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60 Advances in Neonatal Care • Vol. 10, No. 2 • pp. 60-66
State of the ScienceHypoxic Ischemic Encephalopathy and
Hypothermic Intervention for Neonates
Laura D. Selway, MSN, RN
SEARCH STRATEGY
A key word search was conducted using PubMedand the Cochrane
Collection databases. Search termsincluded hypoxic ischemic
encephalopathy, HIE,hypothermia, neonates, and total body and
SHC.Specific search limits included infants only, Englishonly, and
articles published within the last 7 years.Search results yielded 2
large, randomized, con-trolled trials with more than 200 patients
in each trialthat explored hypothermia in neonates. Seven arti-cles
explored neurodevelopmental outcomes, distri-bution of cerebral
lesions, and determinants ofoutcomes. Smaller randomized controlled
trialsexploring hypothermia for neonates were alsoincluded. Other
articles explored the pathophysiol-ogy of HIE and side effects of
hypothermia interven-tions in neonates.
PATHOPHYSIOLOGY OF PERINATALASPHYXIA AND THE DEVELOPMENT OF
HIE
Acute hypoxic brain injury in a neonate can occurfor a variety
of reasons. Any condition that leads todecreased oxygen supply
(hypoxia) and decreasedblood supply to the brain (ischemia) can
lead to this condition. Acute perinatal events such asplacental
abruption, umbilical cord prolapsed,
Address correspondence to Laura D. Selway, MSN, RN, 539Constant
Ridge Ct, Abingdon, MD 21009; [email protected].
Author Affiliation: School of Nursing, The Johns
HopkinsUniversity, Baltimore, Maryland.Copyright © 2010 by the
National Association of Neonatal Nurses.
Perinatal asphyxia and resulting hypoxicischemic encephalopathy
(HIE) occur in 1 to 3per 1000 births in the United States.1-3
Higherrates occur in developing countries with limited diag-nostic
and interventional resources.1 Worldwide,10% to 60% of infants who
develop HIE will die andat least 25% of the survivors will have
long-term neu-rodevelopmental sequelae.2 Hypoxic
ischemicencephalopathy is the primary cause of 15% to 28%of
cerebral palsy among children.3 Hypothermictherapy as either
selective head cooling (SHC) ortotal body cooling as an
intervention for asphyxiatedinfants offers promising results since
its experimen-tal inception in the late 1990s. This article
examinesthe pathophysiology of HIE, identifies infants at riskfor
HIE as a result of perinatal asphyxia, reviewshypothermic
intervention as a primary interventionfor compromised infants, and
describes barriers to itsimplementation.
ABSTRACTPerinatal asphyxia and resulting hypoxic ischemic
encephalopathy (HIE) occur in 1 to 3 per 1000 births in the
UnitedStates. Induced hypothermia as an intervention for
asphyxiated infants offers promising results in reducing
neurodevel-opmental disabilities in surviving infants. Induced
hypothermia and selective head cooling are effective
interventionsfor asphyxiated infants that minimize continued
neuronal damage and decrease neurodevelopmental disability at
18months of age. Identification of affected infants immediately
after delivery and transfer to a facility that provides thistherapy
is necessary to maximize the potential of this intervention.
Standardization of hypothermia protocols withinneonatal intensive
care units is essential for providing hypothermia as a treatment of
HIE in infants. This article exploresthe pathophysiology of HIE,
identifying infants at risk for HIE as a result of perinatal
asphyxia, the use of hypothermicintervention for compromised
infants, and barriers to the implementation of treatment.KEY WORDS:
HIE, hypothermia, hypoxic ischemic encephalopathy, neonates,
perinatal asphyxia, selective head cooling,total body cooling
LINDA IKUTA, RN, MN, CCNS, PHN • Section Editor
2.8HOURS
Continuing Education
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Hypothermia and Neonates 61
uterine rupture, tight nuchal cord, or an acute bloodloss are
risk factors.3
In response to hypoxia, the neonate’s brain convertsto anaerobic
metabolism in an effort to sustain func-tional ability. Anaerobic
metabolism leads to rapiddepletion of adenosine triphosphate,
accumulation oflactic acid, and failure of normal metabolic
activity.4Intracellular pumps lose their efficiency resulting in
anaccumulation of sodium, calcium, and water withinbrain cells. The
resulting cascade of events includes anaccumulation of fatty acids,
increasing oxygen-free rad-icals, cell apoptosis, and cell death.4
Following the acuteinjury and resuscitation, the neonate’s brain
will expe-rience a second delayed insult if there is no
interven-tion, despite restoration of oxygen to the brain.
