Transcript Current Concepts on Pediatric Hip Disorders

Current Concepts on Pediatric
Hip Disorders
Dr. Donald W. Kucharzyk
Pediatric Orthopaedic Surgeon
The Orthopaedic,Pediatric &
Spine Institute
Crown Point, Indiana
“Developmental Dysplasia of
the Hip”
CURRENT CONCEPTS UPDATE
Developmental Dysplasia Hip
TERMINOLOGY
Dysplasia: Abnormal tissue development
Subluxation: Capsular laxity with some
displacement but maintenance of cartilagecartilage contact
Dislocated: No cartilage-cartilage contact
with hip external to the labrum NOW
TERMED “DDH”
Developmental Dysplasia Hip
ETIOLOGY
Genetic Factors: Race..Blacks/Chinese
Twins(34-50%)
Anatomic Factors: Primary Acetabular
Dysplasia…parents of children with DDH
have incidence of shallow acetabulum;
Increased Joint Laxity seen in children
with DDH (33-75%)
Developmental Dysplasia Hip
Mechanical/Environmental: Increased risk in
First Born, young mothers, and molded baby
syndrome; Twins; Oligohydramnios;
Breech(50%)
Breech Incidence: female
1/200
female breech
1/35
female breech FH 1/15
Overall Incidence: Instability 2.7/1000
Dislocation
1/1000
Developmental Dysplasia Hip
ANATOMY
EARLY STAGE: Capsular Laxity
Blunting of Labrum
Ortolani/Barlow Pos.
LATE STAGE: Adduction Contracture
Enlarged Capsule
Hourglass Contracture
Infolded Labrum
False Acetabulum
Developmental Dysplasia Hip
NATURAL HISTORY
Barlow(1962): 58% spontaneous stable at 1
week; 30% stable at 2 months; 12%
remained dislocated
Coleman(1968): 22% spontaneous
correction; 39% dysplastic; 26% dislocated
Wedge(1979): untreated 60% pain
Weinstein(1987): DDH leads to DJD
Developmental Dysplasia Hip
EXAMINATION
Ortolani
Barlow
Allis/Galeazzi
Asymmetrical Thigh Folds
Limited Abduction
Developmental Dysplasia Hip
RADIOLOGIC EVALUATION
Plain Xrays: unreliable intially; useful at
6-8 weeks
Ultrasound: most reliable but level of
dependability related to expertise of
radiologist; useful with treatment
modalities
Developmental Dysplasia Hip
TREATMENT
BIRTH TO SIX MONTHS
Pavlik Harness: fulltime for 4-6 weeks till
hips stable then brace till acetabulum
normal; Failure to reduce in 2-3 weekschange treatment plan
Complications: AVN
Femoral Nerve Palsy
Developmental Dysplasia Hip
SIX MONTHS TO ONE YEAR
Closed Reduction and Casting: must achieve
stable and concentric reduction, human
position for casting, maintain safe
zone(adductor release)
Developmental Dysplasia Hip
TWELVE TO EIGHTEEN MONTHS
Closed Reduction with Adductor Release
followed by Double Hip Spica casting for 4
months
Open reduction: if reduction failure, hip
not stable in a favourable position, or if
reduction not concentric
Developmental Dysplasia Hip
EIGHTEEN TO THIRTY-SIX MONTHS
Open Reduction and Innominate osteotomy
with casting for 6 weeks followed by
abduction bracing for 3 months
Key to Treatment: Capsulorrhaphy
important to maintaining the hip and
promoting development of the acetabulum
Developmental Dysplasia Hip
THREE TO SIX YEARS
Must alter the Natural History
Soft Tissue Release
Open Reduction
Femoral Shortening
Pelvic Innominate Osteotomy
Developmental Dysplasia Hip
SIX YEARS AND OLDER
Unrecognized Complete Dislocation:
Unilateral..should be treated via OR,
Femoral shortening and Pelvic osteotomy;
Bilateral..controversial
Failed Efforts at Reduction: Requires
assessment of the cause of the failure and
then a Salvage Procedure(Shelf, Chiari,
Colonna)
Developmental Dysplasia Hip
Redislocation after Prior Reduction: Due to
unstable reduction caused by acetabular
incompetence, proximal femoral deformity
or osseous necrosis; treatment aimed at
correction of any femoral or acetabular
deformities and reduce the hip
Late Dislocation: Instability..acetabular
deformity
Developmental Dysplasia Hip
TREATMENT
Unilateral Dislocation: Open Reduction with
Femoral Shortening and stabilization of any
