Epiphyseal growth plate - Growth plates have an ordered arrangement of chondrocytes that reflects the chondrogenic events and processes that lead to bone growth. From the epiphysis to the metaphysis, they are arranged as four zones that gradually merge with each other: •zone of resting cartilage (attaches growth plate to epiphyseal bone) •zone of proliferating cartilage (mitosis of chondrocytes occurs here) •zone of hypertrophic (maturing) cartilage (chondrocytes make matrix and enlarge lacunae) •zone of calcified (calcifying) cartilage (matrix is calcifying, chondrocytes are dying or dead attaches the growth plate to the metaphysis) Undifferentiated or Resting Cell Zone: - immediately adjacent to epiphysis are irregularly scattered cartilage cells - this is germinal layer that supplies the developing cartilage cells NB ***- injury to this layer results in cessation of growth - the groove of Ranvier contains cells which flow into the into the cartilage in this layer of the growth plate - the function is to supply chondrocytes for increasing the width of the growth plate Zone of Proliferating Cartilage: - location in which bone length is created by active growth of cartilage cells - on metaphyseal side, cartilage cells become aligned into well-defined columns, known as zone of cellular proliferation - it is at base of these columns that mitotic activity is found - in this small area, two or three cells thick, occurs cell division upon which entire growth in length of bone depends - failure of these cells to thrive results in cessation of growth at end of bone Hypertrophic Cell Zone (Maturation Zone): - layer in which chondrocytes become swollen and vacuolated in process of maturation leading to cell death - they hypertrophy at expense of extracellular matrix, & these enlarged cartilage cells constitute the third zone, or hypertrophic zone - there is no active growth in this layer - columns of cartilage cells extend toward metaphysis, being constantly lengthened by cell division occurring at the base cells nearer the metaphysis begin to undergo changes that ultimately lead to their destruction - this is weakest portion of the epiphyseal plate (Salter Harris fractures occur thru this zone) (NB*** - in rickets, there is failure of calcification which causes accumulation of cells in the hypertrophic layer - juncture between epiphyseal plate & metaphysis is secured by welding of metaphyseal bone to calcified cartilage matrix. - collagen type X, may play a role in the calcification of this cartilage Zone of Provisional Calcification: - area where, w/ death of chondrocyte & production of AP, longitudinal bars of cartilage matrix become calcified - last two cells in column of cartilage cells are in fourth zone, the zone of provisional calcification. - it is in this area that extracellular chondroid matrix becomes impregnated with calcium salt *** - This calcification of matrix is required for subsequent steps, including: - invasion of cartilage cells by blood vessels from metaphysis - destruction of cartilage cells - formation of bone along remaining walls of calcified cartilage matrix Endochondral ossification is the way in which most bones form, including the limb bones. - Small collections of mesenchymal cells cluster together, become chondroblasts and begin to secrete cartilage matrix. - Other cells around them form a perichondrium and a tiny cartilaginous model of a bone has been formed. - Chondrocytes within the model grow and divide and more chondrocytes and matrix is added to the surface by the perichondrium, so the model gets larger. •Osteogenic cells are carried in, too, form the endosteum and begin to lay down bone matrix on the inner surface of the marrow cavity. (This is the primary centre of ossification.) • The marrow cavity expands toward both epiphyses as the cartilage continues to grow. •Eventually secondary centres of ossifcation occur in the epiphyses (at different times) and this traps a thin plate of cartilage between the primary centre and each secondary centre. These are the growth plates of the bone. - Later, the perichondrium is transformed into a periosteum and a thin periosteal collar of bone matrix is laid down around the model's shaft. - The cartilage mineralises and is invaded by a blood vessel from the periosteum. - Cells that accompany the blood vessel erode the now dead cartilage and form the marrow cavity. Intramembranous ossification is the way in which bones like the clavicle, mandible and some skull bones form. •Small collections of mesenchymal cells cluster together, become osteoblasts and begin to secrete osteoid. Other cells around them form a periosteum and a tiny bone has been