Once cerebral perfusion and oxygenation arerestored, a second
cascade of injury will occur at 6 to48 hours because the brain
attempts to restore func-tion.4 Phosphorus metabolites and
intracellular pHare restored; however, the brain has not
recoveredfrom the initial injury and mitochondrial
dysfunctioncontinues. The neonate’s body releases
endogenousinflammatory cells and mediators following the
initialinjury that contribute to ongoing brain injury in thesecond
phase.4 The second stage of brain cell injuryis characterized by
restoration of cellular metabolismwith continued suppression of
electroencephalogramactivity.5 Cell apoptosis and death occur
followinghypoxic injury, and the extent of cell death is
propor-tional to the extent of the ischemic injury.
Perinatal asphyxia progresses to HIE based on thedegree of brain
injury and resulting clinical presenta-tion. Clinical seizures are
the hallmark of resultingencephalopathy following injury.1,4 Sarnat
andSarnat’s criteria for clinical encephalopathy can beused to
determine the degree of neuronal injurybased on the infant’s
symptoms.6 The Sarnat andSarnats criteria include lethargy, stupor,
or coma,with 1 or more of hypotonia, abnormal reflexes (ocu-lomotor
or papillary abnormalities), an absent orweak suck, or evidence of
seizures.6 An amplitude-integrated electroencephalogram (aEEG) can
pro-vide further information about the degree of braininjury.
Moderate to severe voltage changes seen onan aEEG are indicative of
encephalopathy and fur-ther intervention is required to limit brain
injury.1
Perinatal asphyxia and resulting HIE cannot beanticipated prior
to delivery. Neuronal injury is aresult of precipitous events,
rather than a diagnosis orknown complication of the pregnancy.
Asphyxiatedand physiologically depressed infants show no clini-cal
warning of delivery complications that can beanticipated during the
pregnancy. During labor, vari-able and late decelerations of the
fetal heart rate arethe main indicators of a stressed infant at
risk forhypoxic injury.4 Primarily, term infants are at risk
forneuronal injury because of change in blood flow andbrain
metabolic activity after 34 weeks.
There is no known genetic predisposition fordeveloping HIE for
some infants compared withother infants. There is also no evidence
exploringindividual coping and adaptation processes amonginfants
that can blunt neuronal injury followingasphyxia.
THERAPEUTIC HYPOTHERMIA
Mild hypothermia as a treatment for HIE was discov-ered in the
1950s when isolated reports that asphyx-iated infants were
submersed in a cold tub of wateruntil spontaneous respirations
began.7 In the 1980s,it was noted that hypothermic drowning victims
sur-vived submersion for up to 40 minutes with no last-ing
neurologic sequelae and experiments withhypothermia were conducted
following cardiopul-monary resuscitation of adults.7 Studies have
alsoexplored the use of hypothermia with stroke and car-diac
patients.