acetabular defects
Bilateral Dislocations:
Controversial..painful,stiff hips result and
successful reductions uncertain; BEST
results in this group is EARLY DETECTION
AND PREVENTION
Developmental Dysplasia Hip
COMPLICATION’S
Failure to Document Reduction
Brace Failure: inappropriate application,
poor compliance, failure in following the
patient, anatomic obstructions and
excessive laxity
Cast Failure: Narrow safe zone, cast
application problems, and short
immobilization period
Developmental Dysplasia Hip
COMPLICATION’S
Joint Problems: Not addressing the soft
tissue contractures especially about the
capsule(hourglass) and inverted labrum;
Loose redundant capsule; Femoral Head
Malposition;
Femoral Osteotomies: shortens femur,
trendelenberg gait, persistant instability
and no remodeling over 8
Developmental Dysplasia Hip
COMPLICATION’S
Innominate Osteotomies: failure of
concentric reduction and increased femoral
head pressure
Combined Osteotomies: may uncover head
posteriorly, difficult to obtain correct
alignment
Developmental Dysplasia Hip
COMPLICATION’S
Avascular Necrosis: AVOID
Keep Femoral Head Centered
Maintain Acetabular Coverage
Overgrowth of the Greater Trochanter
Early Degenerative Osteoarthritis
Legg-Calves-Perthes Disease
CURRENT CONCEPTS UPDATE
Legg-Calves-Perthes Disease
ETIOLOGY
Chronic sequence of changes initiated by
an avascularity of the femoral head: less
developed blood flow
Specific cause is unknown
Seen age grouping: 4-8 years with range
of 2-12 years
Four-five times more common in males
Bilateral in 10%
Legg-Calve-Perthes Disease
CLINICAL FINDINGS
Prolonged limp
Waddling gait
Pain in groin or thigh
Limited painful motion
Tenderness to palpation over hip
Gluteal Atrophy
Trendelenberg sign Positive
Leg Length Discrepancy
Legg-Calve-Perthes Disease
RADIOGRAPHIC
Diagnostic Changes
Lateral Displacement of Femoral Head
Subchondral Fracture Line
Increased Epiphyseal Density
Smaller Epiphyseal Nucleus than Normal
Legg-Calve-Perthes Disease
Head at Risk Signs
Lateral Subluxation of Femoral Head
Calcification Lateral to Capital Epiphysis
Metaphyseal Cysts
Horizontal Growth Plate
Gage’s Sign: V-shaped Defect
Legg-Calve-Perthes Disease
CLASSIFICATION
Catterall: Based on xray appearance at
the time of maximal resorption
Type I: less than 25% involvement
Type II: 50% involvement, lateral border
spared
Type III: 75% involvement, lateral head
collapse
Type IV: total involvement
Legg-Calve-Perthes Disease
CLASSIFICATION
Salter-Thompson: based on extent of
subchondral fracture line
Group A: less than 50% involvement
Group B: over 50% involvement
Legg-Calve-Perthes Disease
PROGNOSTIC FACTORS
Sex: girls have poorer prognosis than boys
Age at Onset: younger children have better
prognosis than older
Extent of Head Involvement: more involvedWorst Prognosis
Femoral Head Containment: loss of containmentgreater risk of deformity
Legg-Calve-Perthes Disease
PROGNOSTIC FACTORS
Hip Range of Motion: major factor in
pathogenesis
Premature Physeal Closure: asymmetric
growth and inadequate remodeling
Legg-Calve-Perthes Disease
TREATMENT
Goals: good containment and congruence
and reduction of weight on affected area
of femoral head; maintenance of ROM
Legg-Calve-Perthes Disease
Treatment Options:
No Treatment
Intermittent Traction
Abduction Orthosis
Femoral Osteotomy
Pelvic Osteotomy
Legg-Calve-Perthes Disease
No Treatment:
Children under Five require observation
only
Containment Orthosis does not affect
the natural history in children under Five
Legg-Calve-Perthes Disease
Containment Orthosis
Texas Scottish Rite Brace: effects the
natural history
Disadvantages: bilateral useage,
interference with activities of daily living
Brace Use: over Six Years of Age and
with greater than 50% head involvement
Legg-Calve-Perthes Disease
