SPRELIMINARY REPORT

OF CEREBRAL PALSY

Arranged by:

ANNISA HAFIZAH

1614401320211

UNIVERSITY OF MUHAMMADIYAH BANJARMASIN

FACULTY OF NURSING AND HEALTH SCIENCE

INTERNATIONAL CLASS OF NURSING DIPLOMA PROGRAM

ACADEMIC YEAR 2016/2017

1. Anatomy and Physiology

To better understand cerebral palsy, it helps to understand the anatomy of the brain. The
brain is well protected by:

 The scalp
 The skull
 The dura
o A tough 3-layer sheath that surrounds the brain and spinal cord
o Layers include the dura mater (strongest layer), arachnoid mater (middle layer),
and pia mater (closest to the brain)

The brain is a complicated structure containing many parts. These include:

 The cerebrum:
o Made up of two cerebral hemispheres that are connected in the middle
o It is the largest part of the brain
o Each area of the cerebrum performs an important function, such as language or
movement
 o Higher thought (cognition) comes from the frontal cortex (front portion of the
cerebrum)
o Outside of the cerebrum are blood vessels
o There are fluid-filled cavities and channels inside the brain
 The cerebellum:
o Located in the lower, back part of the skull
o Controls movement and coordination
 The brainstem and pituitary gland:
o Responsible for involuntary functions such as breathing, body temperature, and
blood pressure regulation
o Pituitary gland is the "master gland" that controls other endocrine glands in the
body, such as the thyroid and adrenal glands
 The cranial nerves:
o Twelve large nerves exit the bottom of the brain to supply function to the senses
such as hearing, vision, and taste
 The cerebral blood vessels:
o A complicated system that supplies oxygenated blood and nutrients to the brain

The blood supply to the brain is divided into two main parts:

 Anterior cerebral circulation:

o The front of the brain is supplied by the paired carotid arteries in the neck.
 Posterior cerebral circulation:
o The back portion of the brain is supplied by the paired vertebral arteries in the
spine.

Brain injury or malformation in areas that affect mobility before, during, or after birth
causes CP. In addition to the varying areas of the brain that could be affected, as
mentioned above, timing of this injury or malformation is also a variable. Damage to the
developing brain can be caused by:
http://neonatology.ucsf.edu/specialized-care/cerebral-palsy.aspx

 Cerebral Dysgenesis—refers to the brain either not developing fully or growing

abnormally, both of which can include but are not limited to incomplete division or
organization
 Preventricular Leukomalacia—poor myelination by oligodendrocytes prenatally
o Toxins from intrauterine infections cause the poor myelination by permeating the
membranes surrounding the fetus and integrating with the amniotic fluid
 Hypoxic-Ischemic Encephalopathy or Intrapartum Asphyxia—oxygen deprivation for a
long enough duration to permanently damage brain tissue

http://neonatology.ucsf.edu/specialized-care/cerebral-palsy.aspx
 o Oxygen deprivation is common in premature infants who cannot take a big
enough breath of air when they are first born; also infants who are unfortunate
enough to have the umbilical cord wrapped around their neck for too lung suffer
the same way
 Neonatal Stroke—as with adults, blockage to blood vessels supplying nutrients to the
developing brain can lead to permanent tissue death, not allowing for the brain to make
connections to those areas
 Genetic and environmental factors interrupting and disturbing brain cell migration to
their appropriate locations prenatally
 Trauma, infections, or asphyxia in early infancy that damage cell tissue denying the
ability for the brain to make connections to those areas
 Intracranial Hemorrhage
o The bleeding from trauma can lead to a hematoma, which can press on areas of
the developing brain and/or deprive it of blood flow, killing the tissue as a result
1. Definition of Cerebral Palsy

Cerebral palsy (CP) is a heterogeneous group of movement disorders with

various etiologies.

The primary functional difficulty is in movement and posture, i.e. the movement
disorder is not secondary to another neurofunctional disability.

Cerebral palsy is associated with a permanent, non-progressive pathology that formed

in utero or early infancy (before 2-3 years of age).

Cerebral Palsy excludes transient disease processes.

