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NSG 434 - Peds > Peds Musculoskeletal/Neuromuscular Dysfunction > Flashcards

Peds Musculoskeletal/Neuromuscular Dysfunction Flashcards

1
Q

One of the most difficult aspects of illness in a child is

A

immobility

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2
Q

contusion

A

(bruise) is damage to the soft tissue, subcutaneous structures, and muscle
*Escape of blood into tissues causes ecchymosis (black-and-blue discoloration)

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3
Q

Crush injuries

A

occur when children’s extremities or digits are crushed (finger slammed in the car door).

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4
Q

treatment for contusion

A

application of cold.

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5
Q

treatment for crush injury

A

hematomas may require a release of blood by creating a hole at the proximal end of the main with a special cautery device or a heated sterile 18-gauge needle.

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6
Q

dislocation

A

*Displacement of normal position of opposing bone ends or of bone ends to socket
*Occurs when force of stress on ligament is sufficient to cause displacement

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7
Q

what is the predominant symptom of dislocation

A

increased pain with active or passive movement of affected extremity

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8
Q

what is the concern with hip dislocation

A

potential loss of blood supply to head of femur: relocation within 60 minutes provides best chance for prevention of damage to femoral head

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9
Q

sprain

A

trauma to joint from LIGAMENT partially or completely torn or stretched by force

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10
Q

strain

A

microscopic tear io MUSCULORTENDINOUS unit

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11
Q

onset: sprain vs strain

A

sprain: rapid onset of swelling with disability
strain: generally incurred over time

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12
Q

Therapeutic Management ofSoft-Tissue Injuries

A

RICE AND ICES

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13
Q

RICE

A

rest, ice(3o mins at a time), compression, elevation

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14
Q

ICES

A

Ice, Compression, Elevation, Support

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15
Q

what is the most frequently broken bone in childhood

A

distal forearm

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16
Q

fracture

A

broken bone

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17
Q

simple or closed fracture

A

*Does not produce a break in the skin

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18
Q

open or compound fracture

A

*Fractured bone protrudes through the skin

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19
Q

complicated fracture

A

Bone fragments have damaged other organs or tissues

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20
Q

comminuted fracture

A

*Small fragments of bone are broken from fractured shaft and lie in surrounding tissue

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21
Q

growth plate injuries

A

*Weakest point of long bones: The cartilage growth plate (epiphyseal plate)
may affect future bone growth

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22
Q

growth plate injury treatment

A

*May include open reduction and internal fixation to prevent growth disturbances

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23
Q

neonatal bone healing period

A

2-3 weeks

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24
Q

early childhood bone healing period

A

4 weeks

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25
Q

later childhood bone healing period

A

6-8 weeks

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26
Q

adolescence bone healing period

A

8-12 weeks

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27
Q

diagnosis of fracture

A

*Radiographs (X-ray)
*History taking
*Suspicion of fracture in a young child who refuses to walk or bear weight

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28
Q

goals of fracture management

A

*Reduction and immobilization
*Restoring function
*Preventing deformity

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29
Q

fracture treatment

A

reduction and immobilization
splinted or casted to immobilize and protect the injured extremity

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30
Q

Assessment of Fractures: The Six Ps

A

*Pain and point of tenderness
*Pallor
*Pulselessness
*Paresthesia:
*Paralysis:
*Pressure

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31
Q

cast care

A

*Elevate casted extremity for first day
*Observe the extremities (fingers/toes) for swelling, discoloration
*Check movement and sensation of fingers/toes
*Do not allow child to put anything inside the cast
*Cool hair dryer can help with itching

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32
Q

Developmental Dysplasia of the Hip

A

abnormal development of the hip joint found that is congenital

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33
Q

Acetabular dysplasia

A

the mildest form of DDH, in which there is a delay in acetabular development evidenced by osseous hypoplasia of the acetabular roof that is oblique and shallow. The femoral head remains in the acetabulum.

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34
Q

Sublaxation

A

the largest percentage of DDH, incomplete dislocation of the hip. The femoral head remains in contact with the acetabulum, but a stretched capsule and ligamentun teres causes the head of the femur to be partially displaced. Pressure on the cartilaginous roof inhibits ossification and produces a flattening of the socket.

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35
Q

Dislocation

A

the femoral had loses contact with the acetabulum and is displaced posteriorly and superiorly over the fibrocartilaginous rim. The ligamentum teres is elongated and taut.