Containment Orthosis:
Prerequisites for Bracing: full ROM
especially in abduction; no residual hip
irritability; round femoral head
Contraindication: noncompliance
Time of Bracing: 6-12 months
Does not alter the Natural History
Legg-Calve-Perthes Disease
Surgical Treatment:
Advantage over Bracing: period of
restriction less than 2 months; no end point
to determine discontinuation; permanent
improvement in femoral head containment
Indications: bracing contraindicated;
bilateral involvement at different stages;
coverage not obtainable
Legg-Calve-Perthes Disease
Surgical Treatment:
Containment obtained by altering the
acetabulum or femur
Varus Derotational Osteotomy: maximum
coverage of femoral head; disadvantages
include shortening, trendelenburg gair,
nonunion, excessive varus angulation
Legg-Calve-Perthes Disease
Surgical Treatment:
Innominate Osteotomy: anterolateral
coverage with improvement in gait and only
mild lengthening of extremity; disadvantages
include inability to obtain coverage and mild
limb lengthening
Reconstructive Procedures: include valgus
osteotomy, cheilectomy, chairi osteotomy,
trochanteric advancement,or a combination of
above
Legg-Calve-Perthes Disease
69% good
71% good
87% good
86% good
osteotomy
Clinical Results
results with no treatment
results with containment orthosis
results with pelvic osteotomy
results with femoral varus
Legg-Calve-Perthes Disease
Natural History
Age of Disease Onset
Degree of Involvement
Presence of Head at Risk Sign
Age of Patient at Treatment
Stage of Disease at Treatment
Congrous Hip at Skeletal Maturity
The Hip in Myelodysplasia
Muscular Contractures
Hip Subluxation and Dislocation
Acetabular Dysplasia
Stiff Hip
Pelvic Obliquity
The Hip in Myelodysplasia
MUSCULAR CONTRACTURE
Flexion Contracture
More frequent in high lumbar-thoracic level
lesions
Caused by hip flexors unopposed
Spasticity of flexors
Prolonged sitting or lying
Surgery: greater than 2 yrs or greater than
20deg. contracture
The Hip in Myelodysplasia
Surgical Treatment:
Anterior Hip Release: release the
sartorius, rectus femoris, iliopsoas, tensor
fascia lata, and anterior hip capsule
Extension Osteotomy: for persistant
deformity or if hip flexor power needs to
be maintained
The Hip in Myelodysplasia
Flexion-Abduction-External Rotation
Contracture
Common in thoracic level lesions and
complete paralysis of lower extremity
Usually Bilateral
Caused by external rotation of hip in supine
position-contracture in posterior hip capsule
and short external rotators
Surgery: interferes with sitting/brace
The Hip in Myelodysplasia
Surgical Treatment:
Complete hip release: release the
iliopsoas tendon, sartorius, tensor fascia
lata, gluteus medius and minimus, short
external rotators, and the anterior and
posterior capsule. If Bilateral releases at
same time
The Hip in Myelodysplasia
Abduction Contracture
Seen in T2-L2 High level lesions
May cause scoliosis and pelvic obliquity
Caused by contracture of tensor fascia
latae and iliopsoas
Surgery: Pelvic Obliquity, Scoliosis, and
Functional Impairment
The Hip in Myelodysplasia
Surgical Treatment:
Tensor Fascia Latae Release
Yount Procedure
The Hip in Myelodysplasia
Adduction Contracture
Frequent in high level lesion
Occurs with hip subluxations and
dislocations
Caused by spasticity and contracture of
adductor
Surgery: Pelvic Obliquity and
interference with sitting or walking
The Hip in Myelodysplasia
Surgical Treatment:
Adductor Release
Femoral/Pelvic Osteotomy
The Hip in Myelodysplasia
Hip Subluxation and Dislocation
Congenital: seen in sacral lesion; treatment
similar to DDH
Teratologic: no treatment initially; goal is
FUNCTION not reduction
Paralytic: seen in 50-70% of low lumbar
L3-4 lesions, muscle imbalance of adductors
and flexors, frequent before age of 3 yrs.
