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NU 374 > Ch. 33 & 34 > Flashcards

Ch. 33 & 34 Flashcards

1
Q

neuromuscular dysfunction pediatric assessment: inspection & palpation of

A
  • motor function
  • reflexes
  • sensory function
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2
Q

spina bifida cystica is also called

A

aka myelomengocele

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3
Q

what is a neural tube defect

A

when the neural tubes of the brain and spine dont close properly

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4
Q

what is the difference between meningocele and myelomeningocele

A

meningocele: defect of posterior elements of spine w/ extrusion of meninges and CSF (w/out neural elements)

myelomeningocele: defect of posterior elements of spine w/ extrusion of meninges and CSF and neural elements such as the spinal cord elements and nerves
- most severe form of spina bifida
- develops during first 28 days of pregnancy
- 90% of spinal cord lesions
- located at any point on spinal column

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5
Q

how are meningocele and myelomeningocele abnormalities detected?

A
  • in utero (prenatally) or at birth
  • ultrasound of the uterus and elevated maternal AFP or MS-AFP, fetal specific gamma 1-globulin (tested between 16-18 weeks gestation)
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6
Q

myelomeningocele therapeutic management

A

Associated/acquired problems
Parental support
Care of the “sac”
Positioning
General care
Orthopedic concerns
GU function
Bowel control
Prevention

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7
Q

myelomeningocele post-op management

A

Monitoring
Positioning
Parent involvement
Latex allergy??
Home care prep
Prevention of complications and readmissions

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8
Q

teaching for parents of children with myelomeningocele

A

Positioning
Preventing infection
Feeding
Promoting urinary elimination through clean intermittent catheterization
Preventing latex allergy
Preventing signs and symptoms of complications such as increased ICP

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9
Q

duchenne muscular dystrophy

A

X-link trait (M>F)
Genetic counseling
Begin meeting most developmental milestones with delays in gross motor d/t muscle weakness around age 3-7 y.o.
Waddling gait
Muscular enlargement (early) atrophy (later)
Loss of independent ambulation by age 12
Immobility complications
Cognitive impairment

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10
Q

duchenne’s therapeutic management: goals

A
  • maintain optimal function in all muscles (mobility)
  • prevent contractures/complications and maximizing quality of life
  • maintaining cardiopulmonary function
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11
Q

Duchenne’s: What collaborative services are required to maintain function?

A
  • PT: passive ROM, stretching, splinting
  • polysomnography: before onset of daytime sx,
  • no CPAP, maybe sip-puff ventilator
  • tracheostomy
  • MIE (cough assist)
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12
Q

Duchenne’s: What problems/complications can result with disease progression?

A
  • progressive muscle weakness
  • no decline in cognitive function; BUT mild-moderate intellectual disability (lower IQ)
  • neurodevelopment: autism, ADHD, anxiety and mood d/o, OCD (not as common)
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13
Q

Duchenne’s: What nursing interventions should be implemented into a DMD patient’s POC?

A
  • assist patient and family in coping with dx (progressive nature of d/o)
  • design program to promote independence of the child and reduce the predictable and preventable complications associated with the d/o
  • adapt to limitations caused by d/o
  • decisions regarding quality of life, achieving independence, transition to adulthood
  • modify family activities to meet the needs of the child
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14
Q

Duchenne’s: promoting mobility

A

Administering corticosteroids and calcium supplements
Performing passive stretching and strengthening exercises

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15
Q

Duchenne’s: patient teaching

A

Teaching deep breathing exercises
Performing chest physical therapy

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16
Q

Duchenne’s: preventing complications and maximizing quality of life

A

Developing a diversional schedule
Providing emotional support

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17
Q

for neuromuscular disorders like DMD and spina bifida, consider:

A

Growth and development
Care of disabled patient
Family (sibling) support
Coping with ongoing stress & periodic crises
Palliative care
End of life care

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18
Q

cerebral palsy: causes

A
  • prenatal
  • perinatal: infection, trauma, hypoxia
  • postnatal factors
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19
Q

80% of CP cases are linked to

A

perinatal or neonatal brain lesion or brain maldevelopment

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19
Q

4 primary movement disorders of CP

A
  • spastic is most common (80% of cases): upper motor neuron muscular weakness
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20
Q

CP clinical manifestations

A

Delayed gross motor skills
Abnormal motor movements
Altered muscle tone
Abnormal posture
Abnormal reflexes
Associated disabilities

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21
Q

CP nursing management

A

Developmental assessment
MS assessment/neuro assessment
Parent participation and education for normalization
Parent and sibling support
Multidisciplinary approach

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22
Q

CP assessment and maintenance

A

Nutritional needs
Limited mobility concerns (skin, B/B)
Adaptive equipment for age and deficits
Safety precautions (meds, helmet, fall-risk car seat)
Health promotion (immunizations, dental, sensory etc.)