Cerebral Palsy is often accompanied by disturbances of sensation, perception, cognition,

communication, behaviour, epilepsy, and secondary musculoskeletal problems. (Laura
Rogers and Eric Wong, Dr. Peter Rosenbaum, Professor, Pediatrics (McMaster
University)).

Cerebral Palsy (CP), is used to refer to a disorder that arises because of brain damage that
affects movement or posture. (Boyd, D., & Bee, H. (2012) The Developing Child (13th ed).
Boston, MA: Pearson).

Cerebral palsy (CP) is a group of non-progressive, permanent disorders of the development of

movement and posture. (Dev Med Child Neurol Suppl. 2007 Feb; 109():8-14.)
2. Etiology of Cerebral Palsy

Antenatal (~70-80% of causes)

Prematurity and low birth weight

 Greater risk of CP with preterm deliveries (but since most deliveries happen close to
term, most infants with CP (75%) are born after 36 weeks).
o There is a U-shaped association between CP and gestational age, where incidence
of CP is increased in both preterm and postterm babies. The mechanism may be
related to the physiological changes that trigger labour. Parturition is
hypothesized to be partially related to fetal brain maturity, as fetuses with cerebral
 abnormalities tend to be delivered either preterm or postterm.
JAMA. 2010 Sep 1;304(9):976-82.
o Periventricular leukomalacia (PVL) is a condition of underdeveloped white
matter in the brain surrounding the ventricles. It is the leading cause of CP in
preterm infants. PVL is discussed in the Pathophysiology section below.
o Intraventricular hemorrhage (IVH) is predominantly associated with
prematurity and is due to fragility of developing blood vessels in the infant’s
brain. IVH may cause PVL or ischemia in other parts of the brain. See
Pathophysiology for details.

Infections

 Fetoplacental and uterine infection or inflammation can cause initiation of preterm

labour, which can lead to CNS injury and CP. Underdeveloped fetal brains are more
susceptible to inflammation and inflammatory cytokines. These cytokines are
hypothesized to be responsible for the development of PVL.
o Chorioamnionitis is an infection of the chorion and amnion, the two membranes
surrounding the developing fetus. It is the most frequently associated maternal
infection in CP.
o TORCHS is an acronym for perinatal infections: toxoplasmosis, other infections
(varicella zoster, adenovirus, enterovirus), rubella, cytomegalovirus, herpes
simplex virus, syphilis. TORCHS infections are associated with approximately 5%
of all CP cases.

Multiple gestation

 Increases the risk of antenatal complications, such as preterm labour, growth restriction,
low birth weight, and death of a co-twin.
 Death of a co-twin in utero has been shown to induce neuropathologic changes that can
lead to CP in the surviving twin. Prevalence of CP in the surviving twin was found to be
15x higher than average.
 Twinning is the single strongest risk factor for the development of CP.
Pregnancy complications in the mother

 Thrombophilias can lead to placental vascular injury and clotting of the fetal vessels.
 Hemorrhage and preeclampsia (placental abruption, placenta previa, and other causes
of third trimester bleeding) seem to lead to premature delivery, conferring the same risks
for CP as a premature infant according to some evidence.

Perinatal

 Birth asphyxia (~10%) is commonly associated with CP.

 CP is associated with complicated labour and delivery, but there is not a clear
association between CP and the quality of perinatal care.
 Despite the advancement of prenatal and obstetrical care in the past 30 years, the
incidence of CP has remained constant. This may be due to increased survival rates of
premature and low birth weight babies.

Postnatal

 Non-accidental injury
 Head trauma
 Meningitis/encephalitis (including cerebral malaria in the developing world)
 Cardiopulmonary arrest

Obstetrical care (protective factors)

 Magnesium sulfate (used for tocolysis for preterm labour, and to increase the seizure
threshold in mothers with preeclampsia) may reduce the risk of CP according to some
studies, but further research is needed before it is used specifically as a neuroprotective
agent for preterm births.
 Antibiotics used to treat bacterial vaginosis may reduce the rate of preterm delivery. In
women with premature rupture of membranes, antibiotics reduce the risk of
chorioamnionitis.
 Corticosteroids reduce the risk of CP, as steroids inhibit cytokine production, thus
preventing PVL. (Pediatr Neurol. 2009 Mar;40(3):168-74)

