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Neurological Dysfunction
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OverviewNeurological Assessment
Anatomic and Physiologic Changes
Increased Intracranial Pressure
Meningitis
Reye Syndrome
Febrile Seizures
Hydrocephalus
Acute Head Injury
Seizure Disorder
Meningomyelocele
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Neurological Assessment/History
It all begins with the history...
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Neurological Assessment/History
Prenatal Factors:
Maternal Age
Maternal Health
Adequacy of Prenatal Care
Exposure to Teratogens
Family Support
Resources during Pregnanacy
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Neurological Assessment/History
Perinatal Factors
position of fetus
progression of labor
premature ROM/fever
anesthesia/medicationsplacental function
monitoring abnormalities
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Neurological Assessment/History
Postnatal Factors
APGAR scoresmeconium
hypoxia (ABGs)
assisted ventilationhyperbilirubinemia
infections
seizures
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Neurological Assessment/History
Childhood Problems
Growth Parameters
Illnesses/Operations
Immunizations
Exposure to Illness
Injuries
Seizures
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Assess individual
trend on curve
Height, Weight, Head
Circumference ismonitored
Be alert to growth
deceleration
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Neurological Assessment/History
Developmental HistoryAge milestones achieved
School performance
Need for early intervention
Plateau or regression
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Neurological Assessment/History
Family History
sudden death/cardiac problems
genetic conditions/mitochondrial conditions
frequent miscarriages
hypotonia
cerebral palsy
epilepsy
mental retardation
developmental delay
s stemic roblems
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Neurological Assessment/Physical Exam
Observation is the cornerstone of the pediatric exam!
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Neurological Assessment/Physical Exam
Do not require the patient to sit on table or bedunless appropriate
Examine from least painful/intrusive to most
Allow parent to hold the child
Make a game out of the examination
Use familiar toys or objects
Look for symmetry
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Neurological Assessment
General Exam
Note head shape, symmetry, and size
Measure occipitofrontal circumference (OFC)Note general appearance of spine
Note overall tone and symmetry of extremities
Note general appearance and behaviorNote socialization skills and interpersonal interaction
Note interaction with caregiver
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Head Circumference
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Fontanelle Assessment
Assess for overriding,nonmobile sutures
AF = closes 14-18 months
PF = closes 6-8weeks
Fontanelles bulge withcrying and activity
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Components of the
Neurological ExaminationMental State
Cranial NervesMotor
Sensory
Cerebellar
Reflexes
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Mental State: Attention
Note level of infant alertnessNote ability to engage child
Adolescent: ask to spell house
forward and backward
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Mental State: Orientation
Infant: assess quality of awake time, ease of arousal
ability to calm
As child develops can begin to assess orientation aroundage 3-4
Full orientation assessment begins at ages 7-8
The adolescent should respond to all components of the
orientation exam
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Mental State:
Speech and LanguageInfant: note cry (shrill, lusty, weak, silent)1-3 months: Ooh, ah sounds
5-7months: single syllables (dada, baba) babbling12-18 months: 3 words
17-24 months: combines words
By age 2: 50 words18-24 months: begins to learn body parts
**Language is closely related to speech, if a childhas language difficulty suspect hearing loss!!!
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Mental State: Memory
As the child learns memory is constantly in play
Assess fund of knowledge, recognition of objects,evaluate school performance
If note developmental delay where memory ability isin question, refer for neurophsychological testing
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Cranial Nerves: I
OlfactoryRarely tested in children; testing same as adult
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Cranial Nerves: IIOptic Nerve
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Cranial Nerves: II
Optic NerveNote infants ability to fix on face and objects
Binocular vision attempted at 3 monthsElevated disc margins and 20/20 vision by age 2 years
Observe the toddler interacting with the environment
Age 7-8 can begin to use Snellen eye chart
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Cranial Nerves: II
Optic Nerve
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Cranial Nerves:
III, IV, VITested together because they control eye movementIII: Oculomotor:
pupil constriction, holds eye open, movement superiorly,inferiorly, and medially
IV: Trochlear:
moves eye down and outVI: Abducens:
lateral gaze
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Cranial Nerves:
III, IV, VINystagmus:
normal to 3 monthsStrabismus:
may be normal up to 6months
Test Visual Fields:
use brightly coloredtoy
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Cranial Nerves: V
Trigeminal Nerve
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Cranial Nerves: V
Trigeminal NerveInfant: assess ability to suck
Child: assess strength of chewing/biting
Adolescent: clench jaw
Sensation throughout face is assessed in all agegroups
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Cranial Nerves: VII
Facial
Note symmetry of face
Note ability to move face
Strength of eye closure
Have child make funny faceswith you
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Cranial Nerves: VIIFacial
What is this?