Today, the effects of hypothermia on the neonatalbrain following
acute brain injury are well knownand promising. A temperature
reduction by 2�C to4�C decreases the rate of cell death and delays
thecascade of metabolic changes that are normally asso-ciated with
hypoxia.4 As a result, cerebral metabo-lism is reduced, adenosine
triphosphate stores areconserved, anaerobic metabolism effects are
blunted,and free radicals are not released. In addition,hypothermia
can delay secondary brain injury andmitigate present injury in the
neonatal hypoxicbrain.4
CoolCap TrialMild hypothermia for asphyxiated infants emergedin
the late 1990s as a possible intervention for braininjury occurring
between the initial phase and thesecond phase of neuronal damage
associated withHIE. The first randomized controlled trial and
cor-nerstone of hypothermic intervention in neonateswas the CoolCap
trial.6 This trial recruited 234infants with evidence of asphyxia
and resultingencephalopathy from 25 perinatal centers betweenJuly
1999 and January 2002 to participate in the trial.Strict inclusion
criteria in the CoolCap trial hasallowed benchmarking with further
criteria in laterHIE studies. Inclusion criteria of the CoolCap
trialincluded the following6:
1. gestational age 36 weeks or more,2. Apgar score of 5 or less
at 10 minutes following
birth,3. continued need for resuscitation (endotracheal
or mask ventilation) at 10 minutes followingbirth,
4. severe acidosis (pH � 7.00, base deficit � 16mmol/L from
umbilical cord, or an arterial orvenous sample from infant within 1
hour follow-ing birth), and
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62 Selway
5. grade II or III encephalopathy based on theSarnat and Sarnat
criteria.
The CoolCap trial cooled infants (n � 116) to 34�Cto 35�C
rectally via a cooling cap within 6 hours ofdelivery and maintained
a hypothermic state for 72hours. The control infants (n � 118)
received conven-tional care and maintained temperatures of 36.5�C
to37.2�C.
The results demonstrated that infants cooled priorto 6 hours
following delivery had the most potentialto benefit from the
therapy before the second phaseof neuronal damage occurred.6 The
infants hadaEEGs performed prior to the initiation of
therapy.Infants in the cooling group with the most severeaEEG
changes received less benefit from coolingthan infants with less
severe aEEG changes. Thestudy found that the initial encephalopathy
gradingwas more predictive of future adverse outcomes thanthe Apgar
scores or the presenting acidosis.6 Theauthors recommended aEEG
recordings to identifyat-risk infants who could benefit from
hypothermiabefore the small therapeutic window of 2 to 6
hoursfollowing delivery closed.
The CoolCap trial also concluded that largerinfants responded
better to hypothermia than smallerinfants. The authors speculated
that the size of thebrain could affect the temperature to which it
wascooled in relation to outcomes, but more researchwas needed.1,6
Pyrexia (temperature � 38�C) wasclearly associated with worse
outcomes, especially inthe control group, since heat production
increasedcerebral metabolism and exacerbated neuronalinjury.1
Inadvertent warming occurred in both thecooling and control groups
through seizures, inflamma-tory cytokine release, and the use of
servo-controlledheaters.
COMPLICATIONS OF HYPOTHERMIAIN NEONATES
The safety of induced hypothermia and SHC hasbeen studied in
relation to the risk—benefit ratio ofthe treatment in neonates.
Hemodynamic changesassociated with hypothermia remain the major
nega-tive outcome of the intervention. One study8 ana-lyzed the
hemodynamic parameters of 7 cooledinfants by comparing cooling
values with postre-warming values. The most significant side effect
ofcooling was a decrease in heart rate, with a mean of129 beats per
minute compared with a mean of 149beats per minute following
rewarming. Cardiac out-put was reduced to 67% and stroke volume
wasreduced to 77% while the infants were cooled, but allinfants
returned to baseline following rewarming.8None of the infants
experienced an alteration inblood pressure or left ventricular
ejection time as aresult of hypothermia. The authors concluded
thatdespite a decrease in heart rate, stroke volume, and
cardiac output, the infants were able to maintainperipheral
perfusion with normal lactate levels dur-ing the hypothermia phase
with all the parametersreturning to baseline with passive
rewarming.8 Theauthors also cited heart arrhythmias,
hypotensionwith rapid rewarming, and increased blood viscosityas
potential side effects of hypothermia, but no infantin their study
experienced these side effects.
A second study looked at 26 asphyxiated infantswith hypothermia
as an intervention for half of theinfants.9 All of the cooled
infants had some degree ofrenal impairment that resolved with
rewarming. Allof the cooled infants demonstrated a fall in heart
rate,less than 80 beats per minute in 2 infants, whichresolved with
rewarming. One cooled infant had aprolonged QT interval that
resolved followingrewarming. None of the cooled infants required
anincrease in oxygen requirement compared with thecontrol infants.