The Hip in Myelodysplasia
Surgical Treatment:
Reduction of dislocation is controversial
No Quadriceps then soft tissue release
only: community ambulators
Strong Quadriceps then consider open
reduction, correction of muscle imbalance,
release contractures, correct bony
deformities(fem/pelvic)
The Hip in Myelodysplasia
Acetabular Dysplasia
Chiari Pelvic Osteotomy
Shelf Procedure
Varus Derotational Osteotomy
The Hip in Myelodysplasia
The Stiff Hip
Most Serious Problem: Stiff in
Extension..can’t sit; Stiff in Flexion..can’t
stand; Stiff in between..can’t sit or stand
Treatment: Proximal Femoral Resection
and Interpositional Arthroplasty
The Hip in Myelodysplasia
Pelvic Obliquity
Infrapelvic: contracture of abductor and
tensor fascia latae of one hip and
adductors of the opposite
Suprapelvic: uncompensated scoliosis due
to bony deformity of lumbosacral spine
Pelvic: bony deformity of sacrum and
sacroiliac
The Hip in Myelodysplasia
Surgical Treatment:
Infrapelvic: prevention by splinting, ROM
exercises, positioning; fixed contracture-soft
tissue release; severe deformity-proximal
femoral osteotomy
Suprapelvic: control scoliosis by orthosis or
fusion
Pelvic: Fixed Obliquity>20deg. Pelvic
Osteotomy(Lindseth: Triple Transfer)
Transient Synovitis of the Hip
Most common cause of hip pain in childhood
Classic signs include: monoarticular hip
pain, limp, restricted range of motion, and
resolve over several days to weeks
Etiology: active or recent viral infection,
trauma, or allergic hypersensitivity
Transient Synovitis of the Hip
Incidence: 0.4-0.9% of the annual
pediatric hospital admissions; risk of a
child having at least one episode is 3%;
seasonal occurrence in autumn months;
right and left equal occurrence; 2:1 male
to female ratio
Clinical Presentation: average age of onset
is 6 years, acute onset of unilateral hip
pain, groin pain, or thigh pain
Transient Synovitis of the Hip
Clinical Presentation: associated limp and
antalgic gait, refusal to bear weight, Leg
held in flexed attitude and externally
rotated with restricted range of motion,
muscle spasm seen.
Laboratory Studies: nonspecific and normal
Radiographic Studies: negative but
ultrasound is promising
Transient Synovitis of the Hip
Natural History: limited duration of
symptoms with average duration of 10
days; no residual clinical or radiographic
abnormalities; Recent literature reports a
1.5% incidence of the development of
Legg-Calve-Perthes Disease(followup now
important for at least one year)
Transient Synovitis of the Hip
Treatment: Bed rest and relief of weight
bearing on the affected joint until pain
resolves and motion returns; period of
cessation of strenuous activity; observation
and followup for the development of
Perthes.