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Cranial Nerves: VIII
VestibularcochlearInfants: use a bell or snap fingers behind ear
turns head to sound, startles to noise,
By 3 months: quiets to mothers voice
Toddler/child: speech delay may be a sign of hearing
impairment
School age and beyond: formal hearing screening
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Cranial Nerves: IX, X
Glossopharyngeal, Vagus
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Cranial Nerves: IX, X
Glossopharyngeal, VagusAssess ability to swallow, symmetry of uvula , speech
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The posterior fossa surgical approach places the childat risk for IX and X cranial nerve damage
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Cranial Nerves: XI
Spinal Accessory
Note stability of headposition
Ask child and adolescent to
shrug shoulders
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Cranial Nerves: XII
HypoglossalMovement of tongue, observeat rest and have child stick
tongue out and move fromside to side
Note fasciculations (sign of
motor weakness)
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Motor Exam
Note Tone and Strength
Assess Progression of Motor Milestones
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Motor Milestones/Gross
Lifts head to chin, hands to midline: 2 months
Roll over: 2.5 - 5 months
Sit without support: 6 months
Crawl: 6-8 months
Pull to stand: 8-10 months
Walk: 11-15 months
Run: 14-19 months
Walks up steps: 15-22 months
Hop: 3-4 years
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Motor Milestones/Fine
Neat pincer grasp: 9 months
Tower of 4 cubes: 15-20 months
Copy circle: 3 years
Draw a 3 part person: 3.5-4.5 years
Diagonal line: 7 years
Draws cross with same dimensions: 9 years
Draws 3 dimensional cube: 12 years
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Sensory Exam
Pain is felt by all age groups and is subjective
Can begin to test vibration in the preschooler
Other sensory function can not be tested untilschool age years.
Assess for symmetry of sensation
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Cerebellar Exam
Can not perform specific testing until age 3
Preschooler: unipedal hopping, stand on one footSchool Age: walk a straight line, heel to toe walking
Adolescent: finger to nose touch test, assess gait,rapid pronation and supination
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Reflexes
All deep tendon reflexes are tested as in adults
Bicpes, brachioradialis, maxillary, patellar present at
birthAchilles present by 4 months
Triceps present by 6 weeks
May need to distract children to assess reflexes
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Developmental Reflexes
Tongue Protrusion: present from birth
to 3 monthsAutomatic expulsion of solid object when
place in mouth
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Developmental Reflexes
Moro:
Symmetric abduction andflexion of upper extremitieswhen allowed to fall back orwith loud noise
Present from birth to 6 months
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Developmental Reflexes
Plantar Grasp
Place finger undertoes and infant graspsfinger with toes
Dissipates by 9months
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Developmental Reflexes
Palmar Grasp
infant will grasp
object when placed inpalm
Present from birth to6 months
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Developmental Reflexes
BabinskiPresent until 18 months
Indicates myelinization ofmotor tracts
Note: myelinization beginsat birth and is a process
that occurs over time
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Increased Intracranial
Pressure
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Increased Intracranial
PressureMonro Kellie Hypothesis:Brain: 80%
Blood: 10%
CSF: 10%
An increase or decrease in one
cranial content results in anequivalent replacement of theother
When the constant
relationship can not bemaintained intracranialpressure will rise
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Etiology of IncreasedIntracranial Pressure
Mass:
Tumor, Hematoma
CSF Disturbances:
hydrocephalus, exposure to toxins ( ex. CMV),
congenital abnormalities, encephalopathy
Edema:cytotoxic, vasogenic, hypo-osmotic
Increased blood volume:
impaired venous outflow
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Etiology of Increased
