Newborn & Infant Nursing Reviews 16 (2016) 812

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Newborn & Infant Nursing Reviews

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Articles

Brain Injury in Preterm Infants: Pathogenesis and Nursing Implications

Susan Blackburn, RN, PhD, FAAN
Department of Family and Child Nursing, University of Washington School of Nursing, Seattle, Washington

a r t i c l e i n f o a b s t r a c t

Keywords: Preterm infants are at higher risk for neurological alterations, with this risk increasing with decreasing gestational
Periventricular leukomalacia age due to both developmental and destructive elements. This article provides an overview of brain development
Germinal matrix hemorrhage/intraventricular and vulnerabilities in the preterm infant and examines the pathogenesis of three areas of brain injury seen in
hemorrhage preterm infants: periventricular leukomalacia, germinal matrix hemorrhage/intraventricular hemorrhage, and
Cerebellar hemorrhage cerebellar injury). Implications for nursing care of infants at risk for these disorders are discussed.
Preterm infant
2015 Elsevier Inc. All rights reserved.
Brain injury

Preterm infants as a group are at higher risk for neurologic alter-
ations. This is seen across all gestational ages, with the greatest preva-
lence in very low birthweight (VLBW) infants (infants b32 weeks
gestation and 1500 g birthweight). 1,2 VLBW infants are at increased
risk for cognitive, behavioral, attentional, and socialization problems
along with motor decits such as cerebral palsy. The most prominent
long term alterations are cognitive decits unaccompanied by motor
decits.1,2 The prevalence of major disabilities (cognitive, motor, vision,
hearing) increases with decreasing birth weight and gestational age and
are seen in 6% to 8% of infants from 1501 to 2000 g, increasing to 14% to
17% at 1001 to 1500 g and 20%30% in infants weighing b1000 g. 3 The
higher prevalence of cognitive dysfunction (alterations in learning,
memory, language, vision, hearing, attention and socialization, motor is-
sues, and behavioral issues) continues into school age and adulthood
(15% to 25% in those born at b1500 g and over 50% in those b750 g).3,4
Volpe notes that brain injury in preterm infants is a combination
of developmental and destructive elements and the importance of
viewing clinical and anatomic consequences in the context of brain
development.5p.168 Preterm infants are more vulnerable to brain injury
and altered brain maturation because preterm birth occurs at a time
of peak brain growth, synaptogenesis, developmental regulation of
specic receptor populations, and central nervous system organization
and differentiation.6p.1157
Sannia et al. discussed particular areas of brain vulnerability at
different gestational ages and their consequences in terms of disorders
that are most prominent at each age (although these disorders certainly
can occur at any gestation).5 For example from 23 to 26 weeks
gestational age there is rapid development in the cerebellum and
periventricular areas (both of which have germinal matrixes) with risks
of germinal matrix hemorrhage (GMH)/intraventricular hemorrhage
(IVH) and cerebellar hemorrhage (CH) most prominent , although these
Department of Family and Child Nursing, Box 357262, University of Washington,
Seattle, WA, 98195-6272. Tel.: +1 206 543 8218.
E-mail address: sblackbn@UW.EDU.
infants are also at risk for later periventricular leukomalacia (PVL). From
26 to 34 weeks gestational age white matter development is more prom-
inent, especially in the periventricular zone as is PVH; GMH/IVH is less
common after 30 to 32 weeks. From 34 to 36 weeks gestation, cortical vol-
ume increases (half of the cortical volume is achieved in the last 6 weeks
of gestation) and myelinated white matter increases from 35 to 40 weeks.
Later preterm infants most commonly have injury from circulatory im-
pairment (stoke) or asphyxia. In term infants the most common disorders
are perinatal stroke and hypoxicischemic injury.5
The focus of this article is to provide an overview of brain
development and vulnerabilities in the preterm infant and examine
the pathogenesis of three types of brain injury seen in preterm infants:
PVL, GMH/IVH, and cerebellar injury. Finally, implications for nursing
care of infants at risk for these disorders will be discussed.