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23
Q

pain with CP

A

Intense pain may occur with muscle spasms in patients with CP as a result of:
- painful procedures such as injections used to control spasms
- surgical procedures intended to reduce contracture deformities
- anatomical position and gastroesophageal reflux
- physical therapy

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24
Q

medications for pain and spasticity with CP

A

Botulinum toxin A
baclofen (Lioresal)
dantrolene sodium (Dantrium)
diazepam (Valium)

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25
Q

BOTULINUM TOXIN A

A

used to reduce spasticity in muscles of the upper and lower extremities

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26
Q

when BOTULINUM TOXIN A is administered early in the course of the illness it can

A

Prevent muscle contractures
Decrease the need for surgical procedures with adverse effects

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27
Q

BOTULINUM TOXIN A: goal

A

allow relaxation and stretching of the muscle
permit ambulation with an AFO

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28
Q

BOTULINUM TOXIN A: prime candidates

A

children with spasticity confined to the lower extremities

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29
Q

BOTULINUM TOXIN A: side effects

A

Pain at the injection site and temporary weakness

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30
Q

Diazepam

A
  • used frequently but should be restricted to older children and adolescents.
  • Oral administration: little improvement with muscle coordination in children with CP. More effective in decreasing overall spasticity.
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31
Q

Diazepam side effects

A

drowsiness, fatigue, and muscle weakness
hallucinations, mood changes, seizures, nausea, and urinary incontinence.

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32
Q

Baclofen (Lioresal)

A
  • Higher PO doses are associated with significant side effects (ex. drowsiness and confusion); often provide little to no relief of spasticity.
  • Oral administration: little improvement with muscle coordination in children with CP. More effective in decreasing overall spasticity.
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33
Q

Baclofen (Lioresal): side effects

A

drowsiness, fatigue, and muscle weakness.
diaphoresis and constipation (with oral baclofen) hallucinations, mood changes, seizures, nausea, and urinary incontinence.

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34
Q

dantrolene sodium (dantrium)

A

Oral administration: little improvement with muscle coordination in children with CP. More effective in decreasing overall spasticity.

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35
Q

dantrolene sodium (dantrium): side effects

A

hepatotoxicity (dantrolene), drowsiness, fatigue, and muscle weakness.
hallucinations, mood changes, seizures, nausea, and urinary incontinence.

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36
Q

INTRATHECAL BACLOFEN

A
  • Direct infusion of baclofen into the intrathecal space provides relief without as many side effects
  • implantation of a pump to infuse baclofen directly into the intrathecal space surrounding the spinal cord to provide relief of spasticity
  • Provides excellent improvement in comfort
  • Outpatient pump refill q 4-6 weeks
    Abrupt withdrawal, especially at high doses, may result in adverse effects (ex. rebound spasticity, pruritus, hyperthermia, rhabdomyolysis, disseminated intravascular coagulation, multiorgan failure, and death.
  • Goal of treating med withdrawal = reestablishing the medication dosage
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37
Q

INTRATHECAL BACLOFEN: med withdrawal

A
  • in some cases intrathecal baclofen withdrawal may mimic sepsis. Needle inserted into pump to refill.
  • Treatment of med withdrawal: Should see improvements within 1 to 2 hours.
  • Hospitalization and surgery may be required for withdrawal that was the result of pump or catheter failure
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38
Q

gross motor milestones: 6-8 months

A

sits with support

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39
Q

gross motor milestones: 9 months

A
  • concern if not sitting at this point
  • stands while holding
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40
Q