formed. •A little later, blood vessels and nerves invade the bone. •More bone is deposited on the surface by osteoblasts of the periosteum, increasing the size of the bone. Epiphysial Growth Plate The epiphysial growth plate, where cartilage is removed and bone is formed, is marked by four stages (left to right): resting zone, proliferative zone, hypertrophy zone, ossification zone This is the normal fetal growth plate demonstrating the process of endochondral bone formation in a long bone. Congenital Dislocation of the Hip Developmental Dysplasia of the Hip The term "congenital dislocation of the hip" has traditionally been used to describe abnormal infant hips that may progress to dislocation. "Developmental dysplasia of the hip”: denotes the same range of hip problems but also includes hips that are never documented to be dislocated but are poorly developed, as well as hips that are determined to be abnormal after the newborn period. This new term is the the currently preferred term but it is not yet universally employed. Common risk factors: - females (80-90%) - 2/3 are firstborn - breech presentation - large baby - low amniotic fluid - family history. ***If it is unilateral the LEFT (70%) is usually involved - bilateral in only 5% *** But sometimes every one of these factors is absent, and the baby is still affected Incidence : one to two cases per 1,000 children OTHER ASSOCIATED CONDITIONS •Foot deformities ( club feet, metatarsus adductus) •Torticollis •Neuromuscular disorders •Skeletal dysplasias The hip is a 'ball and socket' joint. Various problems can affect the baby's hip as it develops: “Dislocation” - the ball does not lie safely in the socket and is displaced from it “Dislocatable” - although the ball is in the socket it can slip in and out of place “Subluxated” - although the hip is in the socket it is not deeply in place “Dysplastic”- In some children although the hip is in the right place the socket does not grow properly and is too shallow The Ortolani maneuver - the contralateral hip is held still while the thigh of the hip being tested is abducted and gently pulled anteriorly. Positive Test - is the palpable and sometimes audible "clunk" of the femoral head moving over the posterior rim of the acetabulum and “ relocating” in the cavity. The Barlow maneuver - is performed by adducting the hip while pushing the thigh posteriorly. Positive Test - If the hip goes out of the socket "dislocatable" Ortolani and Barlow Maneuvers (Left) Ortolani (Right) Barlow The hips are flexed to 90 degrees; the thumbs of the examiner are placed on the medial proximal thigh, and the long fingers are placed over the greater trochanter These maneuvers cannot be performed in a fussy, crying infant whose muscle activity may inhibit the movement of an unstable hip. The baby must be calm and relaxed . Try any method available The more poorly developed the acetabulum (and thus the more unstable the hip), the less pronounced the "clunk." The Ortolani maneuver must be performed very gently to avoid obscuring the sound of the femoral head passing over a poorly developed posterior acetabulum. ***NB : Audible high-pitched "clicks" without a sensation of instability have no pathologic significance. They should simply be re- examined at a later date NB: If an unstable hip is not detected in the newborn period, a positive Ortolani's test becomes less common. - limited abduction is the predominant physical sign as the hip becomes fixed in the dislocated position. - other signs: an apparent shortening of the femur, asymmetric skin folds and telescoping of the affected hip, are also clues to dislocation. NB: Xrays taken before four months old - before the head of the femur starts to convert from invisible-on-xray cartilage to visible bone (ossification) - are unreliable to rule out hip dysplasia. Ultrasound - of the hip is the best under four months. Coronal sonogram of normal infant hips. (F=femoral head; A=acetabulum) RADIOLOGICALLY 1. supero-lateral migration of femoral head 2. increased acetabular angle 3. small capital femoral epiphysis Treatment If an unstable hip is recognized at birth, treatment consists of maintaining the position of the hip in flexion (knee up towards the head) and abduction (knee away from the centerline) for about 1-2 months. The Pavlik harness is the most widely used device. - The device maintains proper position of the femoral head and allows for "tightening up" of the ligamentous structures as well as for stimulation of normal formation of the hip socket. NB *** The treatment must be continued until the hip is stable and xrays or ultrasound examinations are normal. Pavlick Harness The harness pushes