Brain Development
Brain development in the embryo and fetus is characterized by six
stages. The rst two stages, neurulation (3 to 4 weeks) and prosence-
phalic development or ventral induction (5 to 6 weeks) set up the
basic structure and major components of the brain. Neurulation in-
volves development of the neural tube and neural plate, and closure of
the neural tube (generally between 22 and 28 days). 6 Failure of the neu-
ral tube to close leads to neural tube defects (NTDs) such as anenceph-
aly, spina bida and encephalocele. 6,7 Periconceptional folic acid
supplementation signicantly reduces risk of NTDs.8 Prosencephalic de-
velopment leads to formation of forebrain, midbrain and hindbrain
structures as well as the brain ventricles. Development of the face is
associated with this stage so alterations in brain development are
often accompanied by alterations in facial development.6
The third stage, neuronal proliferation, is characterized by formation
of neurons (most prominent from 8 to 16 weeks), and later glial cells, in
the subependymal germinal matrix. The germinal matrix contains neu-
ronal and glial cell precursors.9 This germinal matrix will remain prom-
inent into the third trimester and is the usual site where GMH/IVH

http://dx.doi.org/10.1053/j.nainr.2015.12.004
1527-3369/ 2015 Elsevier Inc. All rights reserved.
 S. Blackburn / Newborn & Infant Nursing Reviews 16 (2016) 812
arises in preterm infants. The germinal matrix thickness begins to
decrease after 24 weeks gestation and has almost disappeared by 36
to 37 weeks. 9 Neuronal proliferation is followed by migration (stage
4) of initially neurons and later glial cells from the germinal matrix to
their eventual loci with the cerebrum. 1,10 Neuronal migration in the ce-
rebral cortex is generally complete by about 5 months gestation; neuro-
nal migration in the cerebellum (which contains its own germinal
matrix) continues into the postnatal period. 11,12 Glial cell migration
continues into the eighth month.
The fth stage of brain development is organization, which begins at
5 months gestation, is most prominent from then until the rst
12 years postbirth, and continues into adulthood. During organization
the central nervous system begins to develop the capacity to act as an
integrated whole and for different areas of the brain to communicate
with each other and other areas of the body. 13 This stage involves devel-
opment of the neocortex (especially from 22 to 36 weeks gestation).13
Major organizational processes include development of axons and den-
drites to link nerve cells (neuron differentiation and arborization), de-
velopment of synapses or points of communication within cells
(synaptogenesis), balancing of excitatory and inhibitory synapses, glial
differentiation and removing excess elements (neurons, synapses, con-
nections) and rening synapses.1,7,13 Preterm infants in the neonatal in-
tensive care unit are in this stage of brain development. The nal stage
of brain development is myelination which lasts from around
8 months gestation until early adulthood. 1,14
Cerebellar Development
The cerebellum derives from the rhombencephalon (hindbrain). The
cerebellar plate (seen by 12 weeks) includes neuroepithelial, mantle
and marginal cellular layers. The neuroepithelium forms the external
granular layer, which migrates inward to form the internal granular
layer of the cerebellum which is comprised of neurons.15 The external
granular layer is a proliferative zone that gives rise to the various cell
types of the cerebellum. 16 Most cerebellar neurons are granular cells
and numbers of neurons in the cerebellum exceed numbers in the
cerebral cortex.15,16 Neuronogenesis in the cerebellar germinal matrix
occurs between 3 and 4 months gestation, with migration from 3 to
8 months.7,14 Cerebellar development accelerates from 20 to 30 weeks
with peak thickness of external granule layer seen at 25 weeks. 15 Cere-
bellar development relies on the reciprocal interactions of excitatory
and inhibitory/regulatory cell types that are rapidly developing in
the third trimester. Between 30 and 40 weeks development continues
at a rapid rate with a greater than 30-fold increase in surface area during
this time. 13,15
Glial Cells
Glia are supporting cells within the central nervous system (CNS)
and continue to divide after birth. There are three types of glia:
(1) myelin-building glia consisting of oligodendrocytes (in CNS) and
Schwann cells (peripheral nervous system); (2) clean-up glia (astroglia,
microglia) that remove waste, especially when neurons die and ll up
vacated space; and (3) guiding glia such as radial glia in the CNS
which guide the migrating neurons from the germinal matrix to their
eventual loci within the cerebral cortex (these become astrocytes after
brain maturation and Schwann cells that guide regenerating axon to
target after peripheral damage). 1,6,13,17 Astrocyctes, oligodendrocytes
and microglia are particularly vulnerable in the preterm infant.