Signs and symptoms

Signs of cerebral palsy include the following:

 History of gross motor developmental delay in the first year of life

 Abnormal muscle tone: The most frequently observed symptom; the child may present as
either hypotonic or, more commonly, hypertonic, with either decreased or increased
resistance to passive movements, respectively; children with cerebral palsy may have an
early period of hypotonia followed by hypertonia. A combination of axial hypotonia and
peripheral hypotonia is indicative of a central process.
 Definite hand preference before age 1 year: A red flag for possible hemiplegia
 Asymmetrical crawling or failure to crawl
 Growth disturbance: Especially failure to thrive
 Increased reflexes: Indicating the presence of an upper motor neuron lesion; this
condition may also present as the persistence of primitive reflexes
 Underdevelopment or absence of postural or protective reflexes

The patient’s overall gait pattern should be observed, and each joint in the lower and upper
extremity should be assessed for signs of cerebral palsy, including the following:

 Hip: Excessive flexion, adduction, and femoral anteversion make up the predominant
motor pattern; scissoring of the legs is common in spastic cerebral palsy
 Knee: Flexion and extension with valgus or varus stress occur
 Foot: Equinus, or toe walking, and varus or valgus of the hindfoot is common in cerebral
palsy. (Hoda Z Abdel-Hamid, MD, 2012 Assistant Professor, Department of Pediatrics,
University of Pittsburgh School of Medicine)
3. Pathophysiology

Preterm infants

The premature neonatal brain is susceptible to two main pathologies: intraventricular

hemorrhage (IVH) and periventricular leukomalacia (PVL). Although both pathologies
increase the risk of CP, PVL is more closely related to CP and is the leading cause in preterm
infants. The term PVL describes white matter in the periventricular region that is
underdeveloped or damaged (“leukomalacia”). Both IVH and PVL cause CP because the
corticospinal tracts, composed of descending motor axons, course through the
periventricular region.

Intraventricular hemorrhage (IVH)

IVH describes bleeding from the subependymal matrix (the origin of fetal brain cells)
into the ventricles of the brain. The blood vessels around the ventricles develop late in the
third trimester, thus preterm infants have underdeveloped periventricular blood vessels,
predisposing them to increased risk of IVH. The risk of CP increases with the severity of
IVH.

Periventricular leukomalacia (PVL)

IVH is a risk factor for PVL, but PVL is a separate pathological process. The
pathogenesis of PVL arises from two important factors: (1) ischemia/hypoxia and (2)
infection/inflammation.
 Ischemia/hypoxia: The periventricular white matter of the neonatal brain is supplied by
the distal segments of adjacent cerebral arteries. Although collateral blood flow from two arterial
sources protects the area when one artery is blocked (e.g., thromboembolic stroke), this
watershed zone is susceptible to damage from cerebral hypoperfusion (i.e., decreased cerebral
blood flow in the brain overall). Since preterm and even term neonates have low cerebral blood
flow, the periventricular white matter is susceptible to ischemic damage. Autoregulation of
cerebral blood flow usually protects the fetal brain from hypoperfusion, however, it is limited in
preterm infants due to immature vasoregulatory mechanisms and underdevelopment of arteriolar
smooth muscles.

Infection and inflammation: This process involves microglial (brain macrophage) cell
activation and cytokine release, which causes damage to a specific cell type in the developing
brain called the oligodendrocyte. The oligodendrocytes are a type of supportive brain cell that
wraps around neurons to form the myelin sheath, which is essential for white matter
development. Intrauterine infections activate the fetal immune system, which produces cytokines
(e.g., interferon γ and TNF-α) that are toxic to premyelinating oligodendrocytes. Infections also
activate microglial cells, which release free radicals. Premyelinating oligodendrocytes have
immature defences against reactive oxygen species (e.g., low production of glutathione, an
important antioxidant). IVH is hypothesized to cause PVL because iron-rich blood causes iron-
mediated conversion of hydrogen peroxide to hydroxyl radical, contributing to oxidative
damage.

