Pediatric Orthopaedics

SMF BEDAH ORTHOPAEDIRSUD ULIN BANJARMASIN/

FK UNLAM

dr. Zairin Noor Helmi, SpOT.(K).MM.FICS

COMMON CHILDHOOD MUSCULOSKELETAL CONDITIONS

General Principles of Fractures and Dislocations in Children

Children’s bones bend more before fracture than do adult’s bones (children’s bones are more ductile)The periosteum in children is thicker and more highly developed and often remains intact on the concave side of a fractureChildren’s fractures heal more rapidly and, therefore, require shorter immobilization time than do adult’s fractures

Stiffness across joints after immobilization is less of a problem in children than in adultsChildren’s bones remodel to a greater extent than adults’ do and, therefore, a greater amount of angulation and displacement is acceptable in children than in adults (except intra-articular fractures: angulation or displacement of intra-articular fractures is not acceptable in adults or children)Specific pediatric fractures are discussed by anatomic region within this chapter

Physeal (growth plate) fractures- Classically occur through the zone of hypertrophy of the growth plate but can involve other zones- Usually caused by a torsion (not tension) at the growth plate- Complications of physeal fractures include

* Limb length discrepancies* Malunions* Physeal bars (leading to angular or

longitudinal deformities)-Most common sites for physeal fractures are the distal radius and distal tibia

Classification of physeal fractures (Salter-Harris classification [SH])

General treatment guidelines for physeal fractures* SH I fractures --- initial attempt at gentle closed reduction (may require general anesthesia)* SH II fractures --- initial attempt at gentle closed reduction (may require general anesthesia)* SH III fractures --- intra-articular: often require open reduction to properly align the growth plate* SH IV fractures --- intra-articular: often require open redustion to properly align the growth plate* SH V factures --- generally identified late and have a high complication rate

Growth plate arrest (Fig.5-2)- Physeal bars (bridges) arise as a result of a growth plate injury that leads to an arrest of growth of a portion of the physis: an uninjured portion of the physis may continue to grow- Centrally located bars within the physis lead to arrest of longitudinal growth with resultant shortening of the extremity- Peripheral bars lead to angular deformities - Treatment options include operative resection of the bar or ipsilateral completion of a growth arrest in conjunction with an epiphysiodesis to the contralateral extremity (to equalize the growth disturbance in both extremities)

Greenstick fracture – fractures in children commonly are incomplete and leave a hinge of intact bone and soft tissues similar to the manner in which a green stick from a tree branch breaks (Fig.5-3)Torus (bruckle) fracture – occurs in children at the metaphyseal diaphyseal junction of long bone (most commonly distal radius) as a result of an axial load (see Fg. 5-3)

Childs abuse (battered child syndrome)- A high index of suspicion is needed to make the diagnosis- Most common in children younger than 3 years of age- Unusual histories are a tip-off- Physical exam may show multiple healing skin bruises, burns, etc.- The most common locations for fractures in child abuse are the humerus, tibia, and femur- Skull fractures are common- Skeletal survey (x-rays of the skull, thoracolumbar spine, chest and ribs, pelvis, femur, knees, tibias, fibulas, ankles, wrists, and hands) to search for other fractures in suspected cases (fractures may be healed)- A technetium bone scan may also be helpful to search for other skeletal injuries.

ClubfootI. Etiology

Unknown, possibly multiple factors, including polygenic inheritance, persistence of fetal positioning, primary germ plasma defect, and neuromuscular factors

II. IncidenceA. In whites, 1.2/1000. male > female (2:1); 50% bilateral

III. EmbryologyA.Embryonic position: 30 mm embryo with

equinovarus footB.Fetal position:50 mm embryo with mild

adducted equinovarus foot secondary to tibial growth

IV. PathologyA. Histologic abnormalities in muscle, tendon, and ligament in addition to contractureB. Equinus, hindfoot varus, and foot varus (talonavicular)C. Calcaneus rotates through subtalar joint

in a medial direction and inverts (varus tilting or supination)D. Body of talus may be directed laterally and neck of talus is directed medially (lateral rotation of the talus)