Astrocytes undergo rapid proliferation from 24 to 32 weeks (peak
26 weeks) and are found primarily in deep cortical layers and white
matter. 13 These glia assist with axonal guidance, growth, brain
structural development, and functioning of bloodbrain barrier, that
can release transmitters (such as glutamate) to send signals to neigh-
boring neurons and interact with neurons and synapses to help inte-
grate information. 1,13 Oligodendrocytes during their premyelinating
9
period prior to term, and especially prior to 32 weeks gestation, are es-
pecially vulnerable to hypoxicischemic injury and thought to play a
role in the pathogenesis of periventricular leukomalacia. 18 Microglia
are brain immune cells and macrophages and also have a role in
brain development. 19 Peak numbers are seen in the third trimester. If
activated due to cell damage such as occurs with hypoxiaischemia or
inection/inammation, the microglia release free radicals, cytokines
and glutamate which can lead to further cellular injury. 1,5,13
Pathogenesis of Brain Injury in Preterm Infants
Brain injury in preterm infants is characterized by multiple lesions
including PVL, often with concomitant neuronal/axonal abnormalities,
GMH/IVH that may be accompanied by posthemorrhagic infarction,
cerebellar injury, and posthemorrhagic hydrocephalus. 1 Pathogenesis
of these disorders involves both developmental and destructive
elements. Knowledge of pathogenesis has increased in recent years,
but questions still remain.
White Matter Injury (Periventricular Leukomalacia)
The most common type of brain injury seen in VLBW infants is PVL
occurring in up to 50% of VLBW infants.2 Infants are most vulnerable be-
tween 23 and 32 weeks.4 The primary lesion in PVL is injury to the cere-
bral white matter, but PVL often occurs in conjunction with neuronal/
axonal injury. 2,19 Disruption of glial and neuronal maturation may
lead to later alterations in multiple areas of cerebral development and
later neurodevelopmental problems across multiple domains. 4,20
Two main types of PVL have been described: focal and diffuse. Focal
injury is further subdivided into macroscopic injury, which evolves into
cysts (cystic necrosis) and microscopic injury which evolves to glial
scars (microscopic necrosis). Focal lesion involves degeneration
of axons and glia in the injured area. 4,21 Microscopic injuries are
more common than cystic injuries (which tend to be more severe). 1,4
Diffuse PVL is characterized by damage to pre-myelinating oligoden-
drocytes (pre-OLs) leading to hypomyelination, astrocystosis and
microgliosis.4,11,12 Diffuse white matter injury involves primarily astro-
cytes, microglia and degeneration of pre-OLs and leads to failure of
myelination. 4 In recent years, studies have reported a shift from the
more destructive cystic lesions to less severe chronic injury from the
diffuse form (which are still associated with decreased cerebral growth
and altered neurodevelopmental outcomes). 4 Back noted that this
change to less severe injury is likely related to changes in the timing,
severity, and progression of HI [hypoxicischemic] insults. 4p.3 Diffuse
white matter injury involves primarily astrocytes, microglia and degen-
eration of pre-OLs and leads to failure of myelination. 4,18
The interaction of three, maturation-dependent factors is thought to
increase vulnerability of VLBW infants to PVL. These factors are (1) an
immature vascular supply to the white matter so oxygen delivery is re-
duced; (2) immature cerebral autoregulation, and (3) the vulnerabil-
ities of pre-OLs, which are rapidly differentiating and the major form
of oligodendrocytes in VLBW infants.1,2,5,19 The pathogenesis of cerebral
white matter injury in preterm infants involves hypoxia and/or ische-
mia and infection and/or inammation.1,2,5,19,22 These events result in
the release of extracellular glutamate (leading to excitotoxicity), reac-
tive oxygen and nitrogen species, i.e. free radicals, (leading to oxidative
stress) and proinammatory cytokines (leading to inammation). 22 As
a result of these events, the vulnerable pre-OLs are damaged, microglia are
activated, astrogliosis and scar formation occur, and neuronal/axonal
damage with damage to both the white mater and gray matter may
occur secondary to the original pathologic event.22 Unfortunately, damage
to the pre-OL leads to further release of these toxic substances. Vulnerability
decreases as pre-OLs mature and differentiate into oligodendrocytes.4
PVL injury often occurs in conjunction with neuronal/axonal alter-
ations primarily in the gray matter. Volpe termed the combination of
PVL and concomitant neuronal/axonal injuries the encephalopathy of
10 S. Blackburn / Newborn & Infant Nursing Reviews 16 (2016) 812
prematurity. 2,19 This is the leading cause of neurological disability in
preterm with motor, cognitive, learning, and behavioral sequelae. 1,18
The neuronal/axonal injury involves various areas of the brain including