Excitotoxicity is a process where increased extracellular glutamate levels stimulate

oligodendrocytes to increase calcium influx, which stimulates reactive oxidative species release.
Glutamate is increased because hypoxia causes white matter cells to reduce reuptake of
glutamate due to lack of energy to operate glutamate pumps. Glutamate is also released from
microglial cells during the inflammatory response.
 Term infants

 Circulation and autoregulation of cerebral blood flow are similar to that of an adult in a
full term infant. Ischemic and hemorrhagic injuries tend to follow similar patterns of
those in adults:
o Watershed areas where the three major cerebral arteries end in the cortex. This
is the most common area of injury.
o Basal ganglia damage can cause extrapyramidal or dyskinetic CP.
4. Management

Management of abnormal movements

Numerous medications, including the following, may relieve the movement difficulties
associated with cerebral palsy:

 Botulinum toxin with or without casting: Botulinum toxin (Botox) type A may reduce
spasticity for 3-6 months and should be considered for children with cerebral palsy with
spasticity.
 Phenol intramuscular neurolysis: This agent can be used for some large muscles or when
several muscles are treated, but phenol therapy is permenant.
 Antiparkinsonian, anticonvulsant, antidopaminergic, and antidepressant agents: Although
antiparkinsonian drugs (eg, anticholinergic and dopaminergic drugs) and antispasticity
agents (eg, baclofen) have primarily been used in the management of dystonia,
anticonvulsants, antidopaminergic drugs, and antidepressants have also been tried

Surgery

Surgical treatments used in patients with cerebral palsy include the following:

 Intrathecal baclofen pump insertion: To treat spasticity and/or dystonia [6]

 Selective dorsal rhizotomy: To treat velocity-dependent spasticity [7, 8]
 Stereotactic basal ganglia: May improve rigidity, choreoathetosis, and tremor
 Orthopedic surgical intervention: To treat scoliosis, joint contractures or dislocation

 Nelson Textbook of Pediatrics, 18E.

 Rosenbaum P, Rosenbloom L (2012). Cerebral Palsy. From Diagnosis to Adult Life.
London: Mac Keith Press.

 Children with CP often have multiple developmental issues that are best managed by a
multidisciplinary team of health care professionals. (Hoda Z Abdel-Hamid, MD, 2012
Assistant Professor, Department of Pediatrics, University of Pittsburgh School of Medicine)
 Child Development Teams act as excellent liaisons between the different health care
professionals, and are able to provide a structured program for treatment, suitable to each
child’s needs.
 Health care professionals usually involved in the care of children with CP include:
o Developmental pediatricians
 Monitor and promote the child’s development.
 Connect with other health care professionals as needed.
 Support children and families with the patient’s development in the
context of their individual family and community.
o Occupational therapists
 Implement the use of assistive devices (e.g., wheelchairs, ankle-foot
orthosis (AFOs), walkers, appropriate toys, and adaptations) that can be
made to the home to accommodate the child.
o Speech therapists
 Assist with feeding, as these children often have difficulties with chewing
and swallowing.
 The development of speech language and the provision of non-verbal
communication systems as necessary.
o Physiotherapists
 Assist with the development of muscle control, overcoming weakness,
minimizing spasticity, and preventing contractures.
o Nutritionists
 Malnutrition may be seen in children with feeding difficulties.
 Food must be given in a form that the child is able to chew and swallow.
 Energy-rich supplements may be needed.
 Enteral feeding may also be necessary if oral intake is insufficient to
maintain nutrition via surgical placement of G-tube or GJ-tube.
o Orthopedic surgeons
 Chronic muscle weakness or spasticity can cause orthopedic deformities
that need surgical correction, e.g., dislocation of the hips due to spasticity
of the thigh adductors, deformity of the ankle from calf muscle spasticity.
5. Diagnostic Examination of Cerebral Palsy

A cerebral palsy diagnosis is made by a variety of medical specialist using multiple tests,
which can include neurogical imaging, screenings for disabilities, disorders and coagulation
issues and reflex tests, among others.

