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53 Cards in this Set
- Front
- Back
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Direct Acquired Limb Length Discrepency |
When overriding segments of a fracture are not resolved |
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Indirect Acquired Limb Length Discrepency |
Congenital Infection Mechanical Neurologica Trauma Tumors Table 6.4 for types of Growth retardation vs stimulation |
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Describe Apparent limb length discrepancies |
Cause by joint contractures, angular deformities, hip subluxation or dislocation, pelvic obliquity or spinal segment |
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Limb length Treatment Guidlines |
0-2cm: no treatment 2-4cm: shoe lift 2-6cm: epiphyseodesis(fusion of the epiphyseal plate), shortening 6-20cm: lengthening that may or may not be combined with other procedures >20cm: prosthesis firring PT: Strengthening post surgical, gait training, ROM family education |
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What is Hemimelia |
-Absence or growth shortening of a bone -Fibular is most common/tibia is rare |
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What is Proximal femoral focal deficiency |
Deformity of the proximal portion of the femur. Wide variety of clinical features |
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Describe Epiphysiodesis |
Equalizelimb length by slowing growth in the longer leg. Stops growth in the growth plate but growthcontinues in other growth plates in the limb. Requires planning to estimategrowth velocity and skeletal maturity. |
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Describe Leg Lengthening |
Monolateral or circumferential lengthening device |
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When can upper extremity prosthetics be started |
As early 12-15 months |
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Age ranges for Idiopathic Scoliosis |
Infantile: < 3 years (usually resolves) Juvenile: 3-10 years Adolescent: 10 (skeletal maturity) |
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Describe the Cobb Angle Method |
Used to quantify the size of the curvature using an AP xray view. Angles from vertebrae that are at the greatest tilt on either end. |
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What are the scoliosis screening guidelines? (Table 6.7) |
Girls -3:1 -10x risk of progression and fusion 10 years old - <12 have 3x risk of progression Thoracic and double mj curves -3x risk of progression or nonthoracic curves Growth potential -Greatest increase during growth spurt Curve Magnitude -20% - 20deg // 60% - 30deg // 90% for 50deg Risser stage/skeletal maturity -Risk reduced 2/3 if iliac crest is more than 50% capped |
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What are the guidelines for scoliosis referral? (Table 6.8) |
-If no rib hump at 10 years of age, none of thechildren's curves progressed. -5° scoliometer trunk rotation angle does not needrescreening; significant scoliosis is not presentnor likely to develop. -10° or> scoliometer trunk rotation angle should bereferred to physician -5° to 9° scoliometer trunk rotation angle should berescreened every 6 months until 1 year after theoccurrence of menarche.Source: Bunnell, W.P. C2005l. Selective screening for scoliosis. |
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What are types of congenital joint anomalies? |
Talipes Equinovarus (Club foot) Developmental dysplasia of the hip |
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Etiology of talipes equinovarus |
Unknown Suspected: -Genetics -Arrested embryonic development -NM anomalies - Mechanical uterine restriction |
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Pathology of talipes equinovarus |
Displacement of the navicular, calcaneous, and cuboid bones around the talus |
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Talipes Equinovarus BF&S impairments |
Hindfoot equinus with varus of the forefoot and heel and adducted forefoot |
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Talipes equinovarus activity and participation restrictions |
-Interferes with standing, ambulation, and other upright activities -Difficulty fitting shoes -Cosmesis |
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Talipes Equniovarus interventions |
PT intervention: taping, stretching, parent education on home stretching, developmental stimulation Health-care team: if conservative treatment is not successful then casting &/or surgery maybe considered. Ponseti method (weekly casting), followed by possible achilles tendon release |
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Etiology of Developmental dysplasia of the hip? |
Geneticpredisposition; first born; 80% female Ethnic:increased in Native American, lower in Chinese & Africans Mechanical:breech position, Oligohydramnios(decreased amniotic fluid) Neuromuscular: myelomeningocele |
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Pathology of Developmental Dysplasia of the hip |
-Subluxation/dislocationofthe hip, ordysplasia of the hip -Hypertrophiedridge of cartilage in the superior, posterior and inferior aspects of theacetabulum called a neolimbus |
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Developmental Dysplasia of the hip BF&S impairments |
•Examinewith Ortolani orBarlow signs in neonates < 1 month of age •Unstablehip joint •Limitedhip abduction •Poorhip socket development WB surface •ApparentLLD |
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Developmental Dysplasia of the hip activity and participation restrictions |
-Motor milestone acquisition -Ambulation and other upright activities -Pain -Leg Length inequality negatively affects cosmesis |
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Developmental Dysplasia of the hip interventions |
•Parenteducation •PavlikHarness* for neonates and/or infants (usually 23 hours/day) •Developmentalstimulation •Positioningand ROM •Surgery |
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What are the types of muscular disorders? |
Duchenne's muscular dystrophy Spinal Muscular atrophy Congenital muscular torticollis |
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Etiology and pathology of Congenital Muscular Torticollis |
Etiology: -Usually unclear, current theory is intrauterine or perinatal compartment syndrome Pathology: -Unilateral contracture of the SCM -May lead plagiocephaly if left untreated |