cerebral white matter axons, thalamus, basal ganglia, cerebral cortex,
cerebellum, and brain stem.2,19 During peak vulnerability for PVL, cere-
bral white matter axons are undergoing rapid growth and thus vulner-
able to hypoxicischemic or inammatory damage.19 The two principal
neuron types in cerebral white matter at this time are subplate neurons
(in subcortical white matter) and late-migrating GABAergic neurons
(in central white matter). Both types are transient population but
are critical for development of the cerebral cortical and thalamus. 2,19
Pathogenic sequelae of encephalopathy of prematurity include
hypomyelination, axonal degeneration and impaired cortical and tha-
lamic development and later neurodevelopmental problems. 2,11,12,19
Germinal Matrix Hemorrhage (GMH)/Intraventricular Hemorrhage (IVH)
GMH/IVH affects 12,000 preterm infants in the United States each
year with survivors at increased risk for cognitive and motor disorders
as well as hydrocephalus.9 Risk factors for GMH/IVH include VLBW, his-
tory of hypoxia, birth asphyxia, patent ductus arteriosus, hypotension,
hypercapnia, severe respiratory distress syndrome, seizures, infection,
and any other factor or event that alters venous return, and increased
venous pressure. 1,9,17 IVH is occasionally seen in term infants with
either trauma or birth asphyxia. In the preterm infant, 90% of these
hemorrhages occur within rst 2 days after birth; 10% occur later in
the neonatal period.1,18 Infants may have an acute or subtle (or silent)
presentation with changes in activity and/or tone. Signs of GMH/IVH
may include a falling hematocrit, deterioration in clinical condition
with apnea, bradycardia, and hypotension, generalized tonic seizures
and posturing, altered level of consciousness and tone, altered eye
movements and a full fontanel. 1,17
The germinal matrix in the periventricular area, at head of caudate
nucleus near foramen of Monro is the usual site of initial hemorrhage
in preterm infants.9 The germinal matrix is present and active until 34
to 35 weeks gestation. Blood may be restricted to the germinal matrix,
but often ruptures through the underlying ependymal and enters the
lateral ventricles then 3rd and 4th ventricles. Blood may collect in
subarachnoid space and basal cistern. Ventricular dilation may occur
due to obstruction of cerebral spinal uid ow with development of
post-hemorrhagic hydrocephalus. If the hemorrhage is severe, blood is
also found in white matter due to associated hypoxicischemic insult
affecting this area.1,7,17
Pathogenesis of GMH/IVH is multifactorial and complex, involving
intravascular, vascular and extravascular factors. 1,9,17 Intravascular
hemodynamic factors include periventricular blood ow, immature cere-
bral autoregulation and brain venous hemodynamics. The periventricular
area receives a signicant proportion of cerebral blood ow prior to
32 weeks primarily to support neuroblast and glioblast mitotic activity
within the germinal matrix and later migration of neurons and glial
cells to the cortex.1 Factors that increase cerebral blood ow can lead to
overperfusion of the periventricular region.1,17 Cerebral autoregulation
is the ability to maintain a constant cerebral blood ow within specic
ranges of systemic blood pressure and cerebral pressure.7 Failure of auto-
regulation leads to a pressure-passive system where cerebral blood ow
varies directly with arterial pressure, and alterations in systemic or cere-
bral blood pressure are transmitted directly to the brain and, in particular,
to the area receiving a high proportion of cerebral blood ow, the fragile,
thin walled vessels of the germinal matrix.2,7,17 Thus rapid uctuations in
systemic blood pressure or cerebral blood ow, increase the risk of vessels
rupture. Altered hemodynamics can occur with positive pressure ventila-
tion, rapid volume expansion, secondary to a patent ductus arteriosus, or
with increased systemic blood pressure, caregiving events, handling,
suctioning and other caregiving activities.1,4,7,9,17
Vascular factors include the fragility of the germinal matrix capil-
laries, venous hemodynamics, and vulnerability of vascular ow end
border-zones in the periventricular area to ischemia. 1,9,17 The germinal
matrix is a highly vascularized structure undergoing rapid angiogenesis
(leading to a higher proportion of immature vessels) with a high vascu-
lar density that increases with increasing gestational age. 9 The germinal
matrix capillaries are large, irregular, thin walled vessels. Capillary epi-
thelial cells have a high metabolic activity and are dependent on oxida-
tive metabolism and thus are easily injured by hypoxic events.1 These
factors all increase fragility of the germinal matrix capillaries and the
likelihood of leakage or rupture if transmural pressure increases. The
venous drainage system of the brain at the level of the foramen of
Monro and the caudate nucleus (usual site of GMH/IVH) is another
