Presentation is loading. Please wait.

Presentation is loading. Please wait.

Current Concepts on Pediatric Hip Disorders

Similar presentations

Presentation on theme: "Current Concepts on Pediatric Hip Disorders"— Presentation transcript:

1 Current Concepts on Pediatric Hip Disorders
Dr. Donald W. Kucharzyk Pediatric Orthopaedic Surgeon The Orthopaedic,Pediatric & Spine Institute Crown Point, Indiana

2 “Developmental Dysplasia of the Hip”

3 Developmental Dysplasia Hip
TERMINOLOGY Dysplasia: Abnormal tissue development Subluxation: 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”

4 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%)

5 Developmental Dysplasia Hip
Mechanical/Environmental: Increased risk in First Born, young mothers, and molded baby syndrome; Twins; Oligohydramnios; Breech(50%) Breech Incidence: female /200 female breech 1/35 female breech FH 1/15 Overall Incidence: Instability 2.7/1000 Dislocation 1/1000

6 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

7 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

8 Developmental Dysplasia Hip
EXAMINATION Ortolani Barlow Allis/Galeazzi Asymmetrical Thigh Folds Limited Abduction

9 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

10 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 weeks- change treatment plan Complications: AVN Femoral Nerve Palsy

11 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)

12 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

13 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

14 Developmental Dysplasia Hip
THREE TO SIX YEARS Must alter the Natural History Soft Tissue Release Open Reduction Femoral Shortening Pelvic Innominate Osteotomy

15 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)

16 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

17 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

18 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

19 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

20 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

21 Developmental Dysplasia Hip
COMPLICATION’S Avascular Necrosis: AVOID Keep Femoral Head Centered Maintain Acetabular Coverage Overgrowth of the Greater Trochanter Early Degenerative Osteoarthritis

22 Legg-Calves-Perthes Disease

23 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%

24 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

25 Legg-Calve-Perthes Disease
RADIOGRAPHIC Diagnostic Changes Lateral Displacement of Femoral Head Subchondral Fracture Line Increased Epiphyseal Density Smaller Epiphyseal Nucleus than Normal

26 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

27 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

28 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

29 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 involved- Worst Prognosis Femoral Head Containment: loss of containment-greater risk of deformity

30 Legg-Calve-Perthes Disease
PROGNOSTIC FACTORS Hip Range of Motion: major factor in pathogenesis Premature Physeal Closure: asymmetric growth and inadequate remodeling

31 Legg-Calve-Perthes Disease
TREATMENT Goals: good containment and congruence and reduction of weight on affected area of femoral head; maintenance of ROM

32 Legg-Calve-Perthes Disease
Treatment Options: No Treatment Intermittent Traction Abduction Orthosis Femoral Osteotomy Pelvic Osteotomy

33 Legg-Calve-Perthes Disease
No Treatment: Children under Five require observation only Containment Orthosis does not affect the natural history in children under Five

34 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

35 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

36 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

37 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

38 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

39 Legg-Calve-Perthes Disease
Clinical Results 69% good results with no treatment 71% good results with containment orthosis 87% good results with pelvic osteotomy 86% good results with femoral varus osteotomy

40 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

41 The Hip in Myelodysplasia
Muscular Contractures Hip Subluxation and Dislocation Acetabular Dysplasia Stiff Hip Pelvic Obliquity

42 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

43 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

44 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

45 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

46 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

47 The Hip in Myelodysplasia
Surgical Treatment: Tensor Fascia Latae Release Yount Procedure

48 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

49 The Hip in Myelodysplasia
Surgical Treatment: Adductor Release Femoral/Pelvic Osteotomy

50 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.

51 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)

52 The Hip in Myelodysplasia
Acetabular Dysplasia Chiari Pelvic Osteotomy Shelf Procedure Varus Derotational Osteotomy

53 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

54 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

55 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)

56 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

57 Transient Synovitis of the Hip
Incidence: % 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

58 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

59 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)

60 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.

61 Common Pediatric Hip Disorders
THANK YOU Dr. Donald W. Kucharzyk

62 Cerebral Palsy CURRENT UPDATE

63 Septic Arthritis of the Hip

64 Developmental Dysplasia of the Hip

65 Legg-Calve-Perthes Disease

66 Transient Synovitis of the Hip

67 The Hip in Myelodysplasia

68 Slipped Capital Femoral Epiphysis

69 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

70 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

71 Cerebral Palsy ETIOLOGY
Postnatal: head trauma, vascular insults in the brain, central nervous system infections, kernicterus, hypoxia, and postnatal infections

72 Cerebral Palsy PREVALENCE
1 to 7 per 1000 children throughout most the world Twin pregnancies result in 12 times higher incidence

73 Cerebral Palsy CLASSIFICATION Neuropathic type of motor abnormality
Anatomic region of involvement

74 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)

75 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

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

77 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

78 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.)

79 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

80 Common Types and Management
Cerebral Palsy Common Types and Management


82 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

83 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

84 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

85 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

86 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

87 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

88 Cerebral Palsy SPASTIC DIPLEGIA

89 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

90 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

91 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

92 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

93 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

94 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 hrs and lasts for 3-6 months

95 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

96 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

97 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)

98 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;

99 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

100 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

101 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

102 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

103 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

104 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

105 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

106 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

107 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

108 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

109 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

110 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


112 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

113 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

114 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)

115 Cerebral Palsy Treatment Type 3
Stiff-Knee gait with equinovarus is treated with hamstring releases and tendon lenghtening and transfers Type Hip Flexor and Adductor Spasticity is treated via iliopsoas release and hamstring releases


117 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

118 Cerebral Palsy THANK YOU

Download ppt "Current Concepts on Pediatric Hip Disorders"

Similar presentations

Ads by Google