate a subacute pattern. thermore, because many obstetricians
These studies cannot, however, de- and pediatricians who practice in small
OTHER ADVANCES
lineate if the injury occurred during hospitals will not be expected to en-
labor or within the days before labor Greater awareness of the importance of counter many cases of neonatal en-
and delivery. There are few studies that placental attributes and genetic sus- cephalopathy, an obstetric and neonatal
have imaged infants in the rst day of ceptibility to neonatal encephalopathy data collection tool is provided to serve
life to assist in the timing of ischemic has emerged, although both areas of as a guide for obtaining necessary in-
cerebral injury. MRI can provide mutual investigation are still fairly new. The formation to learn from these cases.
information from diffusion-weighted implementation of hypothermia for the
treatment of neonatal encephalopathy is
imaging, conventional imaging, and mag- CONCLUSIONS
netic resonance spectroscopy, which can a milestone in neonatal medicine and
inform timing. Information regarding represents the culmination of research In the decade since this report was rst
the likely timing is best obtained with spanning decades that has proved the published, considerable advances have
early imaging (rst 2496 hours of potential for neural rescue after peri- been made in the knowledge and
natal asphyxia. The recognition that understanding of the processes con-
life) with further follow-up imaging to
this therapy improves early childhood tributing to neonatal encephalopathy
dene the full nature of the abnor-
outcomes has accelerated the pace of and long-term neurodevelopmental
malities, optimally at 10 days of life
(but with an acceptable window be- investigations to nd other brain-oriented outcome, including the landmark in-
treatments. The fact that greater than troduction of neonatal hypothermia as
tween 7 days and 21 days of life,
40% of neonates undergoing hypother- a therapeutic intervention. Although
depending on the logistics of acquir-
mia treatment still develop adverse full understanding is still elusive, the
ing MRI in the clinical setting).
neurologic outcomes underscores the recommended multi-dimensional as-
It is now accepted that identifying the need to further understand the un- sessment process for neonatal enceph-
predominant pattern of brain injury is an derlying processes in neonatal enceph- alopathy described in this Executive
important predictor of neurodevelop- alopathy. Understanding the underlying Summary and in Chapter 13 reects the
mental outcome for a term newborn with processes, ideally, will yield more ef- current state of scientic knowledge
encephalopathy. It is important to note fective clinical criteria for matching and acknowledges limitations deni-
that most studies that relate patterns of each patient with tailored treatment tively distinguishing hypoxicischemic
injury to neurodevelopmental outcome options. The current emphasis in this encephalopathy from other forms of
undertook imaging after day 7 of life. document is on identication of the neonatal encephalopathy with the ar-
Conventional images provide a robust optimal criteria for the identication ray of clinical tools currently avail-
measure of the nature and severity of of cases in which there is a hypoxic or able. The multidimensional aspect of
injury when performed after 1 week from ischemic contribution to neonatal en- the assessment process is key to re-
the initial insult, which correlates well cephalopathy of recent onset, which cognizing that no single strategy to
with neurodevelopmental outcome. Con- inevitably will be much less stringent identify hypoxicischemic encepha-
ventional MRI in the rst 2496 hours of than dening essential criteria. lopathy is infallible and will achieve
life may underestimate the total extent of 100% certainty of the cause of neonatal
the injury but is better in timing. encephalopathy in all cases. Promoting
In summary, although MRI studies suggest PATIENT SAFETY a multidimensional perspective should
that the period around the time of birth A new and important addition to this stimulate the laboratory, clinical, and
accounts for more than 75% of the report is a review of patient safety epidemiologic research needed to ll
causative period, studies have not sys- efforts directed at preventing neonatal the knowledge gaps and better guide
tematically investigated the extent to which encephalopathy. Enhancing patient treatment and long-term prognosis of
injury may have occurred during the 24 safety requires changing the culture of neonatal encephalopathy, assist fami-
hours before delivery. Therefore, studies of health care delivery from one that lies in care and support of their af-
early (rst 48 hours of life) and serial (eg, names and blames to one that is ded- fected children, and improve clinical
day 1, 4, 10 of life) MRI in termborn en- icated to reducing medical errors practice.
cephalopathic infants are needed and will through a constructive, nonthreatening, The task force recognizes that this
assist in determining the evolution of and professional process. A template is report will require updating as the

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scientic database and knowledge input from the Centers for Disease  Australian Collaborative Cerebral
on this topic expands. Several impor- Control and Prevention* and the Eunice Palsy Research Group
tant areas of research are recom- Kennedy Shriver National Institute of  Child Neurology Society
mended, which are detailed in the text Child Health and Human Development,
of the full document. Those engaged in and the endorsement from the follow-  Japan Society of Obstetrics and Gy-
ing organizations has resulted in necology
research are encouraged to pursue
these areas and others to exert in- a highly peer-reviewed and scientically  March of Dimes Foundation
uence to the degree possible to propel rigorous document:  Royal Australian and New Zealand
this to a high priority for funding and  American College of Nurse-Midwives College of Obstetricians and Gynae-
study.  American Gynecologic and Obstet- cologists
Finally, the task force acknowledges the rical Society  Royal College of Obstetricians and
many consultants and support staff who  American Society for Reproductive Gynaecologists
made this project possible. In addition, Medicine  Society for Maternal-Fetal Medicine
co-publication of this report with the  Association of Womens Health, Ob-  Society of Obstetricians and Gynae-
American Academy of Pediatrics, the stetric and Neonatal Nurses cologists of Canada

The Royal College of Obstetricians and Gynae-


cologists has reviewed and approved the task
force report and provided its ofcial designation
of support in lieu of endorsement.

The information in Neonatal Encephalopathy and


Neurologic Outcome, Second Edition, should not be
viewed as a body of rigid rules. The guidelines are
general and intended to be adapted to many dif-
ferent situations, taking into account the needs
and resources particular to the locality, the insti-
tution, or the type of practice. Variations and in-
novations that improve the quality of patient care
*The ndings and conclusions in this task force are to be encouraged rather than restricted. The
report are those of the authors and do not nec- purpose of these guidelines will be well served if
essarily represent the ofcial position of the they provide a rm basis on which local norms
Centers for Disease Control and Prevention. may be built.

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Neonatal Encephalopathy and Neurologic Outcome, Second Edition
Pediatrics 2014;133;e1482
DOI: 10.1542/peds.2014-0724 originally published online April 28, 2014;

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Pediatrics is the official journal of the American Academy of Pediatrics. A monthly publication, it
has been published continuously since . Pediatrics is owned, published, and trademarked by the
American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois,
60007. Copyright 2014 by the American Academy of Pediatrics. All rights reserved. Print
ISSN: .

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Neonatal Encephalopathy and Neurologic Outcome, Second Edition
Pediatrics 2014;133;e1482
DOI: 10.1542/peds.2014-0724 originally published online April 28, 2014;

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://pediatrics.aappublications.org/content/133/5/e1482

Pediatrics is the official journal of the American Academy of Pediatrics. A monthly publication, it
has been published continuously since . Pediatrics is owned, published, and trademarked by the
American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois,
60007. Copyright 2014 by the American Academy of Pediatrics. All rights reserved. Print
ISSN: .

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