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36
Q

Clinical Manifestations of DDH: infant

A

*Hip joint laxity
*Shortened limb on affected side
*Restricted abduction of hip on affected side
*Unequal gluteal folds when infant prone
*Positive Ortolani test result
*Positive Barlow test result

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37
Q

Ortolani test

A

hip is reduced by abduction

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38
Q

Barlow test

A

hip is dislocated by adduction

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39
Q

Therapeutic Management of DDH: birth to 6 months

A

*Pavlik harness for abduction of hip

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40
Q

Therapeutic Management of DDH: 6 to 24 months

A

*Dislocation unrecognized until child begins to stand and walk; closed reduction and spica cast

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41
Q

Therapeutic Management of DDH: older child

A

*Operative reduction, tenotomy, osteotomy; correction is very difficult after age 4 years

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42
Q

Tenotomy

A

surgical cutting of a tendon

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43
Q

Pavlik Harness care

A

-Skin care
-Check frequently (2-3x/day) for red areas or skin irritation in skin folds and under the straps
-Gently massage healthy skin under the straps once per day to stimulate circulation
-Always place diapers under the straps
-Remove harness only to quickly bathe the infant if allowed by HCP
-Do not adjust the harness

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44
Q

clubfoot

A

a fixed congenital defect of the ankle and foot

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45
Q

Talipes varus

A

*Inversion or bending inward

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46
Q

Talipes valgus

A

*Eversion or bending out

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47
Q

Talipes equinus

A

Plantar flexion with toes lower than the heel

48
Q

Talipes calcaneus

A

*Dorsiflexion with toes higher than the heel

49
Q

Therapeutic Management of Clubfoot: three stages

A

*Correction of the deformity
*Maintenance of the correction until normal muscle balance is regained
*Follow-up to avert possible recurrence

50
Q

*Ponseti method (serial casting)

A

begun soon after birth with weekly gentle manipulation and stretching of the foot and then serial casting for 6-10 weeks

51
Q

Ponseti sandals are used after casting to…

A

maintain the correction and prevent recurrence.

52
Q

Clinical features Osteogenesis Imperfecta

A

-Varying degree of bone fragility and deformity
-Short stature
-Blue sclera
-Hearing loss (occurs between the ages of 20 and 30 years of age)
-Hypoplastic discolored teeth

53
Q

Therapeutic Management of Osteogenesis Imperfecta

A

*No cure
*Primarily supportive care
*Intravenous bisphosphonate therapy
*Rehabilitative (PT OT) approach for prevention of further complications
*Positional contractures and deformities
*Muscle weakness and osteoporosis
*Malalignment of lower-extremity joints

54
Q

parent teaching for osteogenesis imperfecta

A

-Do not hold up by the ankles when changing the infant’s diaper - lift by the buttocks
-Braces and splints can help support limbs, prevent fractures, and aid in ambulation

55
Q

Legg-Calve-Perthes Disease

A

A self-limiting disorder in which there is avascular necrosis of the femoral head.

56
Q

Clinical Manifestations of Legg-Calvé-Perthes Disease

A

*Insidious onset; possible history of limp, soreness, or stiffness; limited range of motion; vague history of trauma
*Pain and limp most evident on arising and at end of activity

57
Q

diagnosis of Legg-Calvé-Perthes Disease

A

history and findings on radiographs and magnetic resonance images (MRI)

58
Q

treatment goal of Legg-Calvé-Perthes Disease

A

Keep head of femur in acetabulum

59
Q

Therapeutic Management of Legg-Calvé-Perthes Disease

A

*Rest, no weight bearing initially
*Nonsteroidal antiinflammatory drugs (NSAIDs)
*PT or range-of-motion exercises help restore hip motion.
*Surgery in some cases
*Home traction in some cases

60
Q

Idiopathic Scoliosis

A

*Complex spinal deformity in three planes
*Lateral curvature
*Spinal rotation, causing rib asymmetry
*Thoracic hypokyphosis

61
Q

Diagnostic Evaluation ofSpinal Curvatures

A

*Standing radiographs to determine degree of curvature
*Asymmetry of shoulder height, scapular or flank shape, or hip height
*In addition to primary curve, compensatory curve often present to align head with gluteal cleft

62
Q

Therapeutic Management ofSpinal Curvatures

A

*Team approach to treatment
*Bracing
*Exercise
*Surgical intervention for severe curvature (instrumentation and fusion)
*Harrington rods
*Luque rods

63
Q

Osteomyelitis

A

*Infectious process in the bone
*May be caused by exogenous or hematogenous sources

64
Q

what is the most causative organism of osteomyelitis

A

Staphylococcus aureus

65
Q

clinical manifestations of osteomyelitis

A

Acute and chronic inflammation, fever, pain, necrotic bone
*Signs/symptoms begin abruptly, resemble symptoms of arthritis and leukemia
*Marked leukocytosis