E. Navicula is displaced medially F. Cuboid is often subluxated mediallyG.Plantar fascia is tight

V. X-Rays FindingsA. Increased lateral calcalcaneotibial angle

(>125 ) secondary to ankle equinus

B. Decreased lateral talocalcaneal angle (<35 , 35-50 normal) and anteroposterior (AP) talocalcaneal angle (<20, 20-40 normal) secondary to hindfoot varus)C. Abnormal AP talo-first metatarsal angle

(zero is normal) secondary to talonavicular subluxation

VI. Prognosis A. Condition worse if:

1. Teratogenic (eg, arthrogryposis, myelodysplasia) 2. Short, far, rigid foot with severe mid

foot crease 3. Boat-shaped heel, severe, adductus

varus, atavistic short first toe 4. Delayed treatment and failure to

respond

VII. Treatment A. Postnatal: corrective manipulation and

(correct adduction, heel varus, and thenequinos) every 1-2 weeks for 3 months, then holding cast or brace until surgery (50 %

effective) B. Surgery

1. One-stage posteromedial release of tight structures

2. Ideally, 4-8 months but up to 6 years of age

3. Turco posteromedial or extensive subtalar release by Mckay or Simon techniques

4 .Cincinnati incision is often utilized (fig. 3-2)

5 .Structures that are released a. Achilles tendon Z-lengthening

b. Posterior release of ankle and subtalar joints, including calcaneofibular and posterior talofibular ligaments

c. Z-lenghtening or release of posterior tibialis d. Superficial medial release of the subtalar joint:

superficial deltoid (calcaneotibial and tibionavicular ligament),calcaneonavicular (spring ligament) and talonavicular ligament dorsally

e. Deep medial release: the bifurcated ligament (calcaneocavicular and calcaneocuboid) and enough

talocalcaneal interosseous ligament .

f. Plantar release and lateral release of dorsal calcaneocuboid joint if necessary C. Postoperative management

1. Smooth K-wire through talonavicular joint and talocalcaneal joint, occasionally calcaneocuboid joint

2. Three months postoperative casting 3. Many months of splinting, particularly if tibialis

anterior and peroneal muscles are weak

VIII. Salvage Procedures A. Resistant deformity of the foot 1. Forefoot: Heyman-Herndon

tarsometatarsal capsulotomies or metatarsal osteotomies

2. Midfoot: a. Midtarsal osteotomies (Japas or

Dome) b. Open wedge of first cuneiform or

talus (medial column lengthening)

c. Close wedging of os calcis and/or cuboid (lateral column shortening)

3. Hindfoot: Dwyer osteotomy of os calcis, sliding osteotomyB. Triple arthrodesis: resistant foot 12 years old

1 .Residual deformities 2 .Overcorrected planovalgus deformity

Congenital Hip DislocationI. Incidence A. Occurs in 4 – 10 per 1000 cases,

considerable racial variation B. Sixty percent are first born, female > males (6:1)

C. Increased in breech delivery and oligohydramnios

D. The left hip in 60%, bilateral in 20%

E. Associated conditions: muscular torticollis, metatarsus adductus, calcaneovalgus

F. Postnatal influence: increased incidence when hips are kept in extended and

adducted positions G. Associated diseases: Ehlers-Danlos

syndrome, Larsen’s syndrome, myeolomeningocele, arthrogryposis

II. Pathology of Late CasesA. Defective acetabulum growth (frontal acetabular inclinationB. Femoral antervesionC. Capsular constriction D. Inverted labrum in dislocation and everted in subluxationE. Shortened inferior transverse ligamentF. Pulvinar and tight Iliopsoas

III. Clinical FindingsA. Ortolani test: reduction maneuver by gently abducting and lifting the involved femurB. Barlow test: a provoactive test to detect a dilocatable or subluxable hipC. Decreased abduction ( the best test after age of 2 months)D. Galeazzi sign: apparent shortening of fe femur when hips flexed to 90 E. Prominent and higher greater trochanter