area of vulnerability. The U-shaped turn in the venous drainage system
at this location and blood enters the great vein of Galen predisposing
to turbulent venous ow and an area vulnerable to increased intravas-
cular pressure. 1,7 In addition, the pliable skull of the preterm can easily
be deformed, obstructing the major venous sinuses and increasing
venous pressure.17
Extravascular factors include the lack of germinal matrix blood ves-
sel support and brinolytic activity within the germinal matrix. The ger-
minal matrix blood vessels are embedded in a gelatinous material
decient in supportive mesenchymal elements, thus providing poor
support for the fragile blood vessels, with a paucity of pericytes (con-
tractile cells embedded in basal membrane that wrap around capillaries
to provide support). 1,9 The immature infant also has immature astro-
cyte processes which also decrease vessel support. 20 The brinolytic ac-
tivity in the periventricular area means that a small initial bleed may not
clot off and be localized, but continue to enlarge and rupture into the
ventricles and/or cerebral parenchyma. 1,7
Cerebellar Injury
The cerebellum has long been recognized for its role in balance, posture
and motor control, and more recently for its role in the development of cog-
nitive, learning, language, and behavioral as well as motor function.10,14,23,24
The cerebellum acts as a node in distribution of neural networks with inter-
connections with thalamus and parietal and prefrontal cortex, integrates
sensory information and is important in socialization skills.1,17,25
The cerebellum is one of the later areas of the brain to mature. During
late second trimester and third trimester, when preterm infants are in
the neonatal intensive care unit, the cerebellum undergoes rapid growth
and complex, critical developmental processes.10,25 From 24 to 40 weeks
gestation, cerebellar volume increases 5-fold and surface area increases
more than 30-fold.1,5,15,26 Cerebellar growth and development are pri-
marily due to an increase in external granule cell numbers, granule cell
migration and initial establishment of cerebellar neuronal circuitry.16,25
The cerebellar germinal matrix reaches its maximum around 25 weeks,
then decreases rapidly.5 This secondary germinal matrix in the cerebel-
lum is vulnerable to bleeding. Preterm birth has been reported to lead
to decreased thickness in the external granular layer, increased packing
density of internal and external granular layer cells and decreased densi-
ty of cerebellar specic glial bers that are important for the migration of
granule cell (neuronal) precursors from the external to internal granular
layer.12,17 Injury to the cerebellum during this time can impair growth
and development and alter the developmental trajectory.25
Three mechanisms have been proposed for the alterations seen in
the cerebellum in VLBW infants: (1) direct injury (usually due to cere-
bral hemorrhage) leading to atrophy and growth failure; (2) indirect
cerebellar injury or underdevelopment associated with cerebral injury;
and (3) underdevelopment without any evidence of direct or indirect
injury (e.g., prematurity itself may be associated with impaired cerebel-
lar development due to unknown causes).23,27 Indirect injury involves
cerebellar injury in areas contralateral to the cerebral injury that leads
to decreased blood ow and metabolism in the contralateral cerebellum
resulting in decreased growth and cerebellar hypoplasia.23 The indirect
injury occurs via a process called crossed cerebellar diachisis. 14,15 This
means that disruption of activity in one area of the brain area can affect
 S. Blackburn / Newborn & Infant Nursing Reviews 16 (2016) 812
the organizational and function of other remote areas to which it is con-
nected via ber tracts.14
The incidence of CH is unknown but has received increased attention
in recent years due to improved imaging techniques. 25 Data suggest
that CH is more common than previously thought especially in infants
b750 g. 25,27 Studies based solely on neuroimaging (i.e. not including
postmortem reports), report an incidence of about 3% in VLBW and up
to 8.7% to 9% in infants b750 g.25,27 There have been increased investi-
gations into and recognition of CH in recent years with the advent of
cranial ultrasound (CUS) through sites other than the anterior fonta-
nelle (in particular the use of the posterolateral fontanelle, or mastoid
view) and availability of magnetic resonance imaging (MRI). 24,28
The exact etiology of CH in preterm infants is unclear, but includes
factors similar to that of GMH/IVH, which arises in the primary germinal
matrix. Proposed mechanisms for CH include immature cerebral auto-
regulation, increased venous pressure, fragility of the germinal matrix
blood vessels, altered GM coagulation, and vaso-occlusive injury leading
to bilateral infarcts of the cerebral hemispheres. 24,28,29 CH occurs rarely
in term infants and is usually secondary to birth trauma.