66
Q

diagnosis for osteomyelitis

A

*Bone cultures obtained from biopsy or aspirate
*Radiographs: May appear normal at first
*Bone scans for diagnosis

67
Q

Therapeutic and Care Managementbof Osteomyelitis

A

*Prompt, vigorous intravenous antibiotics for extended period (3 to 4 weeks or up to several months)
*Monitor hematologic, renal, hepatic responses to treatment
*Complete bed rest and immobility of limb
*Pain management concerns
*Long-term intravenous access (for antibiotic administration)
*Long-term hospitalization/therapy

68
Q

typical antibiotics for osteomyelitis

A

*Typically nafcillin or clindamycin

69
Q

Juvenile Idiopathic Arthritis

A

utoimmune disease - inflammation in the joint synovium and surrounding tissue with eventual erosion, destruction, and fibrosis of the articular cartilage.
-Can affect one or multiple joints

70
Q

peak onset of Juvenile Idiopathic Arthritis

A

*1 to 3 years of age

71
Q

clinical manifestations of Juvenile Idiopathic Arthritis

A

*Systemic onset (high fever, rash, hepatosplenomegaly, pericarditis, pleuritis, lymphadenopathy)
*Chronic inflammation of synovium with joint effusion, destruction of cartilage, and ankylosis of joints as disease progresses

72
Q

diagnosis of Juvenile Idiopathic Arthritis

A

*Affected children: 90% have negative rheumatoid factor
*No definitive diagnostic tests
*Elevated sedimentation rate in some cases
*Antinuclear antibodies common, but not specific for juvenile idiopathic arthritis
*Leukocytosis during exacerbations

73
Q

Oligoarthritic

A

involves ≤4 joints

74
Q

Polyarthritic

A

involves ≥5 joints

75
Q

Psoriatic arthritis

A

*enthesitis and undifferentiated

76
Q

Therapeutic Management of Juvenile Idiopathic Arthritis

A

*No specific cure
*Nonsteroidal antiinflammatory drugs (ibuprofen and naproxen)
*Disease-modifying antirheumatic drugs (methotrexate)
*Biologic disease-modifying antirheumatic drugs (tumor necrosis factor inhibitors such as Humeria, and Remicade)
*Glucocorticoids

77
Q

Cerebral Palsy

A

*group of permanent disorders of the development of movement and postures, causing activity limitations that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain

78
Q

Cerebral Palsy is characterized by

A

*abnormal muscle tone and coordination

79
Q

causes of cerebral palsy

A

*Gross abnormalities of the brain
*Vascular occlusion
*Laminar degeneration
*Effects of low birth weight
*ANOXIA
*Hypoxic infarction or hemorrhage

80
Q

Diagnostic Evaluation of cerebral Palsy

A

*Infants at risk: Require careful assessment during early infancy
*Neurologic examination and history: Primary means of diagnoses
*Neuroimaging
*Metabolic and genetic testing

81
Q

Clinical Manifestations cerebral Palsy

A

*Delayed gross motor development
*Abnormal motor performance
*Alterations in muscle tone (flaccid or hypertonic)
*Abnormal postures
*Reflex abnormalities
*Associated disabilities

82
Q

Goals of Therapy for cerebral Palsy

A

*To establish locomotion, communication, and self-help skills
*To achieve optimal appearance and integration of motor functions
*To correct associated defects as effectively as possible
*To provide educational opportunities adapted to the child’s capabilities
*To promote socialization experiences

83
Q

Therapeutic Management of Cerebral Palsy

A

*Ankle-foot braces: May be worn
*Orthopedic surgery: To correct spastic deformities
*Pharmacologic agents: To treat pain related to spasms and seizures
*Botulinum toxin A injections
*Dental hygiene
*Physical/occupational therapy

84
Q

Prognosis of Cerebral Palsy

A

*Moderate impairment: 85% of patients can achieve ambulation
*Cognitive impairments: In 30% to 50%
*Growth affected
*Survival dependent on comorbid conditions

85
Q

Neural Tube Defects

A

congenital deformities of the brain and spinal cord caused by incomplete development of the neural tube, the embryonic structure that forms the nervous system

86
Q

myelomeningocele

A

hernia of the spinal cord and meninges

87
Q

Spina Bifida

A

*Failure of the neural tube to close during the embryo’s early development (approximately 3-4 weeks after conception)

88
Q

factors causing spina bifida

A

*Maternal obesity
*Maternal diabetes mellitus
*Low vitamin B12 level

89
Q

prophylaxis for spina bifida

A

folate and b12 helps folate be used properly

90
Q

Therapeutic Management of Neural Tube Defects

A

-Postnatal: Prevent trauma to membranous cyst
-Hydrocelphalus common
-Monitor urinary output (Neuropathic (neurogenic) bladder dysfunction)
-Use of incubator or warmer to maintain temp
-Observe for early signs of infection, temp instability, irritability, and lethargy.
-Prevent drying of the sac
-Change dressings frequently
-Orthopedic considerations - DDH, clubfeet, scoliosis
-latex allergy

91
Q

favorable outcome for neural tube defects

A

close neural tube defect within the first 24-72 hours after birth

92
Q

Duchenne Muscular Dystrophy

A

A human genetic disease caused by a sex-linked recessive allele (so seen in MALE); characterized by progressive weakening and a loss of muscle tissue.