 Using Neuroimaging to Diagnose Cerebral Palsy

Magnetic resonance imaging (MRI) is a test that uses a magnetic field and pulses
of radio wave energy to make pictures of the brain. MRI often gives different
information about structures in the brain than can be seen with an X-ray, ultrasound, or
computed tomography (CT) scan. MRI also may show problems that cannot be seen with
other imaging methods. It can also sometimes be combined with magnetic resonance
spectroscopy (MRS), which can help understand what is going on not just on th structural
level, but also on the metabolic level.

MRI of the baby’s brain can identify a brain injury, such as a lesion in the brain,
in the majority of cases of cerebral palsy. In addition, MRI may provide information
regarding the timing of the brain insult. MRI abnormalities in babies with cerebral palsy
include hypoxic ischemic lesions, such as those associated with hypoxic ischemic
encephalopathy (HIE) and periventricular leukomalacia (PVL).

 Screening for Problems Associated with Cerebral Palsy

Screening for intellectual disability, eye and hearing problems, speech and
language disorders, and disorders of mouth muscle function must be performed as part of
the initial assessment for cerebral palsy because these problems are commonly associated
with cerebral palsy.

 Using EEG Testing to Diagnose Cerebral Palsy

An electroencephalogram (EEG) must be performed when there are features that

suggest the child has epilepsy. The reason for this is because seizures occur in about
45% of children who have cerebral palsy. Epilepsy and seizure disorders must be
promptly diagnosed and treated because seizures can worsen brain damage, which can
cause the cerebral palsy to be more severe. Furthermore, seizure activity can cause
additional brain injuries – injuries that cause problems in addition to the cerebral palsy.

 Screening for Coagulation Problems to Diagnose Cerebral Palsy

Some children with hemiplegic cerebral palsy or MRI findings that show cerebral
infarction (brain tissue death caused by oxygen deprivation (HIE)) may have a blood
clotting disorder called prothrombotic coagulation disorder. It is standard practice to
screen for coagulation abnormalities in such patients so that this disorder can be properly
managed. Children with hemiparesis, which is less severe than hemiplegia, should be
tested for HIE.

 Using Reflex Tests to Diagnose Cerebral Palsy

In normally developing babies, most developmental reflexes pertaining to posture

disappear when the baby is between 3 and 6 months of age. These reflexes do not
properly function or disappear when a child has cerebral palsy. Therefore, delay in the
disappearance of a developmental reflex may be an early indication of cerebral palsy.
Exaggerated developmental reflexes are also an early sign of cerebral palsy.

Testing the tonic labyrinthine reflex (TLR) is very important. The TLR is a
primitive reflex found in newborns. With this reflex, tilting the head back while lying on
the back (supine) causes the back to stiffen and arch backwards, the legs to straighten,
stiffen and push together, the toes to point, the arms to bend at the elbows and wrists, and
the hands to become fisted or the fingers to curl. The presence of the TLR past the first 6
months of life may indicate that the child has cerebral palsy. In children with cerebral
palsy, the TLR may even be more pronounced.
6. Complication of Cerebral Palsy

Some people with CP have associated disorders, such as impaired intellectual

development, seizures, failure to grow and thrive, and vision and sense of touch problems.

Roughly a third of patients with CP have mild intellectual impairment, another third are
moderately or severely impaired, and the remainder are intellectually normal. Mental
impairment is most common in children with spastic quadriplegia.

As many as half of all patients with cerebral palsy have seizures in which uncontrolled
bursts of electricity disrupt the brain's normal pattern of electrical activity. Seizures that recur
without a direct trigger, such as a fever, are classified as epilepsy. Seizures generally are
tonic-clonic or partial.

Tonic-clonic seizures spread throughout the brain, typically causing the patient to cry
out, followed by unconsciousness, twitching legs and arms, convulsive body movements, and
loss of bladder control.

Partial seizures are confined to one part of the brain and may be simple or complex.
Simple partial seizures cause muscle twitching, chewing movement, and numbness or
tingling. Complex partial seizures can produce hallucinations, staggering, random movement,
and impaired consciousness or confusion.