the femoral head toward the socket, and usually, relocation of the femoral head will occur within 3-4 wk. The Pavlik harness is approximately 95% successful in dysplastic or subluxated hips and 80% successful in true dislocations. If a spontaneous reduction does not occur by splinting, then a surgical closed reduction (manipulation under anesthesia) is done and the child is placed in a hip spica cast. In the older infant from 6-18 Mo, surgical closed reduction (manipulation under general anesthesia) is the major method of treatment. After 18 months of age - the progressive deformities become so severe that major open surgical intervention is necessary to realign the hip. Including; open reduction , tendon releases , pelvic and femoral osteotomies ***It is important to carefully examine the newborn child and investigate and refer as needed. TOE-WALKING INTRODUCTION zMay be normal prior to age 3 zAfter age three {Shortened heel cord zHabitual toe-walking {Rule out neurologic causes such as cerebral palsy as spinal dysraphism HISTORY zOften positive family history zBilateral {Think of other diagnosis if unilateral PHYSICAL z Gait {Toe-walk z Standing {Flat {Toeing-out {Forefoot splaying z Dorsiflexion limited z Neurologic Exam {Rule-out other causes TREATMENT zNatural History {Not well delineated {Many do not resolve spontaneously {Benign? treatment zHeel-cord stretching and gait retraining {Night splint zSerial casting {Ankle-foot orthosis zSurgery {Heel-cord lengthening CLUBFOOT INTRODUCTION zCongenital Talipes Equinovarus {Hindfoot equinus {Subtalar joint varus {Cavus {Forefoot adduction zMay be unilateral or bilateral zFamilial tendency HISTORY & PHYSICAL z Noted at birth z If unilateral {Foot and calf smaller z Deep creases z Check for flexibility z May be associated with torticollis, and hip and spine abnormalities RADIOLOGY z Anteroposterior and lateral weight-bearing films TREATMENT zSerial casting {+ heel-cord tenotomy zSurgery for failures zRecurrence rate not insignificant {Follow throughout growth POSITIONAL CALCANEOVALGUS INTRODUCTION zMarked dorsiflexion of entire foot at the ankle joint zMild and flexible eversion of the subtalar joint zLikely due to intrauterine malpositioning HISTORY & PHYSICAL zPresent at birth zUsually able to bring foot out into inversion and plantarflexion zRule out congenital vertical talus {Fixed equinus and valgus of the hindfoot {Rigid dorsiflexion of midfoot on hindfoot zRadiographs normal: R/O CVT TREATMENT zPassive stretching exercises to hasten correction may be used FLATFOOT INTRODUCTION zImportant to differentiate flexible from rigid flatfoot {Flexible flatfoot not usually problematic HISTORY zRigid flatfeet may be painful and can be associated with increased ankle sprains in tarsal coalition (abnormal connections between some of the tarsal bones) PHYSICAL z Flexible {Arch returns with sitting or tiptoe standing {Normal subtalar and midtarsal motion {Check dorsiflexion with forefoot supinated z Locks subtalar joint z R/O tight achilles physical z Tarsal Coalition {May be painful to move or palpate subtalar joint or other tarsal bones {Subtalar motion often decreased {Pes planus and ankle valgus may not be striking RADIOLOGY z Normal in flexible flatfoot z Oblique views and Harris view may help view a coalition TREATMENT zFlexible flatfoot {None needed {May improve spontaneously {Usually asymptomatic {May try an orthotic to improve function or alleviate pain {Rarely surgery required treatment zTarsal Coalition {Rest/activity modification {Antiinflammatories {Physiotherapy {Orthotics {Casts {Surgery: resection or fusion IDIOPATHIC SCOLIOSIS INTRODUCTION zFrontal plane spinal deformity associated with torsional malalignment of the spinal column zFirst rule out other causes of scoliosis CLASSIFICATION z Idiopathic z Neuropathic z Myopathic z Congenital z Associated with neural tissue defect z Neurofibromatosis z Mesenchymal z Traumatic z z z z z z Soft tissue contactures Osteochondrodystrophies Tumor Rheumatoid disease Metabolic Related to lumbosacral area z Thoracogenic z Hysterical z Functional HISTORY zDeformity {When noted {Progression {Pain zNeurologic Symptoms zGrowth Indices PHYSICAL z Cutaneous back lesions {Pigmentation {Dimpling/sinuses {Hair patches z Thoracopelvic balance z Leg length discrepancy physical z Range of motion z Rotational prominence z Neurologic examination RADIOLOGY z Coronal and Sagital (3 foot standing films) {Abnormal vertebrae {Vertebral rotation {Cobb angle {Risser Sign z Convexity determines sidedness z Other tests as needed TREATMENT zNatural History {Why we need to treat {Who we need to treat PROGRESSION DURING GROWTH Risser Sign < 19 