gross motor milestones: 10 months

A

pulls to standing

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41
Q

gross motor milestones: 12 months

A

walks with assistance

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42
Q

gross motor milestones: 15 months

A
  • walks wall, unaided
  • gait is wide-based
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43
Q

gross motor milestones: 18 months

A
  • runs well, unaided
  • gait is wide-based
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44
Q

gross motor milestones: 2 years

A
  • goes up and down stairs, two feet per step, without assistance
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45
Q

gross motor milestones: 2.5 years

A
  • jumps on both feet
  • may walk on tiptoes
  • concern if cannot jump by school age
  • hand dominance is appropriate around 2.5-3 years (earlier is a concern of CP)
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46
Q

gross motor milestones: 3 years

A
  • stands on one foot (few seconds)
  • goes up stairs 1 foot per step, comes down 2 feet per step
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47
Q

gross motor milestones: 4 years

A
  • hops on one or both feet
  • goes up and down stairs like an adult (1 foot per step)
  • heel and tiptoe walk
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48
Q

gross motor milestones: 5 years

A

skips

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49
Q

gross motor milestones: 7 years

A
  • balance on one foot for 20 seconds
  • should be coordinated
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50
Q

growth and development is dependent on

A

the child
- not every child will be sitting at 6 months
- we give a little time before concerned (like around 3 months)

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51
Q

MS assessment should include

A
  • gait
  • posture
  • curvature of the spine
  • muscle strength: arms, hands, legs
  • ROM: extremities, joints
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52
Q

signs and symptoms of fractures

A
  • Swelling
  • Pain or tenderness
  • Deformity
  • Diminished functional use of affected part
  • Bruising
  • Muscle rigidity
  • Crepitus** (direct pressure on spot that hurts, hear crunching)
  • Hx of injury may be lacking due to age
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53
Q

common variations in growth development

A
  • bowleg or genu varum
  • knock knee or genu valgum
  • pigeon toe or toeing in
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54
Q

toddlers carry their weight in

A

their abdomen
- the abdomen will protrude
- lordosis
(developmentally this is okay, around 4/5 years this will go away)

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55
Q

bowleg (genu varum)

A
  • Lateral bowing out of the tibia
  • Bow seen when standing
  • Outward curvature of femur & tibia
  • Normal in TODDLERS
  • Abnormal past the age of 2-3 years
  • Common in African-American Children
  • not > 2” between knees
  • concern if causing issues to get or if one-sided
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56
Q

knock-knee

A
  • Opposite of genu varum
  • Measure distance between malleoli
  • Normally present in 2-7 years of age
  • past age 7 is concerning
  • not > 3” between ankles
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57
Q

pigeon toe or toeing in

A
  • Most common gait problem in young children
  • Can result from a rotational deformity of the hips, legs, or feet
  • internal rotation of bones in the hips, legs, feet
  • Most common is r/t hips (W sitting)
  • Can test leg/hip forms by assessing Babinski (plantar)
  • Usually self-corrects with growth
  • usually goes away by 8 years
  • refer if unilateral or is getting worse
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58
Q

tibial torsion

A

tibia turn inward
- pigeon toe/toeing in

59
Q

femoral antiversion

A

thigh bone (femur) turns inward
- pigeon toe/toeing in

60
Q

metatarus adductus

A

feet turns inward
- pigeon toe/toeing in

61
Q

vit D is given through

A
  • nutrition and sun
    (rice cereal, orange juice, whole milk)

Breastfed babies usually begin taking Vit D supplementation because there is a limited amount of Vit D in human milk.

affects cognition and development if not enough

62
Q

rickets

A
  • the softening and weakening of bones in children, usually because of an extreme and prolonged vit D deficiency
  • consider family hx too
  • very thin long bones, swollen joints
  • protrusion of sternum (necklace appearance)
63
Q

s/sx of rickets

A

Delayed motor development
Injury
Pain, loss of sensation, tingling
Muscle weakness, loss of function of an extremity
Interferes with usual ADL’s or play