Common Pediatric Hip Disorders
THANK YOU
Dr. Donald W. Kucharzyk
Cerebral Palsy
CURRENT UPDATE
Septic Arthritis of the Hip
Developmental Dysplasia of the Hip
Legg-Calve-Perthes Disease
Transient Synovitis of the Hip
The Hip in Myelodysplasia
Slipped Capital Femoral Epiphysis
Cerebral Palsy
Cerebral Palsy is a term used to describe
various clinical syndromes whose common
feature is the abnormal control of motor
function by the brain
Abnormal control results in a disorder of
movement, posturing, and sometimes
sensory functioning
Cerebral Palsy
ETIOLOGY
Can occur in the prenatal, perinatal, and
postnatal
Prenatal: maternal infection, maternal drug or
alcohol, or congenital malformation of the brain
Perinatal: trauma, placental complications,
hypoxia, low birth weight, prematurity, and
breech
Cerebral Palsy
ETIOLOGY
Postnatal: head trauma, vascular insults in
the brain, central nervous system
infections, kernicterus, hypoxia, and
postnatal infections
Cerebral Palsy
PREVALENCE
1 to 7 per 1000 children throughout most
the world
Twin pregnancies result in 12 times higher
incidence
Cerebral Palsy
CLASSIFICATION
Neuropathic type of motor abnormality
Anatomic region of involvement
Cerebral Palsy
NEUROPATHIC TYPE
Spastic: upper motor neuron syndrome,
velocity-dependent increase in tonic stretch
reflexes(muscle tone) with exaggerated
tendon reflexes, may see weakness,loss of
muscle control,
interference with balance, joint
contractures(pyramidal)
Cerebral Palsy
Athetoid: type of dyskinesia seen with
purposeless writhing movements that are
aggravated when the child is frightened or
excited; dystonia can occur with
atherosis(extrapyramidal)
Ataxia: uncommon, disturbance of
coordinated movement, most notable when
walking, intention tremors
Cerebral Palsy
ANATOMIC PATTERNS
Quadriplegia: involvement of all four limbs,
mental retardation, drooling, dysarthria,
dysphagia, seizures; cause is severe
hypoxia; initial presentation floppy baby
Diplegia: both lower extremities are
involved with upper involvement to some
but lesser degree; caused by prematurity
and perivent. hemorrhage
Cerebral Palsy
Hemiplegia: one side of the body is
involved with upper being more involved
than the lower; cause due to focal trauma,
vascular or infectious lesion; seizure
disorders seen,limb growth affected with
the involved smaller
Double Hemiplegia: bilateral and
symmetrical involvement with upper more
than lower
Cerebral Palsy
DIAGNOSIS
History: not a genetic disease; search for
possible etiologies; assess benchmark
developmental milestones especially
sitting(6 mo.), crawling(8 mo.), cruising(9
mo.), and walking(12 mo.)
Cerebral Palsy
Physical Examination: to determine tha
grades of muscle strength and selective
control, to evaluate the muscle tone and
determine type, to evaluate the degree of
deformity or muscle contracture at each
major joint, to assess linear, angular, and
torsional deformation, and to appraise
balance,equilibrium,and standing/walking
posture
Cerebral Palsy
Common Types and Management
Cerebral Palsy
SPASTIC QUADRIPLEGIA
Cerebral Palsy
Only 20% of these children will walk
Goals aimed at maintaining balanced,
comfortable sitting
A Straight Spine and Level Pelvis
Mobile Painless Hip that Flex and Ext
Mobile Knees that Flex and Ext
Plantigrade Feet
Management of malnutrition and seizures
Cerebral Palsy
Hyperkyphosis: due to weak spinal extensor
musculature and a resultant long C-shaped
kyphosis posturing of the entire spine that’s
flexible
Scoliosis: seen in 25% of the patients,
it develops earlier and is more progressive;
less responsive to orthotic use and more
likely to require surgery
Cerebral Palsy
Hip Disorders: limitation of motion,
contractures,valgus inclination, subluxation
and dislocation seen; causative factors
include muscle imbalance, acetabular
dysplasia, pelvic obliquity, femoral
anteversion, increased hip valgus, and lack
of weight bearing; common before the age
of 6 and in children with limited abduction
and flexion contractures
Cerebral Palsy
Hip Management: Best treatment early is the