degrees 20 – 29 degrees 0–1 22% progression 68% progression 2-4 1.6% progression 23% progression PROGRESSION AFTER MATURITY Thoracic Curves <60 degrees Thoracic Curves 60 – 80 degrees Lumbar Curves <31 degrees Lumbar Curves >31 degrees 6 degrees/24 years 28 degrees/24 years 0 degrees/24 years 18 degrees/24 years PULMONARY FUNCTION zThoracic curves >60 degrees {Decreased vital capacity zThoracic curves >80 degrees {Dyspnea TREATMENT zThree P’s {Psychosocial issues {Progression {Pulmonary function treatment zObservation {Small curve (<20 degrees?) {Repeat x-rays every 4 months zCobb angle zProgression treatment zOrthotics {Growing child {>20 degree curve? {Progression (>5 degrees) treatment treatment z Surgery {Large curves {Progression despite bracing SCHEUERMANN DISEASE INTRODUCTION zStructural kyphosis of the thoracic, thoracolumbar, and lumbar spine zEtiology unknown HISTORY zAge >10 years of age zDeformity zPain {At deformity or area of compensation {Worse with sitting, standing, or physical activity PHYSICAL z Rounded shoulders z Angular kyphosis {Rigid {pigmentation RADIOLOGY z Coronal and Sagital (3 foot standing films) {Vertebral wedging z >50 on 3 consecutive {Irregular end plates {Schmorl Nodes {Decreased disk space {Cobb angle TREATMENT zNatural History {Rapid progression during growth spurt {Not clear whether it progresses at maturity treatment zObservation {Mild deformity {Repeat x-rays every 4 - 6 months zCobb angle zProgression zExercise/physical therapy {Improve muscle tone/posture and flexibility treatment treatment SPONDYLOLYSIS & SPONDYLOLISTHESIS INTRODUCTION zSpondylolysis: defect in the pars interarticularis zSpondylolisthesis: Slipping forward of one vertebrae on the next HISTORY zMay be asymptomatic zPain usually noted during adolescent growth spurt {Worse with activities {May rarely get radicular pain zDeformity {Scoliosis {Postural changes PHYSICAL z Decreased forward bending {Hamstring tightness z Tenderness on deep palpation in lumbosacral area z Large slips {Flattening of the buttocks {Step-off at lumbosacral junction z Scoliosis z Neurologic examination may be abnormal RADIOLOGY z Standing posteroanterior and lateral lumbosacral spine, spot lateral, and oblique views { Pars interarticularis defect { Slipping z Bone scan, CT, or MRI sometimes needed for Dx TREATMENT zNatural History {Progression usually during the adolescent growth spurt zRare at maturity treatment zObservation {Asymptomatic {Repeat x-rays every year if mild zReduction of activity/physiotherapy {Symptomatic {Orthotic if not settling or if acute injury treatment z Surgery {Repair of the defect (<L4) {Arthrodesis Assessing Limb Alignment In Children (when to “reassure” and when to “refer”) GENERAL INTRODUCTION: • Torsional and angular malalignment are the most common musculoskeletal complaints encountered by pediatricians and family physicians • Parents and family members have great concern for the child's appearance and gait • Spontaneous resolution of these problems is the norm and the primary care provider can, in most cases, treat these with careful observation • Referral to Orthopedic surgeon only when deformity is severe NATURAL HISTORY: During gestation, the lower limb internally rotates, bringing the great toe to the mid line. External rotation then occurs in the femur and tibia throughout the remainder of development to skeletal maturity. Some may have a familial tendency and others are attributable to intrauterine positioning. NORMAL TORSION OF THE FEMUR: In the normal adult, the head and neck of the femur are angulated by 12 degrees relative to the femoral condyles as noted in the illustration below. ANTEVERSION: is an increase in the angle of the head and neck of the femur relative to the frontal plane of the body This represents a normal femur abnormally positioned in the acetabulum. The net effect of this positional relationship is an externally rotated leg. RETROVERSION: is a decrease in the angle of the head and neck of the femur relative to the frontal plane of the body. This represents a normal femur that is abnormally positioned relative to the acetabulum. The net effect of this positional relationship is an internally rotated leg. NB** Average adult has 10° of externally rotated foot. - Intoeing of greater than 10° and out-toeing of more than 30° are considered abnormal, but rarely with a functional problem. Complete History - Pregnancy, birth, and development to rule out pathological causes for the deformity. - Type of deformity, onset, progression, and prior treatment. - Parents concerns regarding future gait, function, and cosmesis abnormality. - Family history of musculoskeletal deformities similar