Intracranial PressureOther:
hypoxic injury, diffuse brain injury,
encephalopathies, infections
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Clinical Manifestations
Infant:
tense, bulging fontanelle
separated cranial suturesMacewen sign (cracked pot sound)
high-pitched cry
irritability
feeding intolerance
seizures
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Clinical Manifestations
Children:
headache
altered level of consciousnessvomiting (projectile)
visual changes
pupillary signsseizures
motor dysfunction
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Late Signs
Depressed level of consciousness
unilateral/bilateral dilated pupils
sluggish or non-reactive pupils
respiratory abnormalities
decerebrate or decorticate posturing
Cushing Triad: hypertension, bradycardiawidened pulse pressure
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Cerebral Perfusion Pressure
The goal of increased ICP management is to maintaincerebral perfusion pressure
CPP = MAP - ICP
Normal = 60 - 100 mm Hg
NOTE* All ICP interventions are customized to patient
response (examples given in class)
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Medical Management
Maintain oxygenation
saturation at 100%
CO2 = 30-35
Control Ventilation
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Medical Management
Glucocorticoidsused for focal edema as in tumor
Maintain normal blood sugar:
hypoglycemia increases secondary injury andworsens edema
hyperglycemia increases cerebral edema,
morbidity, and mortality
Surgery:
ICP monitor/CSF drainage
hemicraniotomy or lobectomy
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Nursing Interventions
Positon head in neutral position to promote venous outflow
Elevate head of bed
Avoid extreme hip flexion
Avoid high peep on ventilator (increases intrathoracicpressure and thus, ICP)
Avoid noxious stimuli
Advocate for only the necessary invasive procedures
Maintain an ETT suctioning protocol that minimizes ICPelevation
Promote adequate sedation and pain control
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Nursing Interventions
Maintain normal to hypothermia
Every 1 degree of temperature elevation
increases cerebral metabolism by 5-10%AVOID SHIVERING
Use acetominophen aggressively
Control the environment (low lights,decrease sound, move patient to quiet area
of unit, direct staff and visitors tominimize noise)
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Bacterial Meningitis
Acute inflammationof the meningessecondary to abacterial agent
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Epidemiology
1993: 2 cases per 100,000 children
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Etiology
3 pathogens account for > 80% of bacterial meningitis
Streptococcus pneumonia = pneumococcal meningitis
Neisseria meningitidis = meningococcal meningitis
Haemophilus influenzae = Hib meningitis
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Symptomatology
Classic Triad: severe headache, fever, nuchal rigidity
Insidious nonspecific illness that starts with fever,malaise, irritability, and vomiting that progressesrapidly over 2-4 days
Notable petechial rash in 50% of meningococcal cases
Illness often becomes fulminating in < 24 hours and is
often associated with a poor outcome
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Symptomatology
As the meningesbecome affected the
patient develops:
photophobia
nuchal rigidity
headache
increased ICP
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Symptomatology/Infant
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Symptomatology/ Kernigs Sign
Inability to extend knee with hip flexion
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Symptomatology
Brudzinski Sign
When the patient is supine, passively flexing the
neck produces involuntary flexion of the kneesand hips
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Management
Prevention through vaccination
Early identification and rapid treatment with
antibiotic therapyManagement of ICP
serial head circumference measurements in theinfant
Maintain fluid and nutrition status
Address skin integrity
Psychosocial support of patient and family
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Aseptic Meningitis
Also called nonbacterial or viral meningitis
Most common type of meningitis75,000 cases per year are reported in the U.S.