Children with moderate-to-severe cerebral palsy—especially those with spastic

quadriplegia—often experience failure to grow or thrive. Infants fail to gain weight
normally, young children may be abnormally short, and teenagers may be short for their age
and may have slow sexual development. These phenomena may be caused by a combination
of poor nutrition and damage to the brain centers that control growth.

Some patients, particularly those with spastic hemiplegia, have muscles and limbs that
are smaller than normal. Limbs on the side of the body affected by CP may grow slower than
those on the other side. Hands and feet are most severely affected. The affected foot in cases
of hemiplegia usually is the smaller of the two, even in patients who walk, suggesting the
size difference is due not to disuse but to a disrupted growth process.

Vision and hearing problems are more common in people with cerebral palsy than in the
general population. Differences in the left and right eye muscles often cause the eyes to be
misaligned. This condition, called strabismus, causes double vision; in children, however, the
brain often adapts by ignoring signals from one eye. Because strabismus can lead to poor
vision and impaired depth perception, some physicians recommend corrective surgery.

Patients with hemiparesis may have hemianopia, a condition marked by impaired vision
or blindness in half of the visual field in one or both eyes. A related condition, called
homonymous hemianopia, causes impairment in the right or left half of the visual fields in
both eyes.
 Sensations of touch or pain may be impaired. A patient with stereognosis, for example,
has difficulty perceiving or identifying the form and nature of an object placed in their hand
using the sense of touch alone.

Hip dislocation, curvature of the spine (scoliosis), incontinence, constipation, tooth decay
(dental caries), bronchitis, skin sores, and asthma are other complications commonly
experienced by people with CP.
7. Nursing Care in Cerebral Palsy Patient

A. Assessment

1. General Data
Includes the patient's identity and the person in charge of the patient
No registration :
Patient's name :
Age :
Mother's name :
Father's name :
Family health history :

2. Medical history
Health history related to prenatal, natal and post natal factors and circumstances around
birth.

3. Complaints and clinical manifestations

Observe the manifestations of cerebral palsy, especially those associated with
achievement of development:

- Deceleration of gross motor development

Common manifestations, delays in all motor achievements, but increased in line with
growth.
- Abnormal motor display
Unilateral use of unilateral hands, abnormal asymmetrical crawling, standing or tiptoing,
involuntary or uncoordinated movements, poor sucking, feeding difficulties, persistent
tongue sprue.
- Changes in muscle tone
Increased or decreased resistance to passive movements, opistotonic posture (excessive
back arch), feeling stiff in holding or dressing, difficulty in using diapers, stiffening or
not bending on the hips and knee joints when pulled into a sitting position (early sign).
- Posture abnormal
Maintain a higher hips from the body on the stomach, cross or extend the foot with
plantar feet flexed in supine position, shoulder abduction arm, flexed elbow, fist
clenched.
- Reflex abnormalities
Primitive infantile reflex persists (Tonic neck reflex is present at any age, not settled
above 6 months of age), Moro reflex, plantar, and clashing or hyperactive, Hiperefleksia,
ankle clonus and stretch reflexes appear in many muscle groups in rapid passive
movement .

- Companion abnormalities (may exist, or not).

Subnormal learning and reasoning (mental retardation in about two-thirds of individuals).
Damage behavior and interpersonal relationships. Other symptoms that can also be found
in cerebral palsy are:
1) Intelligence below normal
2) Mental retardation
3) Sucking or eating disorders
4) Irregular breathing
5) Impaired development of motor skills (eg reaching for something, sitting, rolling,
crawling, walking)
6) Speech disorder (dysarthria)
7) Impaired vision
8) Hearing loss
9) joint contractures
10) Restricted Movement

B. Physical Examination
a. Musculuskeletal: spasticity, ataxia
b. Neurosensory:
 - High noise-capturing noise
- Speech disorder
- Children drool
- Lips and tongue moves by itself
c. Nutrition: less intake