The authors found that coagu-lopathies within the cooling group
were not signifi-cant when compared with the control group.
Therewas no difference in the rates of
thrombocytopenia,intraventricular hemorrhage, or abnormal
coagula-tion tests in the cooled group when compared withthe
control group.9 An additional study3 found noassociation with an
increase in hemorrhagic lesions ininfants cooled to 33�C to 34�C
when examining basalganglia and white matter lesions in
asphyxiatedinfants.
Studies examining the side effects of hypothermiaacknowledge
transient hemodynamic changes incooled infants who resolve with
passive rewarming.3,8,9All studies recommend hypothermia for
asphyxiatedinfants as the benefits of preventing continued
neu-ronal damage outweighed the transient hemodynamicside effects.
The original CoolCap trial data did notspecifically address side
effects, but the same data wereused in other trials focusing on
side effects and thesafety of hypothermia.
NEURODEVELOPMENTAL OUTCOMESFOLLOWING HYPOTHERMIA IN NEONATES
Using the original data obtained from the CoolCaptrial,
investigators were able to follow up with theinfants who
participated in the study to evaluate neu-rodevelopmental outcomes
at 18 months of age.6 Ofthe original 234 infants who participated
in theCoolCap trial, 218 infants were available for follow-up at 18
months. Investigators defined severe neurode-velopmental disability
as a triad of symptoms, includ-ing gross motor function of 3 to 5
(nonambulant, sitswith support, or infants with no
self-mobility),Bayley mental development index less than 70,
andbilateral cortical visual impairment served as thethreshold
indicators for severe neurodevelopmentaldisability.6 The authors
found that 73 of the 110infants in the control group (66%)
experienced death
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or severe disability by 18 months compared with 59of 108 infants
in the cooled group (55%). It was alsonoted that for infants with
the most severe changesin aEEG recordings prior to treatment,
hypothermiahad offered minimal neuroprotective benefit andthat some
infants incurred too much brain damagefrom the initial injury to
benefit from any interven-tional treatment.6
Rutherford et al3 explored cerebral lesions foundin HIE infants
who underwent cooling comparedwith normothermic infants. Cooling in
this particu-lar study was divided into infants who had SHC
andinfants who had whole body cooling (WBC).Cerebral lesions
related to asphyxia and HIE aremost commonly found in the basal
ganglia and thal-amus and are associated with the development
ofcerebral palsy.3 Less commonly, lesions are found inthe white
matter of the brain and are associated withlater cognitive
impairments.3 Eighty-six infants wereenrolled in the study by
Rutherford et al to determinewhether cooling altered the severity
and pattern oflesions found in infants with HIE. Thirty-four
cooledinfants (20 were whole body cooled and 14 wereselective head
cooled) and 52 normothermic infantswere evaluated following
recovery from an acutehypoxic injury. The study found that the
prevalenceof intraventricular hemorrhage was the same for all3
groups but that the 2 cooling groups had a decreasein number and
severity of basal ganglia and thalamiclesions.3 In the control
group, 46 of the 52 infants(88%) had basal ganglia and thalamic
lesions present.Seven of 14 infants (50%) in the SHC group and 15
of20 infants (75%) in the WBC group had basal gangliaand thalamic
lesions present. Approximately 40% ofinfants with significant basal
ganglia and thalamuslesions will have white matter infarction but
in thisstudy there was no decrease in the incidence ofsevere white
matter lesions in the cooled infants.3
Shankaran et al10 conducted a large hypothermiatrial with 208
enrolled infants with similar inclusioncriteria to that of the
CoolCap trial. The researchersrecruited infants from 15 perinatal
centers from July2000 to May 2003. Two hundred five infants
receivedfollow-up neurodevelopmental assessments at 18 to22 months.
Death or moderate or severe disabilityoccurred in 44% of the
infants in the cooling group (n � 102) and in 62% of the infants in
the controlgroup (n � 103). Table 1 illustrates the infants
strati-fied based on disability from Shankaran’s results.