Frequently underreported because of the mild natureof the disease
Peak in summer and fall
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Etiology
enteroviruses
arboviruses
herpesviruses
85%-90% caused by enterovirus
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Symptomatology
Usually milder than those of bacterialmeningitis and resemble influenza
duration of symptoms usually 1-2 weeksafter onset
headache, nuchal rigidity, photophobia,malaise, and nausea
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Management
Provide supportive care
May give Acyclovir if HSV suspected
Patient education
Patient is expected to recover without neurologicalsequelae
If symptoms become severe the nursing care isconsistent with that of patients with bacterial
meningitis
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Reye Syndrome
Toxic encephalopathy associated
with hepatic dysfunction
Potential associationwith aspirin therapyand influenza andvaricella
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Symptomatology
Fever
Profoundly impaired consciousness
Disordered hepatic function
increased ammonia levels
Advances to coma and brainstem dysfunction
5 stages are correlated to the severity of illness
Definitive diagnosis is by liver biopsy
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Management
Early diagnosis and aggressive therapy
Manage increased ICP
Do not use aspirin for fever management
Family education
Psychosocial support
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SEIZURE CLASSIFICATION
SITE OF BRAIN
AFFECTED
DETERM INES
CLI NI CAL
EXPRESSI ON OF
THE SEI ZURE
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PathophysiologyPathophysiologyEpileptogenesis originates from an imbalance between
cerebral excitation and inhibition. In a seizure, abnormal
neuronal pathways are established that lead to abnormal
electrical firing - Core Curriculum 2003
Three neurotransmitters involved in seizures:
1. Gamma-aminobutyric acid (GABA) 2. Glutamate
3. N-methyl-D-asparate (NMDA)
GABA = inhibition
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facilitates activity of
chloride channels
making the cell
membrane more
negatively charged
opens potassium
channels leading to
post-synaptic inhibition
of impulse
closes calcium channels
which stabilizes the cell
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Glutamate = Excitation
Most important excitatory
transmitter involved in
seizures
NMDA is a receptor subtype
which is implicated in
propagation of seizures
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Medication Therapy
All anticonvulsants affect cognitive function
NEVER withdraw medication abruptly
Wean medication over a prolonged period
Be aware of blood level before administering the dose
Review side effect panel closely
Most anticonvulsants interact with other drugs
Provide detailed patient education
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Nursing Interventions
Assist with developing an individualized medicationadministration plan
Monitor drug levelsAssess for symptoms of drug toxicity
Patient safety
Initiate seizure precautionsFacilitate socialization with others
Dispel myths
F b il S i s
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Febrile Seizures
Most common form of childhood seizures
Most common between ages of 6mos - 3 years
The fever usually exceeds 101.8 before the seizure
Usually occurs during the temperature rise
Lasts less than 5 minutes
95% will not develop epilepsy or have brain damage
Control by reducing the temperature with antipyreticsand tepid bath
Education and emotional support are the most important
intervention.
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Acute Head Injury
Injuries are the leading cause of death in children over 1year of age
Estimated 300 per 100,000 children per year have atraumatic brain injury
The head of the infant and toddler is large and heavy in
relationship to other body parts making it most likely tobe injured
Male > Female
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Types of Injury
Concussion
Contusion and Laceration
Fractures
Epidural Hemorrhage
Subdural Hemorrhage
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Concussion
Most common injury
a traumatically
induced alteration ofconsciousness
LOC is not required
pathogenesisunclear;may be a resultof shearing forces
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Contusion/Laceration
Visible bruising andtearing of cerebral tissue
Common in occipital,frontal, temporal lobes
symptoms may be
indistinguishable fromconcussion
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Epidural Hemorrhage
blood accumulates between the dura and the skull
generally arterial
uncommon in children under 4 years of age
the classic clinical picture is rarely evident
the symptom free period can often last longer than
48 hours
symptoms: irritability, headache, vomiting
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Subdural Hemorrhage
bleeding between dura and the cerebrum
10 times more common than epidural hematoma
peak incidence at 6months of age
develops more slowly
subdural and retinal hemorrhages = evaluation forShaken Baby Syndrome
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FB Menu
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FB Menu
Pearls of Head Injury Management
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Pearls of Head Injury Management
