L11 MSK Impairments Flashcards
Connective tissue disorders
EDS
JIA
Hemophilia
Scleroderma
Dermatomyositis
Bony disorders
- arthrogryposis multiplex congenital
- osteogenesis imperfecta
- Scurvy
- Rickets
- Fractures
- Limb-length discrepancy
- scoliosis
- dysplasia
- legg-calve perthes
- SCFE
- Clubfoot, pes planus
Ehlers Danlos Syndrome
- heterogeneous group of connective disoders
- affects 1/5,000 people
- abnormal collagen synthesis, can leads to skin hyperextensibility, laxity, fragility, delayed wound healing, atrophic scarring, easy bruising, bleeding
- 13 types of EDS
Classic Ehlers Danlos
- abnormal colalgen type V
- autosomal dominant inheritance
- impairments include developmental delay, HE, atrophic scarring, slow wound healing, hernias, easy bruising, structural cardiac abnormalities
Hypermobility EDS
- unknown etiology
- impairments include skin laxity, velvet skin, joint HE, frequent dislocations
Vascular EDS
- abnormal collagen type 3
- unknown etiology or autosomal dominant inheritance
- impairments include, arterial, intestinal fragility, varicose veins, easy bruising, unusual facial features
Kyphoscoliosis EDS
- defiiciency of an enzyme that provides stability to collagen
- autsomal recessive
- impairments include joint laxity, scoliosis from birth, sclera fragility, hypotonia in infants
Arthroclasia EDS
- abnormal collagen type 1
- autosomal dominant
- joint hypermobility, frequent dislocations, kyphoscoliosis, skin fragility, easy bruising, hypotonia
Dermatosparaxis EDS
- abnormal collagen type 1
- autosomal recessive
- sagging, redundant skin with soft feeling, easy bruising, hernia, premature rupture of fetal membranes
Most common types of EDS
- classic
- hypermobility
- vascular
- kyphoscoliosis
- arthroclasia
- dermatosparaxis
Activity considerations for EDS
- caution with PA putting bones, joints, skin at risk
- social stigma
- care or avoidance of strenuous weight bearing or contact sports
- weight training (vEDS)
- postural considerations (kEDS)
- stress on skin or skin trauma (dEDS)
Juvenile Idiopathic Arthritis
- exclusion classification for all types of arthritis of unknown origin affecting kids before 16
- prevalence is 11-20/100,000
- likely involves cytokines signaling proteins
- 7 main categories
Categories of JIA
- systemic
- persistent and extended olgioarthritis
- polyarthritis
- enthesitis-related
- psoriatic
- undifferentiated
Systemic JIA
- typically most painful, diagnosed in young kids from 5-15
- onset preceded by fever and rash for 2 weeks
- involvement of heart, inflammation lung, swollen glands, liver/spleen enlargement, abdominal pain, anemia, growth stunt
- generally symmetrical and multiple joints
- small % of kids present with macrophage activation, which results in inflammatory s/s, insufficient liver function, neuro changes. should see immediate care
Oligoarthritis
- no fever, most common JIA subtype
- persistent = asymmetrical, affecting ≤ 4 joints, onset is prior to 6 yo, less severe, mostly LE
- extended = involvement of UE, more severe form, longer duration
- 10-30% have eye inflammation
Polyarthritis
- RA factor + –> ≥5 joints, + RA factors in 2 blood tests 2 months apart. Typically females, usually symmetrical, swelling. Prognosis not favorable
- RA factor - –> ≥5 joints, presents similar to oligoarthritis, no significant joint swelling, contractures/stiffness
Therapeutic Considerations for JIA
- education
- pain management
- deformity prevention
- ROM interventions
- strengthening
- proprioceptive training
- joint protection by avoiding end range, maintaining motion
- functional abilities
- physical fitness
Hemophilia
- missing protein required for clotting
- defect in gene on x chromosome
- impairments present as joint destruction, premature arthritis, chronic pain, muscle atrophy, ROM limitations, nerve compression, severe bleeding
- activities: pain and psychosocial limitations, limitations to activity and play
Bone changes with recurrent bleeds
- deformity-valgus, subluxation, widening of bone
- atrophy of heads of bones
