current concepts on pediatric hip disorders dr. donald w. kucharzyk pediatric orthopaedic surgeon...
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Current Concepts on Pediatric Hip Disorders
Dr. Donald W. KucharzykPediatric Orthopaedic Surgeon The Orthopaedic,Pediatric & Spine Institute Crown Point, Indiana
“Developmental Dysplasia of the Hip”
CURRENT CONCEPTS UPDATE
Developmental Dysplasia Hip
TERMINOLOGYDysplasia: Abnormal tissue developmentSubluxation: Capsular laxity with some
displacement but maintenance of cartilage-cartilage contact
Dislocated: No cartilage-cartilage contact with hip external to the labrum NOW TERMED “DDH”
Developmental Dysplasia Hip
ETIOLOGYGenetic 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 1/15Overall Incidence: Instability 2.7/1000 Dislocation 1/1000
Developmental Dysplasia Hip
ANATOMYEARLY 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 HISTORYBarlow(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% painWeinstein(1987): DDH leads to DJD
Developmental Dysplasia Hip
EXAMINATIONOrtolaniBarlowAllis/GaleazziAsymmetrical Thigh FoldsLimited Abduction
Developmental Dysplasia Hip
RADIOLOGIC EVALUATIONPlain Xrays: unreliable intially;
useful at 6-8 weeksUltrasound: most reliable but level of
dependability related to expertise of radiologist; useful with treatment modalities
Developmental Dysplasia Hip
TREATMENTBIRTH TO SIX MONTHSPavlik Harness: fulltime for 4-6 weeks
till hips stable then brace till acetabulum normal; Failure to reduce in 2-3 weeks- change treatment plan
Complications: AVN Femoral Nerve Palsy
Developmental Dysplasia Hip
SIX MONTHS TO ONE YEARClosed Reduction and Casting: must
achieve stable and concentric reduction, human position for casting, maintain safe zone(adductor release)
Developmental Dysplasia Hip
TWELVE TO EIGHTEEN MONTHSClosed 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 MONTHSOpen 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 YEARSMust alter the Natural HistorySoft Tissue ReleaseOpen ReductionFemoral ShorteningPelvic Innominate Osteotomy
Developmental Dysplasia Hip
SIX YEARS AND OLDERUnrecognized 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
TREATMENTUnilateral 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’SFailure to Document ReductionBrace 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’SJoint 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’SInnominate 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’SAvascular 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
ETIOLOGYChronic sequence of changes initiated by an
avascularity of the femoral head: less developed blood flow
Specific cause is unknownSeen age grouping: 4-8 years with range of
2-12 yearsFour-five times more common in malesBilateral in 10%
Legg-Calve-Perthes Disease
CLINICAL FINDINGSProlonged limpWaddling gaitPain in groin or thighLimited painful motionTenderness to palpation over hipGluteal AtrophyTrendelenberg sign PositiveLeg Length Discrepancy
Legg-Calve-Perthes Disease
RADIOGRAPHICDiagnostic 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
CLASSIFICATIONCatterall: 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
CLASSIFICATIONSalter-Thompson: based on extent of
subchondral fracture line Group A: less than 50% involvement Group B: over 50% involvement
Legg-Calve-Perthes Disease
PROGNOSTIC FACTORSSex: girls have poorer prognosis than boysAge at Onset: younger children have
better prognosis than olderExtent of Head Involvement: more
involved- Worst PrognosisFemoral Head Containment: loss of
containment-greater risk of deformity
Legg-Calve-Perthes Disease
PROGNOSTIC FACTORSHip Range of Motion: major factor in
pathogenesisPremature Physeal Closure:
asymmetric growth and inadequate remodeling
Legg-Calve-Perthes Disease
TREATMENTGoals: 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
Clinical Results69% good results with no treatment71% good results with containment
orthosis87% good results with pelvic
osteotomy86% good results with femoral varus
osteotomy
Legg-Calve-Perthes Disease
Natural HistoryAge of Disease OnsetDegree of InvolvementPresence of Head at Risk SignAge of Patient at TreatmentStage of Disease at TreatmentCongrous Hip at Skeletal Maturity
The Hip in Myelodysplasia
Muscular ContracturesHip Subluxation and DislocationAcetabular DysplasiaStiff HipPelvic Obliquity
The Hip in Myelodysplasia
MUSCULAR CONTRACTUREFlexion 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
ETIOLOGYCan occur in the prenatal, perinatal, and
postnatalPrenatal: 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
ETIOLOGYPostnatal: head trauma, vascular
insults in the brain, central nervous system infections, kernicterus, hypoxia, and postnatal infections
Cerebral Palsy
PREVALENCE1 to 7 per 1000 children throughout
most the worldTwin pregnancies result in 12 times
higher incidence
Cerebral Palsy
CLASSIFICATIONNeuropathic type of motor
abnormality Anatomic region of involvement
Cerebral Palsy
NEUROPATHIC TYPESpastic: 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 PATTERNSQuadriplegia: 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
DIAGNOSISHistory: 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 walkGoals aimed at maintaining balanced,
comfortable sittingA Straight Spine and Level PelvisMobile Painless Hip that Flex and ExtMobile Knees that Flex and ExtPlantigrade FeetManagement 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 low-intensity 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 PalsyManipulation 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 gait-eliminates 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 lenghtening-transfer 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 casesHistory of Head Trauma or Intracranial
hemorrhage is frequent causeAll 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 PalsyTreatment: 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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