Peds Musculoskeletal/Neuromuscular Dysfunction Flashcards
(115 cards)
1
Q
One of the most difficult aspects of illness in a child is
A
immobility
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)
3
Q
Crush injuries
A
occur when children’s extremities or digits are crushed (finger slammed in the car door).
4
Q
treatment for contusion
A
application of cold.
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.
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
7
Q
what is the predominant symptom of dislocation
A
increased pain with active or passive movement of affected extremity
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
9
Q
sprain
A
trauma to joint from LIGAMENT partially or completely torn or stretched by force
10
Q
strain
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microscopic tear io MUSCULORTENDINOUS unit
11
Q
onset: sprain vs strain
A
sprain: rapid onset of swelling with disability
strain: generally incurred over time
12
Q
Therapeutic Management ofSoft-Tissue Injuries
A
RICE AND ICES
13
Q
RICE
A
rest, ice(3o mins at a time), compression, elevation
14
Q
ICES
A
Ice, Compression, Elevation, Support
15
Q
what is the most frequently broken bone in childhood
A
distal forearm
16
Q
fracture
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broken bone
17
Q
simple or closed fracture
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*Does not produce a break in the skin
18
Q
open or compound fracture
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*Fractured bone protrudes through the skin
19
Q
complicated fracture
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Bone fragments have damaged other organs or tissues
20
Q
comminuted fracture
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*Small fragments of bone are broken from fractured shaft and lie in surrounding tissue
21
Q
growth plate injuries
A
*Weakest point of long bones: The cartilage growth plate (epiphyseal plate)
may affect future bone growth
22
Q
growth plate injury treatment
A
*May include open reduction and internal fixation to prevent growth disturbances
23
Q
neonatal bone healing period
A
2-3 weeks
24
Q
early childhood bone healing period
A
4 weeks
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later childhood bone healing period
6-8 weeks
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adolescence bone healing period
8-12 weeks
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diagnosis of fracture
*Radiographs (X-ray)
*History taking
*Suspicion of fracture in a young child who refuses to walk or bear weight
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goals of fracture management
*Reduction and immobilization
*Restoring function
*Preventing deformity
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fracture treatment
reduction and immobilization
splinted or casted to immobilize and protect the injured extremity
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Assessment of Fractures: The Six Ps
*Pain and point of tenderness
*Pallor
*Pulselessness
*Paresthesia:
*Paralysis:
*Pressure
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cast care
*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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Developmental Dysplasia of the Hip
abnormal development of the hip joint found that is congenital
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Acetabular dysplasia
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.
34
Sublaxation
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.
35
Dislocation
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.
36
Clinical Manifestations of DDH: infant
*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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Ortolani test
hip is reduced by abduction
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Barlow test
hip is dislocated by adduction
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Therapeutic Management of DDH: birth to 6 months
*Pavlik harness for abduction of hip
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Therapeutic Management of DDH: 6 to 24 months
*Dislocation unrecognized until child begins to stand and walk; closed reduction and spica cast
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Therapeutic Management of DDH: older child
*Operative reduction, tenotomy, osteotomy; correction is very difficult after age 4 years
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Tenotomy
surgical cutting of a tendon
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Pavlik Harness care
-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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clubfoot
a fixed congenital defect of the ankle and foot
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Talipes varus
*Inversion or bending inward
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Talipes valgus
*Eversion or bending out
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Talipes equinus
Plantar flexion with toes lower than the heel
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Talipes calcaneus
*Dorsiflexion with toes higher than the heel
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Therapeutic Management of Clubfoot: three stages
*Correction of the deformity
*Maintenance of the correction until normal muscle balance is regained
*Follow-up to avert possible recurrence
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*Ponseti method (serial casting)
begun soon after birth with weekly gentle manipulation and stretching of the foot and then serial casting for 6-10 weeks
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Ponseti sandals are used after casting to...
maintain the correction and prevent recurrence.
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Clinical features Osteogenesis Imperfecta
-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
Therapeutic Management of Osteogenesis Imperfecta
*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
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parent teaching for osteogenesis imperfecta
-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
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Legg-Calve-Perthes Disease
A self-limiting disorder in which there is avascular necrosis of the femoral head.