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Congenital Muscular Torticollis BF&S impairments |
•Headis tilted toward involved side and chin is rotated toward opposite side. •LimitedROM in lateral flexion toward uninvolved side and rotation toward involved side •Skewedvertical and midline orientation |
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Congenital Muscular Torticollis activity and participation limitations |
-Cosmesis -Distorted orientation may interfere with play -Limited ROM may impede dressing -Developmental delay |
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Conservative treatment of CMT |
Positioning, ROM, strengthening through activation of head and trunk muscles as the infant gains control of upright postures |
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Congenital Muscular Torticollis activity and participation limitations |
Prognosis with PT is excellent within 3 months and remains high if initiated in the first year |
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Congenital muscular torticollis interventions |
•Environmentalchanges such as arranging the child’s crib and changing table to promoteturning the head to look at caregivers. •Stimulatingactive head turns to toys or interesting sounds. •Towelrolls may be used to prevent the head from falling into shortened position. |
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Home program for CMT |
Ways to handle, feed, carry, and position the baby Activities to encourage midline head and trunk postures Gentle A or PROM of cervical spine |
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Etiology of Duchenne Muscular dystrophy |
-X Linked Recessive trait -Defect on the Xp21 portion of the X chromosome |
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Pathology of Duchenne Muscular Dystrophy |
-Muscle composition abnormalities -Progressive degeneration of muscle fibers variation in fiber size -Connective and adipose tissue deposits |
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Duchenne Muscular Dystrophy BF&S impairments |
Progressive muscle weakness -Proximal > Distal -Hip flexion and ITB contractures -Progressive Scoliosis Psuedohypertrophy -Enlargement without increased strength Respiratory muscle weakness Progressive Scoliosis |
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Duchenne Muscular Dystrophy activity and participation limitations |
-Fatal in adolescence or early adulthood -Motor skill regression -Loss of ambulation -Hip and knee flexion contractures and progressive scoliosis are accelerated -Gowers Sign |
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Duchenne Muscular Dystrophy interventions |
-Child and Family Education -ROM program -Strengthening and fitness programs -Ambulation and mobility aids as dz progresses -Resp exercises and secretion elimination -Adaptive equipment to ease caregiving as limitations progress -Referral to support systems |
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Etiology of Spinal muscular atrophy |
-Hereditary -Autosomal recessive genetic disease -Deletion or mutation of the Survival Motor Neuron-1 gene located at chromosome region 5Q |
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Pathology of Spinal muscular atrophy |
Unclear -Includes non-progressive loss of anterior horn cells -Sequelae of the disease process is progressive and fatal as the child outgrows his/her muscle capacity -3 different types |
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Spinal Muscular Atrophy BF&S impairments |
-Depends on the type -Hypotonia -Muscle weakness and atrophy (proximal >distal) -Absent/dec in DTR -Gradual loss of function -Resp complications is main cause of death |
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What muscles are typically uninvolved in Spinal muscular atrophy |
Diaphragm Sternothyroid Sternohyoid Involuntary muscles of the intestines, bladder and heart |
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Type 1 SMA (Onset, death, motor limitations) |
Onset: 0 - 6mo Death: <2 year (with no intervention) Limits: Does not sit |
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Type 2 SMA (Onset, death, motor limitations) |
Onset: 7mo - 18mo Death: > 2 years Limits: Does not stand |
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Type 3 SMA (Onset, death, motor limitations) |
Onset: > 18mo Death: Adults Limits: Stands and walks alone |
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Spinal Muscular Atrophy interventions |
Depends on type -ROM, strength, maintaining development and function -Power Mobility -Assistive Technology -Caregiver education -Focus on quality of life |
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How is idiopathic toe walking diagnosed? |
Diagnosis of exclusion Etiology and pathology is unknown |
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Idiopathic toe walking BF&S impairments |
-Loss of ankle ROM -Shortened Achilles tendon -Lack of muscle coordination -Delays in language development, gross and fine motor skills, visual motor development, sensory integration, behavioral problems |
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Idiopathic toe walking activity and participation limitations |
•Frequentfalls or stumbles with ambulation •Painin the foot or leg •Maylimit mobility and self-care activities •Difficultlywearing shoes •Maynot be able to run or ascend stairs •Influencedby method of treatment_1" |
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Interventions for Idiopathic toe talking |
-AFO -Serial Casting -Calf stretches -Strengthening -Gait training -Balance/posture -Sensory integration -NM estim -Botox -Surgery |
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Cerebral Palsy BF&S impairments |
Scoliosis Pelvic obliquity/misalignment Hip subluxation/dislocation Foot & Ankle misalignment - equinovalgus, limitation in DF |
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Intervention for cerebral palsy |
Strengthening, family education, functional activities, botox, surgery, serial casting, ROM, positioning |
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Down Syndrome BF&S Impairments |
Hypotonicty Pes planus, pes valgus Atypical gait AA joint instability |
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Intervention for Down syndrome |
Family education, fitness program, strengthening, functional activities |