- loss of motion
- osteophyte formation
- bone cysts
- changes in shape of bones
Juvenile Dermatomyositis
- inflammation, vasculitis, proximal more than distal muscle weakness and rash, includes skin and GI
- inflammatory cells predominantly B cells around blood vessels in septa between muscle
- autoimmune disease, unknown etiology
- focus on movement and function, avoid resistive exercises
Juvenile Scleroderma
- localized or systemic, involves skin of face, upper trunk, hands, arms, internal organs
- autoimmune disorder, unknown etiology
- involves fibrous thickening and hardening of skin, can lead to severe joint and tissue contractures
- may affect posture, rib cage mobility, limb length, muscle growth, skin changes
Arthrogryposis Multiplex Congenital
- deficit in motor unit, leading to severe fetal weakness
- fetal immobility, causes hypoplastic jt development and contractures
- unclear cause, occurs in utero
Impairements in arthrogryposis multiplex congenital
- contractures
- hip subluxation
- jaw, tongue ROM limitations
- limbs appear tubular, lack of normal creases
- diminished muscle mass, strength
- mobility difficulties, difficulty w/ADLs
- poor grasp, handwriting, feeding
- speech difficulty
Typical contracture patterns
- shoulder: adduction, IR
- Elbow: extension
- wrist: flexion and ulnar deviation
- finger: flexion, thumb in pam
- hip: flexion, abduction, ER
- knee: flexion
- clubfeet
Osteogenesis Imperfecta
- defects in type 1 collagen
- increased bone turnover
- genetic cause
- often short stature, poor tooth formation, hearing loss, blue sclera, translucent skin, triangle face
- osteoporosis, ligamentous laxity, scoliosis, propensity for fractures
- fragility limits play and ADL opportunities, mobility limitations
Scurvy
- decreased thickening of bone cortex and epiphyseal plates
- decreased bone available for calcification
- caused by insufficiency of vitamin C
- fragile bones, can fracture. Limits options for play
Rickets
- deficiency interferes with bone calcification
- caused by deficiency of vitamin D
- long bones bend under body weight
- may interfere with play, ADLs
Fractures
- peak for typically developing, health children in early adolescence
- bone turnover is high at this age
- mineralization may lag behind height, weight growth
Risk of subsequent fracture increases ____ after first fx
- 2-3x
- increases w/decreased calcium intake, first fx before 5 yo, and obesity
Epiphyseal Fracture
- fracture through growth plate
- may cause growth arrest
- about 20% of peds fractures
Salter Harris Classification
- determines extent of growth plate involvement
- Type 2 is the most common
- type 5 has poor prognosis
- type 1-2 = does not completely cross epiphysis
- type 3-4 = crosses epiphyseal border
- type 5 = crushing injury
Growth arrest
- complete may lead to significant limb length inequality
- asymmetrical may result in angular deformities if portion of bone keeps growing
usually happens in type 3-4
Greenstick Fracture
- occur in long bones when force breaks the cortex on side of impact and bends the other
- causes angular deformity
- refer to ortho physician
Treatment of fracture depends on
extent of involvement
follow WB precautions, and advise/education with AD as necessary
Nondisplaced/displaced treatment
Non = typically treated with cast
Displaced = closed or open reduction
Limb Length Discrepancy
- anatomical/osseous
- functional (soft tissue, joint)
- can assess with direct measurement (tape measure, imaging) or functional (postural, mechanical)
Potential Cause for Limb Length Discrepancy
- congenital
- infection/inflammation
- mechanical
- neurological
- trauma
- tumors
- others
Congenital LLD
examples include hip dysplasia, club foot, giantism, hemophilia
Infection/Inflammation LLD
examples include epiphyseal plate destruction, infection, JIA, increased blood flow
Mechanical LLD
examples include long term immobilization, traumatic aneurysms
Neurological LLD
examples include spina bifida, CP, polio
Trauma LLD