COOLING AND REWARMING
Since the CoolCap Trial, researchers have exploredvarious
methods of cooling and the degree of coolingrequired to mitigate
neuronal injury resulting fromHIE. The original CoolCap was a
cooling deviceshaped as a hat that circulated water to maintain
theinfant’s rectal temperature at 34�C to 35�C. Selective
head cooling seemed ideal because the infant’s brainproduces 70%
of total body heat and systemic sideeffects of hypothermia would be
minimal with onlythe infant’s head cooled.2 However, new
researchindicates that WBC enables the infant to reach adeeper
level of hypothermia, and deep internal brainstructures benefit
from temperatures of 33�C.3,10Shankaran et al10 chose WBC for their
randomizedcontrol trial since WBC provides even cooling to allbrain
structures affected by hypoxic injury. Becausethe thalamus,
internal capsule, and basal ganglia ofthe brain are most sensitive
to hypoxic injury, WBCachieved homogenous hypothermia compared
withSHC, which tends to cool the periphery of the brainrather than
the central brain. The hemodynamic sideeffects of hypothermia do
not differ between SHCand WBC.8 Stratified studies have divided
cooledinfants into SHC and WBC and into differing degreesof cooling
that complicate the results and delay trans-lation into
practice.3,9 Cooling temperatures rangedfrom 33�C to 35� via
rectal, skin, and esophagealmeasurements in the studies, with no
standardizationevident.1,2,5,6,10
Once the infant has been in a hypothermic state for48 to 72
hours, the process of rewarming begins. Aswith the cooling of
infants, the process of rewarminginfants varied among trials. In 1
study, active rewarm-ing occurred over 3 to 6 hours with the
discontinua-tion of the cooling device and the addition of
blanketsand a radiant warmer.8 Wyatt et al1 and Shankaran et al10
rewarmed infants slowly, no faster than 0.5�Cper hour until
temperature was normothermic.
However, one point on temperature is clear.Temperatures greater
than 38�C following acute neu-ronal injury increased cerebral
metabolism andintensified injury. The CoolCap trial
cautionedagainst inadvertent warming of infants in both thecontrol
and cooled groups through seizure activityand the use of
servo-controlled warmers.1
LIMITATIONS AND GAPS INTHE LITERATURE
The current literature on mild hypothermia is variablein
translation and future application. The CoolCap
TABLE 1. Outcomes at 18 to 22 monthsof age10
Cooled Infants Controlled Infants (n � 102) (n � 103)
No. of deaths 24 38
Cerebral palsy, % 19 30
Blindness, % 7 14
Hearing aid use, % 4 6
Hypothermia and Neonates 63
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64 Selway
trial was the first multicenter, randomized controlledtrial to
evaluate hypothermia as an effective interven-tion following
perinatal asphyxia. Subsequent studieshave used the original
inclusion criteria and incorpo-rated recommendations from the
CoolCap trial sonow neonates must be enrolled within 6 hours
ofdelivery to qualify for a hypothermia study and anaEEG is most
often the diagnostic tool used to deter-mine baseline neuronal
abnormality.
The neurodevelopmental outcomes of hypother-mia are promising
but have not been validated byrepeated studies. The studies that
examined neurode-velopmental outcomes all measure different
outcomecriteria and continue to demonstrate high rates of
dis-ability despite treatment. Despite discouraging ratesof
disability, hypothermia still has benefits if initiatedpromptly and
uniformly. Healthcare providersshould acknowledge that the severity
of the initialhypoxic injury is most prognostic of the infant’s
out-comes, regardless of intervention. Another limitationof
neurodevelopmental outcomes is time. Becausehypothermia is
relatively new, there are no data onhow these infants will progress
as they age and howthey will perform in cognitive exercises.
In summary, what is known about hypothermia asan intervention
for neonates with traumatic braininjury is that it is safe and
affords minimal hemody-namic side effects. Hypothermia should be
initiated assoon as possible because the therapeutic window closes6
hours after initial injury at delivery. Hypothermia hasdecreased
the degree of neurodevelopmental disabilityfor some infants, but
infants with more severe neuronalinjury may not respond to any
intervention.