F. Extra skin folds and widened perineum in bilateral

G. Increased lordosis, particularly with bilateral cases and positive Trendelenburg sign (hip should be held in

extension to prevent false-negative by iliopsoas muscle in hip flexion)

H. Hip dysplasia associated with abduction contracture or the contralateral hip

1. Pelvic obliquity and apparent leg length discrepancy

2. Secondary to intrauterine packing problem3. Positive Ober test; abduction contracture the hip.

I. Teratologic dislocation (1%)1. Arthrogryposis, paralytic, sacral agenesis,

chromosomal abnormalities, etc2. Generally do not respond to nonoperative

management

IV. X-Ray Findings (Fig 3-5)A. Unreliable before 4-6 weeks, may be

taken to rule out teratologic dislocations or proximal femoral focal deficiency

B. Von Rosen view (45 abduction and 25 internal rotation) may be more useful for infants but there can be false negative

resultC. Acetabular index: <30 is normal, but there is a wide variation during the first year

D. Lateral and superior migration of the femoral head (ie, proximal femoral metaphysis is lateral to Perkin’s line)

E. Delayed ossification of the femoral head (should appear during first 6-12 months; compare with the opposite side)

F. Shenton’s line is broken in the dislocated hip

G. Center edge (CE) angle of Wiberg: <20 – 25indicates subluxation of the femoral head (use after 4 years of age)

H. Arthrogram1. Very useful in ruling out mechanical blocks to reduction of the infant hip, such

as hourglass constriction of the capsule by the psoas muscle

2. Confirms the shape and congruence of the femoral head and the acetabulum

3. Medial space >3-5 mm indicates failure of closed reduction

I. Ultrasound1.Most effective prior to ossification of the proximal femoral head2.Can be used to diagnose subluxable hip or

to confirm concentric reduction in the Pavlik harness3.Gaining increasing use

J.CT scan: can be used to document concentric reduction in a cast

V. TreatmentA. Newborn to 6 months of age: Pavlik harness

1.Minimum 2 months’ duration or about twice the child’s age2.Obtain an X-Ray or Ultrasound 1 week

after being in brace3.A 95 flexion using the anterior strap,

and safe zone abduction (45 – 60 ) using the posterior strap

4.Wean if the hip is stable in extension5.Discontinue Pavlik harness if it does not

relocate the hip after 1 month of use6.Avoid extreme positions to prevent

osteonecrosis

B. Between 4 and 6 months and 18 months of age1. Traction is required because hipcontracture is developed and the hip does not reduce

2. Closed reduction under anesthesia with adductor tenotomy if necessary and spica cast: may be appropiate until 3 years of

age in selected individuals

3. Traction: skin traction with 30 -45 flexion and 30 abduction. Two to 3 pounds of weight is used until the head is down to the level of triradiate cartilage (home traction can be

done for about 3 weeks)4. Percutaneous adductor tenotomy may be

done zone if the adductors are tight or safe zone is narrow

5.Hip spica cast: 110 flexion and safe zone abduction (30 – 60 ) and 10 – 20 internal rotation for 6 months’ duration a.Fiberglass cast preferredb.Single cut CT scan may be done to

confirm reduction in doubtful cases6.Ocassional open reduction may be necessary

in 12 to 18 month- old children if closed reduction fails or when extreme positioning is required to maintain reduction

Legg-Calve-Perthes Disease (Coxa Plana )I. Incidence A. Occurs during 4-8 years of age (80%)

B. Incidence:1:1000 (varies by region and race)C. Males>FemalesD. Ten percent bilateral but usually not simultaneous low socioecoomic group