CH usually begins in the cerebellar hemispheres in layers that
include the germinal matrix and may extend to involve areas of the
cerebral cortex and white matter and, if large, put pressure on the
pons. 5 The most vulnerable time seems to be between 23 and
27 weeks gestation. 25 Risk factors include low gestational age, low
birthweight, and hypoxicischemic events. 25 Two forms of CH have
been usually reported: focal hemorrhage (often in association with
IVH) and a milder form with multiple small lesions. A recent study iden-
tied six types: extrusion of subarachnoid hemorrhage into the cerebel-
lums, small folial hemorrhage, bleeding in the cerebellar germinal
matrix, bilateral lobal hemorrhage, extensive lobar hemorrhage involv-
ing the vermis and contusional hemorrhage secondary to birth trauma.30
CH accompanied by supratentorial injury has a high mortality. 23,25,28
CH ranges from mild unilateral focal injury to extensive hemorrhage
that involves both cerebellar hemispheres as well as the vermis (area
between the hemispheres) that may or may not be associated with
supratentorial injury. 28 CH presentation may be silent, may present
with diffuse signs such as apnea, bradycardia, eye deviations, and al-
tered tone, or less commonly the infant may present with catastrophic
deterioration. 17,28,30 A recent study reported unexplained episodes of
motor agitation in many infants later diagnosed with CH, hypothesizing
that the damage from the hemorrhage reduced the usual motor inhibi-
tory effect of the cerebellum.30
CH can also lead to damage and altered development in other areas
of the brain in addition to the cerebellum.10,24 Outcomes are related to
the site of the hemorrhage, extensiveness of the damage, and presence
of supratentorial IVH.24 CH may alter subsequent cerebellar growth and
development. 10,28,29 VLBW infants tend to have a smaller cerebellum
into childhood and young adulthood. 31 Studies on preterm infants
with isolated CH are limited. A study of infants b32 weeks gestation
found that neurologic abnormalities were more common in infants
with CH including expressive language, cognitive, and behavioral
decits as well as abnormal autism screening. 10,28,29,32 Early disruption
of the cerebellum has been suggested as a risk factor for development
of autism spectrum disorders. 5,32 Abnormal cerebellar ndings are
frequently reported in postmortem studies of autism. 28 Decreased
cerebellar volume has been associated with supratentorial IVH but not
with the severity of PVL. 33,34 Impaired cerebellar growth in VLBW is
also associated with undernutrition, infection, postnatal steroids and
supratentorial injury. 33,34 A recent analysis of studies examining out-
comes of preterm infants with cerebellar injury reported that decreased
cerebellar volume was associated with impaired neuromotor and
cognitive performance.23 In general, in this study, direct cerebral injury
(such as CH) was associated with long term motor, cognitive and
language impairment with behavioral and socialization difculties;
indirect injury with cerebellar underdevelopment and hypoplasia; and
underdevelopment without evidence of direct injury with lower
11
cognitive abilities and an increased frequency of behavioral and psycho-
logic issues in adolescences and young adults.23
Implications for Nursing Care
White matter injury/PVL, GMH/IVH and cerebellar injury have simi-
lar factors in their etiology and pathogenesis, namely immaturity of the
preterm infants brain (developmental elements) and vulnerabilities to
damage from destructive events, most prominently hypoxia/ischemia
and infection/inammation. There are currently few specic interven-
tions to treat these disorders, thus the primary emphasis of nursing
care is on preventative, protective and supportive care. Back notes that
Factors such as improving nutrition, preventing infections, reducing
neonatal stress, and implementing earlier behavioral interventions may
all play a role in mitigating the impact of neuronal dysmaturation.4p,12
Prevention of brain injury in preterm infants begins in the perinatal
period with prevention of preterm birth, perinatal asphyxia and birth
trauma and use of prenatal glucocorticoids. 9,17 Nursing management
after birth involves recognition of factors that increase the risk of brain
injury, implementation of strategies to reduce the risks, and supportive
care. Ongoing assessment of fetal and neonatal oxygenation and perfu-
sion is important in order to recognize subtle alterations and intervene
early to avoid cerebral hyperperfusion and stabilize cerebral blood ow
and pressures.17
Prevention and risk reduction activities include interventions to
avoid/reduce hypoxia or asphyxia events and rapid alterations in cere-