What is not known about hypothermia forneonates is the ideal
cooling temperatures, method ofcooling, or duration of cooling
because data have var-ied across studies. The duration of therapy
in thestudies ranged from 48 to 72 hours and it was
oftendiscontinued early for perceived hemodynamic insta-bility of a
decreased heart rate related to hypother-mia. Unfortunately,
rewarming practices of cooledinfants vary as much as the initial
cooling practices.
Neurodevelopmental outcomes are prematurebecause of the short
amount of time that the interven-tion has been available. It is
apparent that more researchis required despite encouraging outcomes
to date.
IMPLICATIONS FOR NURSING PRACTICE
Access to hypothermia for infants with acute asphyxiaat delivery
varies across the United States. An anony-mous survey about
hypothermia and HIE was sent tothe 809 medical directors of
neonatal intensive careunits in the United States in October 2005.
Only 28of the 441 respondents (6.4%) offered cooling as
anintervention for HIE at their institution.11 Of therespondents
who cooled infants, 64% offered totalbody cooling and 25% offered
head cooling, the
remainder a combination of both interventions. Langet al11
reported that the majority of institutions thatoffered cooling were
academic centers, with an aver-age patient census greater than 40.
Approximatelyhalf (57%) of the centers offered Extra
CorporealMembrane Oxygenation. Overwhelmingly, 69.1% ofthe
responders felt that they “need more data” todetermine whether
hypothermia was an effectiveintervention for infants with HIE.11 A
major limitationof this survey was the convenience sample model,
butit offers a glimpse into the access issue for infants bornin
community hospitals with acute asphyxia and anarrow therapeutic
window for successful interven-tion with hypothermia.
Nursing is central to the identification of infants atrisk for
developing HIE as a result of acute asphyxiaat delivery. After the
initial hypoxic injury, infantsmay appear to recover, but this
leads to a false senseof safety because a second phase of neuronal
injurywill inevitably follow. Ideally, infants at risk for
HIEshould be transferred to a treatment center within 6hours to
prevent further brain injury and to initiatehypothermia. Education
about the clinical presenta-tion of asphyxia, presence of seizures,
and criteria forhypothermia should be mandatory for all labor
anddelivery, newborn nursery, and neonatal intensivecare unit
nurses, regardless of whether hypothermiais practiced at that
institution or not.
Although it is essential to initiate hypothermia forat-risk
infants as soon as possible, it is equally imper-ative that it is
initiated in a controlled manner and ina setting with hypothermia
expertise. The transferringhospital should not begin hypothermic
proceduresindependently prior to transfer. Efforts to avoid
over-heating the infant should be made. If the patient can-not be
transferred within 6 hours of delivery, coolingcan be initiated in
transport, but only under the direc-tion of the accepting
institution.12 Whole body cool-ing is easier to initiate than SHC
in transport with icepacks and the use of ambient air temperature
whilecontinuously monitoring rectal temperatures.
Care of the infant receiving either SHC or totalbody cooling
requires a whole systems approach(Figure 1). In addition to
managing the cooling appa-ratus, supportive care of the infant is
essential.Promotion of oxygen and ventilation is important.Not all
infants who qualify for hypothermic therapywill require mechanical
ventilation. However, care-ful attention should be paid to avoid
hypoxia, hyper-oxia, or hypercarbia.13,14
Cooling will frequently result in a mild decrease inresting
heart rate. However, bradycardia (a heart rateless than 80 beats
per minute) may indicate that theinfant needs to be warmed
slightly. In addition, per-fusion should be maintained and
hypotension shouldbe treated with volume expansion or
vasopressordrugs as appropriate. Monitoring of intake and outputis
essential because infants with asphyxia injury may
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also develop oliguria secondary to acute tubularnecrosis or
“syndrome of inappropriate antidiuretichormone” release.14
Total parental nutrition will be required to main-tain
appropriate blood glucose and provide for nutri-tion. Hypoglycemia
and hyperglycemia should beavoided.14 In addition, electrolytes,
including sodiumand potassium, should be monitored, along
withcoagulopathy studies.