64
Q

common causes of immobilization

A
  • Disability
  • Congenital Defects
  • Neuromuscular conditions
  • Prolonged mechanical ventilation and sedation
  • traction
  • surgery
  • infections and injuries impairing: MS, integumentary, neurological
65
Q

immobility effects: muscular system

A
  • decreased muscle mass
  • atrophy
  • wasting
66
Q

interventions for muscular system

A
  • ROM exercises
67
Q

immobility effects: skeletal system

A
  • bone damage (d/t calcium)
  • hypercalcemia
  • higher risk of fractures
68
Q

skeletal system interventions

A
  • calcitonin
  • IVF/ fluids
  • biphosophate therapy
69
Q

immobility effects: CV system

A
  • blood clots
  • heart has to work harder
70
Q

CV system interventions

A
  • anticoagulants
  • pulses above and below site of injury
71
Q

immobility effects: respiratory system

A
  • PNA
72
Q

respiratory system interventions

A
  • incentive spirometer
  • blow bubbles
  • blow cotton balls
  • anything to encourage breathing
73
Q

immobility effects: GI system

A
  • constipation
74
Q

GI system interventions

A
  • increase fiber and fluids
75
Q

immobility effects: integumentary system

A
  • breakdown
  • shearing with movement
76
Q

integumentary interventions

A

lotions, massage, position changes

77
Q

immobility effects: renal

A

renal calculi d/t hypercalcemia

78
Q

immobility effects: neurosensory

A
  • unusual pressure
  • pain
  • ultimately can lead to decreased sensation
79
Q

renal system interventions

A

calcitonin (to prevent calcium kidney stones)

80
Q

neurosensory interventions

A

position changes

81
Q

immobility effects: metabolism

A
  • decreased BMR
  • increased diuresis, natriuresis
  • depletion of nitrogen and calcium
82
Q

metabolism interventions

A
83
Q

psychosocial effects of immobilization

A

depression, isolation

84
Q

possible regression in milestones

A

example: bedwetting, picky eater, personality changes
- should return to normal/ resolve within a few days of discharge
- it is normal for a child to regress in the hosptial setting

85
Q

5 P’s of ischemia

A

pulselessness
pain
pallor
paresthesia
paralysis

  • reassess post-intervention too
86
Q

ischemia

A

lack of blood flow to a certain area
- concern with casts

87
Q

fracture complications

A

Circulatory impairment

Nerve compression syndromes

Compartment syndromes

Physeal damage: growth plate damage
- deformity of doesn’t heal right

Nonunion: fracture was casted but still did not heal correctly

Malunion: casted but was misaligned

Infection: osteomyelitis

Renal calculi: d/t hypercalcemia, urinary stasis

Pulmonary embolism (chest pain & dyspnea): #1 thing we are concerned about

88
Q

compartment syndrome

A

Severe pain
Decreased/lack/deficit sensation
Edema
Paleness
Pulse changes
Motor weakness

89
Q

prevention of compartment syndrome

A

prevention = CSM assess/reassessment

90
Q

compartment syndrome management

A
  • assess the 5 P’s
  • notify ortho
  • remove any mechanically obstructive materials
  • do not elevate if compartment syndrome is suspected
  • if not improved, do a fasciotomy
91
Q

why may compartment syndrome happen in a casted child?

A

cast became too tight
- if not treated and ischemia develops, will lose limb

92
Q

fasciotomy

A

surgical intervention for compartment syndrome
goal:
- decrease arterial spasms
- increase blood flow

93
Q

cast care: application

A
  • Anticipatory guidance (burning with drying)
  • Age approp. explanations
  • Distraction with application (age approp.)
  • Petal edges PRN
  • Teach CSM checks
94
Q

cast care: anticipatory guidance

A
  • Cutter sounds
  • Warmth
  • Caked skin
  • Atrophy
95
Q

traction is used for

A

Provide rest for the extremity
Prevent deformity
Reduce muscle spasms
Immobilize fracture site
Proper realignment
Allow healing time before surgery or casting (callus formation)
pain relief

96
Q

manual traction

A
  • applied by the examiner’s hands
97
Q

skin traction

A
  • 5-7 lbs.
  • attached to skin indirectly.
  • Used if temporary or light force is needed.
98
Q

skeletal traction

A
  • 25-40 lbs.
  • attached directly to the bone using tongs, pins, or screws
99
Q

what to look out for with traction

A

infection:
- fever
- swelling
- pain
- heat

100
Q

halo traction

A
  • screws going into the scalp
101
Q

traction managment

A
  • maintain traction
  • assess the skin and CMS
  • distraction and education; quiet play
102
Q

tortocollis

A
  • kink in the neck
  • can be congenital or acquired
  • plagiocephaly: flattened back of head (one sided)
  • brachiocephaly
103
Q

treatment of torticollis

A
  • get them off their head
  • tummy time
  • get their focus towards the opposite side as the kink
  • gentle stretches/passive ROM (left and right motion of head)
  • surgery if severe or unable to correct
104
Q

developmental dysplasia of hip (DDH)