prevention of the dislocation-these lead to
pain
Hip at Risk: often progress to subluxation and
dislocation unless treated; Treatment consists
of lenghtening the adductors and flexors,
tenotomy or elongation of the psoas
Cerebral Palsy
Hip Subluxation: uncovering of more than
one-third of the femoral head; the
subluxated hip has increased valgus and
anteversion; Treatment requires
corrective proximal femoral osteotomy and
if acetabular dysplasia exists then
corrective pelvic osteotomy as well
Cerebral Palsy
Hip Dislocation: If seen within one year:
open reduction, soft tissue releases,and
proximal femoral osteotomy combined with
acetabular procedures; If seen after one
year: when the hip is painless-no
treatment and if painful-proximal femoral
resection and muscle interposition
Cerebral Palsy
SPASTIC DIPLEGIA
Cerebral Palsy
Most diplegic’s walk although delayed usually
around 4 years of age
Motor improvement reaches a plateau by the
age of 7, if not ambulatory by then, there is
less likelihood of it
Severity of involvement of the lower
extremity is important to walking
Seizure disorder,flaccidity,persistent primitive
reflexes,or dislocated hip are deterrents to
walking
Cerebral Palsy
Categories of ambulators:
Community: walk indoors and outdoors
with use of braces or crutches
Household: walk only indoors and with
apparatus, able to get in and out of chair
or bed without assistance
Nonfunctional: walk in PT but otherwise
are wheelchair bound
Cerebral Palsy
Children with spastic diplegia are less
often afflicted with scoliosis, seizures,
speech impairments and major problems in
other systems as are quadriplegics
Treatment includes drugs,physical
therapy,intramuscular injections,
casting,orthotics,dorsal rhizotomy and
musculoskeletal surgeries
Cerebral Palsy
Drugs: systemic muscle relaxants,
antispasmodics, and neuroinhibitory
medications have been tried without
success: Intrathecal Baclofen has shown
promise as it interfers with the release of
excitatory transmitters and decreases
lower extremity spasticity for up to 8
hours: acts on the spinal cord synaptic
reflexes
Cerebral Palsy
Physical Therapy: improves joint
contractures, motor status, and social
motivation; maintain or improve joint range
of motion, regain muscle strength,
maximize ambulation, and improve function
Recent advances in the use of lowintensity transcutaneous electric
stimulation on weaker antagonistic muscles
at night shows promise
Cerebral Palsy
Intramuscular Injections: help weaken a
muscle and thereby balance the forces across
a joint, the most common muscle injected is
the gastrocnemius-to reduce equinus
Botox functions to block the myoneural
junction and the release of acetylcholine from
the synaptic vesicles; effect seen in 12-72
hrs and lasts for 3-6 months
Cerebral Palsy
Botox may be repeated after 2 weeks and
up to six injections given at the site of
desired response; contraindicated in the
presence of fixed joint contractures
Cerebral Palsy
Manipulation and Casting: can at times be
beneficial in the elongation of tight or
contracted musculotendinous units or joint
capsules; inhibition casting reduces normal
muscular tone and when combined with PT and
braces post casting, improvements are seen
Orthotics: prevent deformity, improve function
by substituting for a weaker muscle, or to
protect a weakened muscle
Cerebral Palsy
Orthotics: common types include UCBL
inserts(maintain forefoot,hindfoot,and
subtalar alignment); Solid AFO(spastic foot
with mediolateral instabilty); Articulated
AFO(prevent equinus and extensor thrust and
allow free dorsiflexion); Floor Reaction
AFO(prevents knee flexion crouch and gain
stance phase knee extension during gaiteliminates use of KAFO)
Cerebral Palsy
Selective Posterior Rhizotomy: reduces
spasticity by balancing muscle tone by the
control exhibited by the anterior horn cells
in the spinal cord; limit the stimulatory
inputs from the muscle spindles in the
lower limbs that arrive by the afferent
fibers in the dorsal roots;
Cerebral Palsy
Best patient is the young child(age 3-8 yrs.)