It is generally preferable that infants receivingcooling therapy
be sedated as necessary. Excessactivity or agitation can result in
elevation of bodytemperature. Infants with HIE are at risk for
seizureactivity. Seizures should be identified and treated.13
Advanced practice nurses are pivotal in the appli-cation of
research into practice. They can increasewhat is known about
therapeutic hypothermia forneonates through formalized teaching
arenas, publi-cation, and informal unit-based in-services with
nurs-ing staff. Education should focus on identifying
at-riskinfants who require intervention, describing the ben-efits
of hypothermia, and gaps in the literature regard-
ing hypothermia in neonates. In turn, nurses can edu-cate
families and caregivers about this intervention fortheir infant and
support them emotionally as theirinfant’s prognosis evolves.
Advanced practice nursesshould participate in further research to
contribute tothe knowledge of hypothermia for
neonates.Standardization of hypothermia practice is the goal asmore
is discovered about this life-saving intervention.
References1. Wyatt JS, Gluckman PD, Liu PY, et al. Determinants
of outcomes after head cool-
ing for neonatal encephalopathy. Pediatrics. 2007;119:912-921.2.
Jacobs SE, Hunt R, Tarnow-Mordi WO, Inder TE, Davis PG. Cooling for
newborns
with hypoxic ischaemic encephalopathy. Cochrane Database Syst
Rev. 2007;(4):CD003311.
3. Rutherford MA, Azzopardi D, Whitelaw A, et al. Mild
hypothermia and the distri-bution of cerebral lesions in neonates
with hypoxic—ischemic encephalopathy.Pediatrics.
2005;116:1001-1006.
4. Perlman JM. Intervention strategies for neonatal
hypoxic—ischemic cerebralinjury. Clin Ther. 2006;28:1353-1365.
5. Battin MR, Dezoete JA, Gunn TR, Gluckman PD, Gunn AJ.
Neurodevelopmentaloutcome of infants treated with head cooling and
mild hypothermia after peri-natal asphyxia. Pediatrics.
2001;107:480-484.
6. Gluckman PD, Wyatt JS, Azzopardi D, et al. Selective head
cooling with mild sys-temic hypothermia after neonatal
encephalopathy: multicentre randomised trial.Lancet.
2005;365:663-670.
FIGURE 1.
Infant with cooling cap in place. Used with permission from Dr
Jan Paisely.
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7. Thoresen M, Whitelaw A. Therapeutic hypothermia for
hypoxic—ischaemicencephalopathy in the newborn infant. Curr Opin
Neurol. 2005;18:111-116.
8. Gebauer CM, Knuepfer M, Robel-Tillig E, Pulzer F, Vogtmann C.
Hemodynamicsamong neonates with hypoxic—ischemic encephalopathy
during whole-bodyhypothermia and passive rewarming. Pediatrics.
2006;117:843-850.
9. Battin MR, Penrice J, Gunn TR, Gunn AJ. Treatment of term
infants with headcooling and mild systemic hypothermia (35.0�C and
34.5�C) after perinatalasphyxia. Pediatrics. 2003;111:244-251.
10. Shankaran S, Laptook AR, Ehrenkranz RA, et al. Whole-body
hypothermia forneonates with hypoxic—ischemic encephalopathy. N
Engl J Med. 2005;353:1574-1584.
11. Lang TR, Hartman TKM, Hintz SR, Colby CE. Hypothermia for
the treatment ofneonatal ischemic encephalopathy: is the genie out
of the bottle? Am J Perinatol.2007;24:27-32.
12. Shah PS, Ohlsson A, Perlman M. Hypothermia to treat neonatal
hypoxic ischemicencephalopathy. Arch Pediatr Adolesc Med.
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13. Long M, Brandon DH. Induced hypothermia for neonates with
hypoxic—ischemicencephalopathy. J Obstet Gynecol Neonatal Nurs.
2007;36:293-298.
14. Perlman JM. General supportive management of the term infant
with neonatalencephalopathy following intrapartum hypoxia—ischemia.
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Controversies. Philadelphia, PA:Elsevier; 2008:79-87.
For more than 35 additional continuing education articlesrelated
to neonatal, go to NursingCenter.com/CE.
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