and dissimilar to child's. Physical Exam: ** Assess from hips to toes Gait analysis - check for a heel - toe gait and a limp ( absence of a heel toe gait may indicate an underlying neurologic disorder such as CP) Foot progression angle - the angular difference between the long axis of the foot and the line of progression the child is moving in - normal is slightly external ( positive value) - in toeing of more than 5 degrees is abnormal and is recorded as a negative value Imaging ** most rotational problems do not need to be evaluated by xray ** may need to image HIPS if suspect DDH or other congenital or developmental abnormality Metatarsus Adductus Metatarsus adductus normal Tibial Torsion: it is the position of the transmaleolar axis relative to the coronal plane of the proximal tibia normal Medial rotation ( prone hip ROM) Normal = 20 to 60 degrees - if > than 70 its abnormal Lateral Rotation - Normal = 30 to 60 - if < 20 its abnormal - place the child prone to evaluate the hip rotation and tibial torsion - roughly internal and external rotation of the hip should be equal in the older child BUT in younger children IR > ER Metatarsus Adductus: Forefoot is adducted at the tarsal-metatarsal joint. - Usually seen shortly after birth and usually resolves with in the first year of life. NB **It may be associated with hip dysplasia (10-15%) - 85% resolve spontaneously. Treatment: - Feet that can be actively corrected to neutral do not need any treatment ( stretching exercises can be given to the parents) - Feet that can not be possibly corrected need serial casting. If a child is > I year old and resistant to serial casting Metatarsal osteotomy and limited medial release may be considered but is rarely needed Tibial Torsion: - Usually presents at 1-2 years of age and resolves by age 3-4 years. - Operative intervention is seldom required except in severe cases (supramalleolar osteotomy). Reserved for children with excessive or asymmetric rotation *** CRITERIA: indicated if the thigh foot angle remains internally rotated > 10 or external tibial torsion > 35 Pearls: - if a child is born with a normal amount of tibial torsion ( often associated with a calcaneovalgus foot) further external torsion does not occur - in kids born with excessive tibial external rotation… spontaneous correction does not occur Femoral Anteversion: most common cause of intoeing in kids < 3 - Internal rotation of the femur seen in 3 to 6 year olds that usually corrects by 10 years of age (F>M). - Usually symmetric increased medial and decreased lateral rotation is seen on examination of a child with intoeing and medially rotated patellae. -Parents should encourage age child to sit cross-legged. ***NB - Spontaneous resolution occurs in 95% of children If the child is older than 10 years and has > 90 IR and < 10 ER femoral derotational osteotomy may be considered for cosmesis only .. IT DOES NOT CHANGE THE CHILDS FUNCTION!! ****Main complication is the development of a new rotational problem while trying to treat the first one Bottom Line: Most cases need only reassurance VARUS OR VALGUS Knock-knee (or genu valgum): the legs are bowed inwards in the standing position. The bowing occurs at or around the knee, so that on standing with the knees together, the feet are far apart. Bowleg (or genu varum): the legs are bowed outwards in the standing position. The bowing occurs at or around the knee, so that on standing with the feet together, the knees are far apart. Normal Development Almost all infants have some degree of bowing There is gradual improvement of the bowing by 18 months and most toddlers do not have bowing after 2 Knock knees begin to appear between 2 and 3 and the greatest amount by age 4 Partial straightening occurs at age 6 to 7 at which time the adult position is reached Normal evolution: from bowlegs (age 2) to knock-knees (age 3) to normal valgus (age 5) 2 3 5 History Family history Nutritional history Birth history and milestones Height and weight chart trends Does pt have associated pain Physical Exam - general ntutritional status and body proportions - measure the intramalleolar or intrafemoral distance for your records - assess for assymetry Imaging - single AP xray of both lower extremities ( an orthoroentnogram without the ruler) - look for abnormalities of the growth plates such as widening or growth abnormalities - can measure the femoral - tibial angle ( 7 degrees of valgus) and metaphyseal- diaphyseal tibial angle(< 11degrees) ***More detailed work up may be needed under the following circumstances: 1. If the bowleg or knock-knee appears outside the age range mentioned above, i.e., bowleg beyond age 3 and knock-knee