93
Q

what protein is absent in the muscles of kids with DMD

A

dystrophin

94
Q

Characteristics of Duchenne Muscular Dystrophy

A

*Progressive muscle weakness, wasting, and contractures
*Hypertrophic calf muscles in most patients
*Progressive generalized weakness in adolescence
*Death from respiratory or cardiac failure

95
Q

what are usually the first symptoms notes in Duchenne Muscular Dystrophy

A

Difficulties in running, riding a bicycle, and climbing stairs

96
Q

diagnosis of DMD is established primarily by

A

blood polymerase chain reaction (PCR) for dystrophic chain mutation

97
Q

confirmation of DMD by

A

*electromyelography, muscle biopsy, and serum enzyme measurement

98
Q

prenatal diagnosis for DMD

A

*as early as 12 weeks of gestation

99
Q

Gower sign

A

a child with DMD attain standing posture by kneeling on all fours and then gradually pushing his torso upright (with knees straight) by “walking” his hands up his legs.

100
Q

Clinical Manifestations of Duchenne Muscular Dystrophy

A

*Waddling gait, frequent falls, Gower sign
*Lordosis
*Enlarged muscles, especially in thighs and upper arms
*Profound muscular atrophy in later stages
*Mild to moderate mental impairment
*Obesity

101
Q

why does lorodosis and waddling gait occur as a result of DMD

A

Lordosis occurs as a result of weakened pelvic muscles, and the waddling gait is a result of weakness in the gluteus medius and maximus muscles

102
Q

what heart condition is seen in DMD

A

cardiomyopathy

103
Q

primary goal of DMD

A

*Maintain function in unaffected muscles as long as possible

104
Q

Therapeutic Management of Duchenne Muscular Dystrophy

A

*No effective treatment established
*Keep child as active as possible
*Range-of-motion exercises, bracing, performance of activities of daily living, surgical release of contractures as needed
*Genetic counseling for family

105
Q

Care Management of Duchenne Muscular Dystrophy

A

*Multidisciplinary team helps child and family cope with chronic, progressive, debilitating disease
*foster independence and activity as long as possible
*Teach child self-help skills
*Provide appropriate health care assistance as child’s needs intensify (e.g., home health, skilled nursing facility, respite care for family)

106
Q

Guillain-Barré Syndrome

A

*Acute demyelinating polyneuropathy with progressive paralysis, immune-mediated disease

107
Q

Guillain-Barré Syndrome is often associated with

A

*viral or bacterial infection or administration of vaccines

108
Q

Hallmark of GBS is

A

acute peripheral motor weakness. The paralysis occurs approximately 10 days after a nonspecific viral infection.

109
Q

Clinical Manifestations of Guillain-Barré syndrome

A

*Initially: Muscle tenderness, paresthesia, muscle weakness
*Paralysis: Rapidly ascends from lower extremities; may involve trunk, arms, face
*Flaccid paralysis, loss of reflexes
*Intercostal and phrenic nerve involvement
*In many patients: Urinary incontinency or retention and constipation

110
Q

Therapeutic Management of Guillain-Barré syndrome

A

Have equipment for intubation at bedside for emergency use
*Possibly steroids, intravenous immune globulin, and plasmapheresis
*Respiratory support
*Medications to prevent complication

111
Q

In acute phase of GBS

A

starts when symptoms begin and continues until new symptoms stop appearing or deterioration ceases; may take as long as 4 weeks.; hospitalized because of respiratory and pharyngeal involvement

112
Q

Plateau phase of GBS

A

symptoms remain constant without further deterioration; may last from days to weeks

113
Q

Recovery phase of GBS

A

patients begins to improve and progress to optimal recovery; it usually lasts a few weeks to months depending on the deficits incurred by the illness

114
Q

Course and Prognosis of Guillain-Barré syndrome

A

*Better outcomes are associated with younger ages; most patients have complete recovery
*In most patients, muscle function begins to return 2 days to 2 weeks after onset of symptoms, but period to complete recovery is prolonged

115
Q

most death with GBS is caused by

A

respiratory failure

NSG 434 - Peds (17 decks)

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