C. Supporting investigation
Clinical examination to identify abnormalities of tone, frequent hypotonics
followed by hypertonic, postural abnormalities and motor developmental delays. CT scan
to detect central nervous system lesions. Positron emission tomography and computerized
photon emission single emission to see brain metabolism and perfusion. MRI to detect
small lesions. Eye and hearing examination is done immediately after the CP diagnosis is
established. Electro-examination Encephalography is performed in patients with seizures
or in hemiparesis class who are both nippy and not. Photo head (X-ray) and CT Scan.
Psychological assessment needs to be done to determine the level of education required.
 D. Nursing Intervention

No. Nursing Diagnosis Goal Intervention Rational

1. Impaired Physical Mobility The child will ■ Perform ■ Delayed
related to decreased muscle attain maximum development development
strength and control physical abilities assessment milestones
possible and record age are common
EXPECTED of achievement with cerebral
OUTCOME: of palsy.
The child reaches milestones (e.g., Once one
maximum reaching for milestone is
physical objects, sitting) achieved,
mobility and all ■ Plan activities interventions
developmental to use gross and are revised to
milestones. fine assist in
motor skills the next skill
(e.g., holding necessary.
pen or ■ Many
eating utensils, activities of
toys positioned daily living and
to play activities
encourage promote
reaching and physical
rolling development.
over) ■ The child
■ Allow time for may perform
the child to tasks more
complete slowly than
activities most children.
■ Perform ■ Promotes
range-of-motion mobility and
exercises increased
every 4 hours circulation, and
for the child decreases the
unable risk
to move body of contractures.
parts. Position ■ A regular and
the frequently
child to promote reevaluated
tendon rehabilitation
stretching program
(e.g., foot assists in
plantar flexion promoting
instead of development.
dorsiflexion, ■ Adaptive
legs extended devices are
instead often
of flexed at necessary to
knees and hips) maximize
■ Arrange for physical
and encourage mobility.
parents
to keep
appointments
with a
rehabilitation
therapist.
■ Teach the
family to
maintain
appropriate
brace wear.
2. Sensory/Perceptual Alteration: The child will ■ Facilitate eye ■ Adaptive
Visual or Auditory related to receive and and auditory devices often
cerebral damage benefit examinations by enhance
from varied forms specialist. sensory input.
of sensory and Promote These devices
perceptual input. the use of need
EXPECTED adaptive devices frequent
OUTCOME: (glasses, changes as the
The child receives contact lenses, child
adequate hearing aids), grows.
sensory/perceptual and ■ Other senses
input to maximize encourage can compensate
developmental recommended for
outcome return those that are
visits to impaired.
specialists.
■ Maximize the
use of intact
senses
(e.g., describe
verbally the
surroundings to
a child with
poor
vision, allow
touching of
objects,
provide visual
materials to
enhance
learning in the
 child with
impaired
hearing, use
computers to
promote
communication).
3. Altered Nutrition: Less than The child will ■ Monitor ■ Insufficient
Body Requirements related to receive nutrients height and intake can lead
difficulty in chewing and needed for normal weight and to
swallowing and high metabolic growth. plot on a growth impaired
needs EXPECTED grid. Perform growth and
OUTCOME: hydration status dehydration.
The child shows assessment. ■ Special
normal growth ■ Teach the techniques can
patterns for family facilitate
height, weight, techniques to food intake.
and other promote caloric ■ Aspiration
physical and nutrient pneumonia is a
parameters. intake: risk for
■ Position the the child with
child upright for poor
feedings. swallowing.
■ Place foods Special feeding
far back in the techniques may
mouth to be
overcome needed.
tongue
thrust.
■ Use soft and
blended foods.
■ Allow extra
time and quiet
environment for
meals.
■ Perform
frequent
respiratory
assessment.
Teach the family
to
avoid aspiration
pneumonia.
Teach
care of
gastrostomy and
tube
feeding
technique as
appropriate.
 BIBLIOGRAPHY

Boyd, D., & Bee, H. (2012) The Developing Child (13th ed). Boston, MA: Pearson

Arch Dis Child Fetal Neonatal Ed. 2008 Mar;93(2):F153-61.

Pediatric Ophthalmology: Current Thought and a Practical Guide, 1E (Wilson

Dev Med Child Neurol Suppl. 2007 Feb;109:8-14