E. Increased incidence in children with older parents, mother smoking during

pregnancy, breech delivery, low birth weight, delayed skeletal maturation, and

low socioeconomic group

II. PathogenesisA. Idiopathic avascular necrosis (AVN) of the femoral head, followed by subchondoral fracture (clinical onset), revascularization and healing ossification processesB. Etiology of AVN is unknown : inflammatory, synovitis, generalized disorder, growth hormone or somatomedin deficiency, traumatic, cartilaginous disorder, vascular or infections are possibilities

III. Clinical and X-Ray FindingsA. Varies in intensityB. Limping, pain in hip and kneeC. Decreased range of motion (abduction and internal rotation)D. X-Ray findings

1. Plain X-Ray: increased joint space, subchondoral lucency, increased

density, fragmentation, deformities2. Arthrogram: assess femoral head deformity and sublxuation wheter containable or hinged with abduction and internal rotation

3. MRI (arthrogram-like image and can differentiate live versus dead marrow) and bone scan (early detection) but not always predictive

V. Differential DiagnosisA. Transiest synovitis (may developed to Perthes)B. Sickle cell, infection, tuberculosis,

Gaucher's disease, rheumatic fever, trauma, and tumors, such as lymphoma and eosinophilic granuloma of the hip

C. Bilateral (multiple epiphysal dysplasia, spondyloepiphyseal dysplasia, trichorhinopalangeal syndrome, pseudoachondroplasia congenita and tarda, sickle cell disease, hypothyroidism)

Slipped Capital Femoral EpiphysisI. General Considertaions

A. One to 3/100.000 incidenceB. Males>females (2.5:1)C.Twenty-five percent biltaeral (15-50% of these present simultaneouslyD.Common during 13-16 years (males) and

11-13 years (females)

E. Increased incidence in overweight or Froelich-type body habitus, slender tall type,

black females; also occurs in hypothyroidism, hypopituitarism, especially

treated with growth hormone, renal osteodystrophy patients, Down syndrome, positive family history

F. Suspect endocrine abnormalities if age of onset is< 10 years or>16 years of ageG. Etiology is unknown

II.ClassificationA. Acute: associated with acyte traumatic injury resulting in a sudden displacement of femoral headB. Acute on chronic: acute exacerbation of symptoms>3 weeks due to minor traumaC. Chronic:history of pain >3 weeks

III. PathogenesisA. Slippage through the zone of

hypertrophyB. Relative retroversion maybe presentC. The epiphysis slips posteriorly and inferiorly,and the leg rotates externally (anteriorly and superiorly)D. Progressive apparent coxa vara and shortening of the leg result

IV. Clinical FindingsA. Chronic or intermittent pain in groin and

referred down the medial aspect of the kneeB. Antalgic gait with externally rotated foot progression angleC. Decreased intenal rotation, abduction, and flexionD. Hip flexion produces external rotationE. Shortening of the femur in severe cases

V. X-Ray Findings (Fig. 3-9)A. Early change seen only on lateral x-ray view 15%

B. On AP projection, there is loss of overhang of epiphysis at the

superolateral aspect of femoral neck (Kline's line)C. Posterior displacement of the epiphysis:

50% slip in one plane gives 39% overlap of the femoral head on the neck, and 50% slip in both planes gives only 18% overlap

D. “Metaphyseal blanch sign of Steel”: early sign of posterior slippingE. The proximal and medial part of the femoral neck does not overlap on the ischiumF. Chronic changes:widening of the physis, scelerosis, and ossification at the junction of the medial femoral neckG. Narrowed joint space and osteopenia of femoral head and acetabulum in chondrolysis

H. Increased bone density and segmental collapse of femoral head in avascular necrosis

VI. TreatmentA. Acute

1.Traction temporarily until surgery (split Russel skin traction is adequate with internal rotation vector)2.In situ pin fixation

a. One pin is adequate for chronic slip and helps to avoid pin

penetrationb. Start anteriorly from base of the neck and aim posteroinferiorly under

fluoroscopic imaging

c. Avoid superolateral quadrant of the femoral head where the posterosuperior retinacular vessels enter

d. Crutch ambulation and partial weight.