A
  • Unknown/Multi-factorial cause (genetic and environmental)
  • seen commonly in children
  • 80% more likely in F than M
105
Q

DDH (develpomental dysplasia of hip) physiologic factors

A

Maternal hormone secretion
Intrauterine position
Joint laxity
Co-existing orthopedic dx’s

106
Q

DDH mechanical factors (think perinatal)

A

Breech presentation
Multiple fetuses
Oligohydramnios
Large infant size
Postnatal positioning

107
Q

DDH genetic factors

A
  • Parent
  • Siblings of affected infants
108
Q

DDH is diagnosed through

A
  • hip ultrasound: for < 6 months
  • x-ray of hip: for > 6 months

can do a physical exam: will hear and feel popping of hip

109
Q

acetabular dysplasia DDH

A
  • acetabular abnormality
110
Q

subluxation DDH

A
  • shifted out of hip socket
111
Q

dislocation DDH

A
  • shifted out of hip socket and goes superior and posterior
112
Q

signs to look for DDH: infant 0-4 weeks

A
  • Hip joint laxity
    • Ortolani
    • Barlow
    • Galeazzi
  • Shortening of thigh on affected side
  • Asymmetric folds (thigh and buttocks)
    • more folds on the affected side
  • Unequal knee height
  • Limited abduction (away from center point)
113
Q

signs to look for DDH: older infant and child

A
  • The leg of affected hip appears shorter
  • Waddling gait
  • Lumbar lordosis (bilat)
    • Trendelenburg sign (pelvis tilts downward when the leg is raised)
  • Spacing between the legs may look wider than normal
114
Q

pavlik harness

A
  • for DDH
  • surgeon puts on
  • stays on
  • need to go back every couple of weeks to have it adjusted by surgeon
  • concerned for skin integrity under the straps
115
Q

pavlik harness: parent teaching

A

Maintain reduction
Removal for bathing (may not be allowed)
Do not adjust
Skin care: no lotion, no powder, massage is okay
Prevention of complications
Normalcy

116
Q

spica cast: care of child, safety & diapering

A

used for DDH!
care of the child
- have to support the child
- will fall over
- emolskin for protection of skin under the arms

safety
- positioning
- clothing

diapering
- double diapering
- sanitary pad and then diaper
- water proof tape around the edges to prevent urine and stool from getting on the cast

117
Q

swaddling DDH

A
  • don’t put babies legs straight down- could pop hip out of socket
  • let legs be in normal position
  • stop swaddling the babies when they start rolling over (aspiration risk)
118
Q

congenital clubfoot

A
  • diagnosed as early as 20 weeks (in utero or at birth)
  • assess for co-existing hip abnorms
119
Q

affected foot: clubfoot

A

Foot and calf size variation
- Affected limb smaller and shorter
- Empty heel pad (no fat pad)
- Midfoot plantar crease
- Calf atrophy

Stiffness in the ankle or foot tendons

Affected foot (feet) lack full range of motion

120
Q

clubfoot goals

A

Correct deformity
Maintenance of correction
Prevention of recurrence

121
Q

treatment of clubfoot

A
  1. Ponseti method-serial casting with stretching
  2. Heelcord tenotomy
  3. Log leg cast
  4. Denis Browne bar and shoe brace
    - If not effective surgical pinning

*this will delay walking
* usually in this several hours a day

122
Q

osteogenesis imperfecta

A
  • Most common pediatric osteoporosis syndrome
  • caused by defect of the genes: colia-1 and colia-2
  • > 11 classifications: type 1 is most common and mildest; type 2 is most fatal (stillborn or die within a few days of birth)
  • Distinguish OI from child abuse
  • NO CURE
123
Q

assessment/ s/sx of osteogenesis imperfecta

A
  • Blue sclera
  • Hearing loss
  • Dentinogenesis imperfect (discolored teeth)
  • Growth restrictions (bc body isn’t growing; so organs cant grow- don’t work properly for age)
  • they do have a normal IQ
  • body doesn’t grow but head grows
124
Q

therapeutic management of osteogenesis imperfecta

A

Supportive treatment
Bisphosphonate therapy
Bone marrow transplantation (experimental)