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Clinical Manifestations of Legg-Calvé-Perthes Disease
*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
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diagnosis of Legg-Calvé-Perthes Disease
history and findings on radiographs and magnetic resonance images (MRI)
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treatment goal of Legg-Calvé-Perthes Disease
Keep head of femur in acetabulum
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Therapeutic Management of Legg-Calvé-Perthes Disease
*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
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Idiopathic Scoliosis
*Complex spinal deformity in three planes
*Lateral curvature
*Spinal rotation, causing rib asymmetry
*Thoracic hypokyphosis
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Diagnostic Evaluation ofSpinal Curvatures
*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
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Therapeutic Management ofSpinal Curvatures
*Team approach to treatment
*Bracing
*Exercise
*Surgical intervention for severe curvature (instrumentation and fusion)
*Harrington rods
*Luque rods
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Osteomyelitis
*Infectious process in the bone
*May be caused by exogenous or hematogenous sources
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what is the most causative organism of osteomyelitis
Staphylococcus aureus
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clinical manifestations of osteomyelitis
Acute and chronic inflammation, fever, pain, necrotic bone
*Signs/symptoms begin abruptly, resemble symptoms of arthritis and leukemia
*Marked leukocytosis
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diagnosis for osteomyelitis
*Bone cultures obtained from biopsy or aspirate
*Radiographs: May appear normal at first
*Bone scans for diagnosis
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Therapeutic and Care Managementbof Osteomyelitis
*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
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typical antibiotics for osteomyelitis
*Typically nafcillin or clindamycin
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Juvenile Idiopathic Arthritis
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
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peak onset of Juvenile Idiopathic Arthritis
*1 to 3 years of age
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clinical manifestations of Juvenile Idiopathic Arthritis
*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
diagnosis of Juvenile Idiopathic Arthritis
*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
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Oligoarthritic
involves ≤4 joints
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Polyarthritic
involves ≥5 joints
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Psoriatic arthritis
*enthesitis and undifferentiated
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Therapeutic Management of Juvenile Idiopathic Arthritis
*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
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Cerebral Palsy
*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
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Cerebral Palsy is characterized by
*abnormal muscle tone and coordination
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causes of cerebral palsy
*Gross abnormalities of the brain
*Vascular occlusion
*Laminar degeneration
*Effects of low birth weight
*ANOXIA
*Hypoxic infarction or hemorrhage
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Diagnostic Evaluation of cerebral Palsy
*Infants at risk: Require careful assessment during early infancy
*Neurologic examination and history: Primary means of diagnoses
*Neuroimaging
*Metabolic and genetic testing
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Clinical Manifestations cerebral Palsy
*Delayed gross motor development
*Abnormal motor performance
*Alterations in muscle tone (flaccid or hypertonic)
*Abnormal postures
*Reflex abnormalities
*Associated disabilities
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Goals of Therapy for cerebral Palsy
*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
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Therapeutic Management of Cerebral Palsy
*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
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Prognosis of Cerebral Palsy
*Moderate impairment: 85% of patients can achieve ambulation
*Cognitive impairments: In 30% to 50%
*Growth affected
*Survival dependent on comorbid conditions
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Neural Tube Defects
congenital deformities of the brain and spinal cord caused by incomplete development of the neural tube, the embryonic structure that forms the nervous system
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myelomeningocele
hernia of the spinal cord and meninges
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Spina Bifida
*Failure of the neural tube to close during the embryo's early development (approximately 3-4 weeks after conception)
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factors causing spina bifida
*Maternal obesity
*Maternal diabetes mellitus
*Low vitamin B12 level
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prophylaxis for spina bifida
folate and b12 helps folate be used properly
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Therapeutic Management of Neural Tube Defects
-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
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favorable outcome for neural tube defects
close neural tube defect within the first 24-72 hours after birth
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Duchenne Muscular Dystrophy
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.
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what protein is absent in the muscles of kids with DMD
dystrophin
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Characteristics of Duchenne Muscular Dystrophy
*Progressive muscle weakness, wasting, and contractures
*Hypertrophic calf muscles in most patients
*Progressive generalized weakness in adolescence
*Death from respiratory or cardiac failure
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what are usually the first symptoms notes in Duchenne Muscular Dystrophy
Difficulties in running, riding a bicycle, and climbing stairs
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diagnosis of DMD is established primarily by
blood polymerase chain reaction (PCR) for dystrophic chain mutation
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confirmation of DMD by
*electromyelography, muscle biopsy, and serum enzyme measurement
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prenatal diagnosis for DMD
*as early as 12 weeks of gestation
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Gower sign
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.
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Clinical Manifestations of Duchenne Muscular Dystrophy
*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
why does lorodosis and waddling gait occur as a result of DMD
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
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what heart condition is seen in DMD
cardiomyopathy
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primary goal of DMD
*Maintain function in unaffected muscles as long as possible
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Therapeutic Management of Duchenne Muscular Dystrophy
*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
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Care Management of Duchenne Muscular Dystrophy
*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)
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Guillain-Barré Syndrome
*Acute demyelinating polyneuropathy with progressive paralysis, immune-mediated disease
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Guillain-Barré Syndrome is often associated with
*viral or bacterial infection or administration of vaccines
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Hallmark of GBS is
acute peripheral motor weakness. The paralysis occurs approximately 10 days after a nonspecific viral infection.
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Clinical Manifestations of Guillain-Barré syndrome
*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
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Therapeutic Management of Guillain-Barré syndrome
Have equipment for intubation at bedside for emergency use
*Possibly steroids, intravenous immune globulin, and plasmapheresis
*Respiratory support
*Medications to prevent complication
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In acute phase of GBS
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
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Plateau phase of GBS
symptoms remain constant without further deterioration; may last from days to weeks
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Recovery phase of GBS
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
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Course and Prognosis of Guillain-Barré syndrome
*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
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most death with GBS is caused by
respiratory failure