a detailed history of the event is critical in diagnosisAssess ABC, LOC, pupils, seizures
crying for > 10 minutes after injury = serious injury
CT scan detects fracture and hematomamoderate concussion without LOC can be managed athome by checking child q 2 hours for 1-2 days
NPO, IVF, daily weights, manage painreview management of increased ICP
psychosocial support
consider mandatory abuse reporting
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Myelomeningocele
Spina Bifida
derived from embryonic
neural tube
1996: 0.32/1000 live births
failure of neural tube closure
symptoms are related to thelevel and severity of thedefect
Preoperative Care
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Preoperative Care
deliver via C-sectiongood neurological exam
strict aseptic technique to prevent infection
lay baby prone, ROMapply moist saline gauze dressing, change q 2 hours
prevent stool from soiling lesion with a stool flap
strict I and O (monitor urine output)Measure head circumference daily
Psychosocial support of parents
Surgical correction usually with first 24 hours
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Postoperative Care
I. Potential for UTI and urinary retention
a. assess urine quantity, color, odor
b. strict I and O
c. straight cath (teach parents and staff)
d. administer antibiotics
e. document postvoid residuals
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Postoperative Care
II. Potential for impaired skin integrity
a. Change diapers as soon as soiled
b. Keep perianal area clean and dry
c. Place child on pressure reducing surface
d. Massage healthy skin during cleansing
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Postoperative Care
III. Potential for Latex Allergy
a. Reduce Latex exposure
b. Educate family and caregivers
c. Pretreatment with antihistamines and steroids
d. cross-reaction banana, avocado, kiwi, chestnute. incidence estimated 18% - 67%
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Postoperative Care
IV. Potential for injury related to neuromuscularimpairment
a. bracing, PT, botox injections
b. tendon release, address scoliosis
c. ROM
d. maintain hips in slight abductione. maintain body alignment and good positioning
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Hydrocephalus
Symptom of underlyingbrain disorder
caused by an imbalancein the production andabsorption of CSF
Congenitalhydrocephalus: 4/1000live births
E l
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Etiology
Impaired absorption of CSF (communicating)
a. Congenital
b. Subarachnoid hemorrhagec. Infection
Obstruction to flow of CSF (noncommunicating)
a. Blockage at or above 4th ventricleb. Most common blockage in aqueduct of Sylvius
c. Tumor
l
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Symptomotology
Infants:
large head circumference (plot on growth curve)
irritabilityextreme lethargy
dilated scalp veins
split sutures, tense or bulging fontanelleseizures
sunset eyes
l
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Symptomotology
Toddler/Young Child
macrocephaly
poor appetite
failure to thrive
double vision/vision changes
loss of previous developmental ability
vomiting
seizures
l
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Symptomotology
Adolescents
headache
vomiting
vision changes/double vision
decline in cognitive/school performance
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Sh M
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Shunt Management
Position on unoperated side immediately post-op
assess for signs of subdural hematoma
manage painstrict I and O
astute abdominal assessment
monitor incision siteprevent infection
routine postoperative care (IS, SCDs etc.,)
L T C id i
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Long Term Considerations
Teach family signs of shunt malfunction and infection
provide reliable patient education/support group
materialsSeizure management (20-25% in first year of life)
encourage patient independence
address learning disabilitiesconsider motor deficits (75% occurrence)
consider ocular problems (25-30% occurrence)
Spinal Muscular Atrophy
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Werdnig-Hoffman Disease
Autosomal recessive trait
progressive weakening ofskeletal muscles
degeneration of anteriorhorn cells of spinal cordand motor nuclei ofbrainstem
Age of onset variable;worse prognosis theearlier the onset
Cognitively normal
M t
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Management
Promote skin integrity
Frequent suctioning, pulmonary toilet
Prevent feeding aspiration
Attend to potential for injury
Normal verbal, tactile, auditory stimulation
Promote social interaction
Intense family psychosocial support
M l D t h
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Muscular Dystrophy
Largest single group of muscular diseases in children
All have a genetic origin
Gradual degeneration of muscle fibers
Progressive muscle wasting and weakness
Etiology unknown; appears to be related to a metabolicdisturbance independent of the nervous system
Most common form: Duchenne muscular dystrophy
M t
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Management
Major emphasis is on assisting the child and family incoping with the progressive, incapacitating, and fatal
nature of the disease
Promote independence
Modify clothing
Education regarding assistive devices
Refer family to support resources