examples include severe burns, damage to plate, femur/tibia fractures, operations, bone graft removal
Tumors LLD
examples include ones that involve growth plate, chemo can destroy bone, vascular malformations
Scoliosis
- curvature of spine, can be structural or nonstructural
- infantile = < 3 yo
- Juvenile = 3-10 yo
- adolescent = 10 yo to skeletal maturity
Adolescent Idiopathic Scoliosis
- may have hereditary component
- 2-3% incidence, prevalent in biological females with curves > 20°
- feature includes rib hump
- can measure with cobb method
Rib hump
- rotational component of scoliosis
- identified by adams forward bend test
Cobb Method
- standard way to quantify curve size
- uses a/p x ray
- angle between the upper border of the upper vertebra and the lower borders of the lowest vertebra
Treatment for AIS
- <20° = exercise
- 20-40° bracing w/exercise
- > 35-40° surgery
schroth method helps to focus on de-rotation, lengthening, stabilization
Developmental Dysplasia of Hip (DDH)
- pathological hip instability
- genetic predisposition, meningocele, mechanical
- galaezzi sign, ortolani sign, barlow maneuver
Mechanical DDH
breech position in utero
insufficient amniotic fluid
Impairments and activity restrictions for DDH
- unstable hip joint
- limited hip abduction, LLD, poor acetabular development
- pain
- difficulty achieving motor milestones, ambulation, increased energy expenditure
Galaezzi Sign
child supine, hip and knee flexion, asymmetrical knee heigh positive with shortened side
Ortolani Sign
child supine, hips to 90°, gentle abduction and upward motion while stabilizing contralateral pelvis, positive with clunk indicating reduction into acetabulum
Barlow Maneuver
same start position as ortolani, gentle adduction while feeling for posterior displacement at hip joint
Pavlik Harness
maintains hip in flexion and abduction
Legg-Calve Perthes Disease
- AVN of femoral head
- most common for kids 5-7 yo, may affects kids between 3-12 yo
- unknown etiology
- loss of blood supply results in shortened femoral neck, trochanteric overgrowth, asymmetrical repair of femoral head
- modified waldenstrom classification
Kids w/legg-calve-perthes disease present with
- limp, tredenlenburg
- pain in hip, knee, and/or thigh
- pain is provoked by activity, relief with rest
- reduced hip ROM, particularly hip abduction, IR
Interventions for LCP Disease
- pain management
- ROM
- strength
- gait mechanics to promote hip congruency
- hip abduction and IR
- surgical (PTs are post)
SCFE
- post displacement of capital femoral epiphysis from femoral neck through weakened physis
- typical onset in prepubescent, ages 10-15
- unclear etiology, can be trauma, mechanical, inflammation, obesity, hormones, genetic
- surgery, may include prophlactic pinning of univolved hip
Impairments for SCFE
- antalgic gait/limp
- pain in grown
- ER posturing
- decreased hip flexion, abduction, IR
- thigh moves into ER when flexed
- pain, long term changes
Slipped SCFE
mild to moderate pain with activity
Unstable SCFE
severe hip pain, unable to walk
Blount Disease
- compression of medial portion of proximal tibia, most often associated with obesity
- lateral bowing tibia, medial knee instability
- pain, progressive joint degeneration
Congenital Talipes Equinovarus
- known as clubfoot
- midfoot cavus/high arch, forefoot adductors, hindfoot varus, ankle equines deformity
- classifications include postural, idiopathic, neurogenic, syndromic
- surgery, serial casting, achilles surgery, bracing, taping, stretching
Metatarsus Adductus
metatarsals adducted toward midline, assessed with straight line through calcaneus through long axis of foot
may or may not need intervention
Pes Planus
flexible flat feet
may or may not need intervention
Sports PT peds considerations
- child physiology
- repetitive loading
- shear stress to articular cartilage
- overuse injury
- apophysis, often occur with excess compression or traction forces across joint during sport
Osgood-Schlatter Disease/Sever’s Disease
- excess stress on major tendon insertions
- OS = tibia
- sever = calcaneus