125
Q

osteogenesis imperfecta: care goals

A

Decreasing incidence of fx’s
Decreasing pain
Increasing growth
Improving bone metabolism
Optimizing function
Collaborative care

126
Q

osteogenesis imperfecta: nursing care

A
  • Handling with care
  • Diaper changes
  • Support with positioning
  • Manual b/p’s: decreases risk of fractures
  • Bisphosphate therapy
  • Caution with live vaccines
  • Frequent head repositioning
  • Routine dental care
  • Child and Family education
  • Support network
127
Q

juvenile idiopathic arthritis (JIA)

A

Genetic susceptibility is not understood
Unknown cause (autoimmune)
s/sx before age 16
Peak onset:
2-4 yrs. and
10-14 yrs.
F>M
90% children have neg. RF

Chronic inflammation of synovium with joint effusion, destruction of cartilage, and ankyloses of joints as disease progresses

128
Q

forms of JIA

A

Pauciarticular: involves two or more joints

Polyarticular: more then five joints

Systemic: affects organs, lympadeonpthy, fever

129
Q

JIA s/sx

A

Stiffness (am)
Edema
Warmth (no erythema)
Tenderness
Loss of motion
Pain (variable)
Growth restrictions (severe cases)
Different from adult onset

*discomfort after rest is key

Symptoms may “burn out” and become inactive

130
Q

medical management of JIA (drug therapy)

A

NSAIDS (start with)
DMARD’s (methotrexate)
- GI upset, infection, WBC, fetal risks
Biological DMARD’s (humara)
- causes malignancy
Glucocorticoids

131
Q

physical management of JIA (non-pharm)

A

PT/ROM
Water therapy
Splinting overnight (to prevent footdrop)
Surgery if physical mgmt. unsuccessful

132
Q

JIA goals

A
  • relieve pain
  • promote general strength: diet, exercise, sleep/rest
  • encourage involvement in age appropriate activities
133
Q

JIA nursing management

A
  • facilitate compliance
  • comfort measures
  • participation in ADLs
  • exercise with nighttime splinting
134
Q

scoliosis

A
  • most common spinal deformity
  • may be congenital or develop during childhood
  • most commonly idiopathic
  • complex spinal deformity in 3 planes:
    -lateral curvature
    -spinal rotation causing rib asymmetry
    -thoracic hypokyphosis
135
Q

scoliosis screening

A
  • want to screen young bc once puberty/growth plates close, not much can be done
  • scoliosis x-rays
136
Q

scoliosis exam

A
  • scapulary hump
  • lordosis
  • kyphosis
137
Q

scoliosis brace

A
  • wear for 23 hours a day
  • slows progression
  • allows time for skeletal maturity
138
Q

scoliosis checks

A

girls: 10 and 12 years
boys: 13 and 14 years

actually do them younger*

139
Q

degrees/grades of scoliosis

A

mild: 10-25° - wait and see
moderate: 25-45° - bracing
severe: > 45° - surgery

140
Q

scoliosis labs

A
  • CBC
  • CMP
  • PT/PTT
  • imaging
141
Q

patient education post-surgery for scoliosis

A
  • log roll
  • pillow splinting for cough
142
Q

scoliosis therapeutic management

A
  • Treatment is based on magnitude, location, type of curve, age, skeletal maturity, and other disease dx’s
  • bracing
  • boston or wilmington braces
  • exercise with bracing
143
Q

scoliosis operative management

A
  • For progressive or severe curves that does not respond to more conservative measures
  • Spinal fusion-technique is surgeon’s preference
  • Psychological and physiological care
144
Q

scoliosis: pre-op care

A
  • blood work/blood loss plan
  • teaching (PCA, log-rolling, tubes)
145
Q

scoliosis: post-op care

A
  • Early recognition of complications
  • PCA, early mobilization, skin, I/O, Resp

NU 374 (18 decks)

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