bral blood ow, prevent uctuations in systemic blood pressure, pre-
vent hyperosmolality, and prevent/minimize uctuations in cerebral
pressures.17,35 Fluctuations in cerebral blood ow can be reduced by op-
timizing ventilation, use of synchronized ventilation (assist control or
synchronized mandatory ventilatory modes, and suctioning only as
needed and not routinely.9 Hypertonic solutions and volume expanders
are administered slowly with careful monitoring of vital signs. Since sei-
zures can alter cerebral blood ow and pressures, seizures must be
promptly recognized and treated.17,35
Carefully monitor vulnerable infants and maintain oxygenation and
perfusion to prevent initial and further damage. Vital signs, oxygen
saturations, blood gases, blood pressure, tone, activity and level of con-
sciousness are assessed.17,35 Other general supportive measures include
maintenance of oxygenation, ventilation and perfusion pressures, cor-
rection of acidbase abnormalities, avoiding or reducing noxious proce-
dures and crying, limiting unnecessary handling and stimulation,
nutritional support, and temperature control. 17,35 Provide physiologic
support with maintenance of oxygenation, perfusion, normothermia
and normoglycemia.
Activities that can increase intracranial pressure or cause wide
swings in arterial or venous pressure are avoided or minimized when
possible. 17 Place the VLBW infant in a neutral position with the head
in midline and avoid exing the neck. Avoid turning the head sharply
and turn the body as a unit. Turning the head sharply to the side can in-
crease cerebral pressures by obstructing the ipsilateral jugular vein.25,36
Raise the head of the bed slightly to reduce intracranial pressure. Avoid
raising head and feet above head, such as with diaper change.17,36 Avoid
use of constricting headbands (such as tight bilirubin masks) that can
increase cerebral pressures and alter blood ow.17
Use of individualized developmentally supportive care interventions
such as containment or swaddling during aversive procedures (for ex-
ample, during endotracheal suctioning) may promote greater physio-
logic stability during these procedures and a more rapid return to
baseline.17 Reduce environmental stressors and minimize physical ma-
nipulations and handling of vulnerable infants to reduce the risk of hyp-
oxia and uctuations in arterial blood pressure and cerebral blood
ow. 17,35 Recognition and prompt management of pain and stress are
also important as procedural pain and stress are associated with altered
brain maturation, function and growth.4,3739
12 S. Blackburn / Newborn & Infant Nursing Reviews 16 (2016) 812
Parent care involves recognition and discussion of parental concerns
about their infant's immediate and long term prognosis and teaching re-
garding the infants problems, their implications, and management. Par-
ents need to be shown how to interact with and care for the infant in a
developmentally appropriate manner with a goal of promoting oppor-
tunities for the parents to interact with their infant while minimizing
stressful events. 17,35 The nurse can model this care for the parents
and provide anticipatory guidance as to how the infant's needs and
care will change as the infant matures. 18p.419 Parents should also be
involved in developing and implementing a developmental plan of
care to their infant to reduce environmental stressors.18p.417
Summary
Preterm infant, especially those who are VLBW, are at risk for
neurodevelopmental injury and later disabilities due to vulnerabilities
of their brain during the time that they are in the neonatal intensive
care unit as well as risk for hypoxia, ischemia, infection and inamma-
tion. Nurses have a critical role in the prevention or expansion of brain
injury in preterm infants during the perinatal period and the extension
of injuries that have already occurred. Major components of nursing
management include interventions to reduce activities that can lead to
hypoxia or asphyxia events, rapid alterations in cerebral blood ow
and pressures and uctuations in systemic blood pressure. Prompt rec-
ognition and management of pain and stress are also critical. Use of in-
dividualized developmentally supportive care, including handling and
positioning techniques, can promote physiologic stability during and
after caregiving and reduce environmental stress. Finally nurses must
collaborate with parents in developing and implementing care plans
for each infant that promote optimal outcomes.
References
1. Volpe JJ. Neurology of the newborn. 5th ed. Philadelphia: Saunders/Elsevier. 2008.
2. Volpe JJ. The encephalopathy of prematuritybrain injury and impaired brain devel-
opment inextricably entwined. Semin Pediatr Neurol. 2009;16:167-78.
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