with spastic diplegia, voluntary motor control,
no fixed contractures, good trunk control, the
ability to walk with good strength and
balance, pure spasticity; Not indicated for
athetosis, ataxia, rigidity, dystonia,
hypotonia, and fixed contractures and
hemiplegia
Results: lasting reduction in spasticity,
increased hip,knee,ankle ROM and gait
Cerebral Palsy
Surgical Intervention: Best results obtained
if all the abnormalities are identified and
corrected at the same surgery; Best timing is
after the child is at least cruising or
ambulating, after age 4-5 yrs but before age
8; Overall, the goal is aimed at restoration
of joint motion, muscle strength, and
improved gait
Cerebral Palsy
 Ankle Equinus
gastrocnemius overactivity
Achilles Tendon Lengthening
 Foot and Ankle Equinovarus
equinus due to gastrocnemius
hindfoot varus due to overactive tibialis
posterior
forefoot supination and varus due to
overactive tibialis anterior
Cerebral Palsy
Forefoot and Ankle Equinovarus
Treatment of hindfoot equinovarus is by split
tibialis posterior transfer
Treatment of forefoot varus and supination
is by split tibialis anterior transfer
Treatment of nonfixed varus of the hindfoot
occurs with forefoot supination is by adding
tibialis posterior lengthening
Cerebral Palsy
Foot and Ankle Equinovalgus
Most common situation seen in diplegia
Muscle imbalance of triceps and weak tibialis
posterior with overpull of peroneal
Ankle Valgus is commonly seen due to this
combincation
Cerebral Palsy
Foot and Ankle Equinovalgus
Treatment of ankle valgus is via AFO or
UCBL inserts if mild and supple
Treatment of ankle valgus that is more
severe will require subtalar fusion:
indications are failure of orthotic use and
lateral subtalar subluxations
Cerebral Palsy
Foot and Ankle Equinovalgus
Severe ankle valgus may require subtalar
arthrodesis, medial displacement osteotomy
of the calcaneus,opening wedge osteotomy
lenghtening osteotomy of the distal
calcaneus, or triple arthrodesis; Must
achieve muscle balance despite the type of
procedure to be performed
Cerebral Palsy
External Tibial Tiorsion
shortens lever arm effect of the foot to
generate plantar-flexion-knee-extension
couple, stance is shortened and pushoff
power compromised
Treatment is derotational osteotomy of
the tibia and fibula
Cerebral Palsy
Knee Flexion Deformity
associated with hip flexion contracture and
crouched gait, caused by spastic and tight
hamstrings; in addition, occassionally the
rectus femoris will be spastic resulting in
stiff-knee gait post hamstring lenghteningtransfer will be required
Cerebral Palsy
Knee Flexion Deformity
Hip extensor power is lessened by
hamstring release
Pre-existing hip flexion contracture and
lumbar lordosis can become increased due
to iliopsoas and this needs to be addressed
Cerebral Palsy
Hip Adduction Contracture
results in scissoring gait and predisposes
the child to subluxation and dislocation of
the hip
functions to stabilize during gait and
provide more effective hip flexor and
extensor activity
Do Not Overlengthen or Overweaken
Cerebral Palsy
In-Toeing
result of excessive femoral anteversion
may be due to increased spasticity in the
internal rotators of the hips, medial
hamstrings, tensor fascia latae, and gluteus
medius
Treatment is derotational femoral osteotomy
Cerebral Palsy
SPASTIC HEMIPLEGIA
Cerebral Palsy
Involvement of one side of the body with the
arm or hand more severely involved than the
lower extremity
Comprises about 30% of all the cases
History of Head Trauma or Intracranial
hemorrhage is frequent cause
All are Community Ambulators
Cerebral Palsy
Classic Presentation: equinovarus of the
foot and ankle, flexion at the knee and
hip, internal rotation of the lower limb,
internal rotation of the shoulder, flexion
of the elbow, pronation of the forearm,
flexion and ulnar deviation at the wrist,
and thumb-in-palm deformity
Cerebral Palsy
Treatment:
Type 1 Hemiplegia
Foot drop gait with steppage due to
weakness anterior tibialis-AFO
Type 2 Hemiplegia
Equinovarus is treated with Achilles tendon
lenghtening and split tibialis posterior
transfer(if active during stance) and split
tibialis anterior transfer(if active during swing)
Cerebral Palsy
Treatment
Type 3
Stiff-Knee gait with equinovarus is treated
with hamstring releases and tendon
lenghtening and transfers
Type 4
Hip Flexor and Adductor Spasticity is
treated via iliopsoas release and hamstring
releases
Cerebral Palsy
ATHETOID CEREBRAL PALSY
Cerebral Palsy
Dyskinesia(abnormal muscle tension and
tone)
Limb movements are involuntary and almost
continously changing
Muscle tension changes with emotional
changes
Gait is random, inconsistent and influenced
by external stimuli
No Basis for Surgical Intervention
Cerebral Palsy
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