beyond age 7 2. If it is unilateral 3. If the intercondylar or intermalleolar distance is more than 6 cm, or is rapidly progressing (more than 11/2 cm within six months) 4. Associated symptoms like pain or limp, or signs of Blount’s disease, rickets, or other disease syndromes CAUSES OF VARUS AND VALGUS LEGS Blount’s disease - a condition of severe bowleg that occurs usually in obese children who walk early. It is progressive, and may require surrgery. Growth disturbance - or epiphyseal dysplasia, which may be a part of a generalized bone growth disturbance. Post-trauma - where injury to the knee causes damage to the growth plate and abnormal growth around the knee. NB*** Metabolic Abnormalities (Rickets etc..) - can cause growth disturbance of the bones in the body, including the knee. Valgus Deformities Knock-knees can also develop as a result of disease processes. Most often the precipitating condition has already been diagnosed and the knock-knees are recognized as a symptom of the condition Treatment: The condition is usually not treated. Surgery may be considered for a condition that persists beyond puberty and in which the separation between the ankles is approximately 8 cm or greater You can reassure parents by telling them to take a picture every 6 months of their child standing to observe the legs straightening out Sometimes children reach adolescence but are unhappy that their 'normal' knock knees have not straightened out enough. A variety of surgical operations are available to help in these cases. But such treatment is not foolproof and has to be timed very carefully. VARUS DEFORMITIES Observe the child both lying down, walking and standing Physiologic bowing always resolves without treatment. Bracing is not needed. ****At age 18 months, differentiating physiologic bowing from tibia vara is important and imaging may be needed. NB**If a bone metabolic disorder is detected, the underlying problem should be treated and genu varum usually resolve. Metaphyseal diaphyseal angle - this angle is formed by lines between metaphyseal beaks& perpendicular to the longitudinal axis of the tibia *** LESS THAN 11 DEGREES IS NORMAL Metaphyseal dyaphyseal angle > 110 . Children with a Metaphyseal-Diaphyseal Angle greater than 11 degrees on a standing radiograph should be watched!!! A metaphyseal-diaphyseal angle > than 20 degrees confirms the diagnosis of Blounts BUT - angles > than 15 most likely have the disease Lower Extremity Evolution Legg Calve Perthes Disease Definition: - self limiting hip disorder caused by a varying degree of ischemia and subsequent necrosis of the femoral head KEY FEATURES : - avascular necrosis of nucleus of proximal femoral epiphysis - abnormal growth of the physis - and eventual remodeling of regenerated bone are the key features of this disorder - usually seen in 4 to 8 yr old boy - male to female ratio: 4-5 to 1 - increased incidence with a positive family history, low birth wt, and abnormal pregnancy / delivery - upto 12% of cases are bilateral but will be at different stages & are asymmetric - age is the key to the prognosis - presenting after 8 has a poor prognosis Pathogenesis: - AVN of femoral epiphysis - articular cartilage is nourished by synovial fluid - continues to grow - cartilage columns become distorted with some loss of their cellular components - they do not undergoe normal ossification, which results in excess of calcified cartilage in the primary trabecular bone - revascularization procedes from peripheral to central - symptoms occur with subchondral collapse and fracture; DIFFERENTIAL DIAGNOSIS bilateral Perthes: - hypothyroidism - multiple epiphyseal dyspasia - spondyloepiphyseal dysplasia tarda - sickle cell unilateral Perthes: - septic arthritis - sickle cell - spondyloepiphyseal dysplasia tarda - gaucher's disease - transient synovitis Clinical Presentation: - pain (often knee pain) - a limp Early phase: - limited abduction of hip & limited internal rotation in both flexion & extension are seen Late phase - antalgic gait (due to pain - Trendelenburg gait Prognosis: - at least 50% of involved hips do well with no treatment - many others will do well up until the age of 50 when anatomic asphericity leads to DJD Age is the key to prognosis: - less than 6 years of age: outcome is good - between 6-8 years of age: results not always satisfactory with containment - greater than 9 years of age: questionable benefit from containment; - children older than 8-9 yrs at initial onset will have poor prognosis and may be expected to have significant symptoms and restricted ROM Non Operative Treatment: - principles of treatment are maintenance of ROM & containment of femoral head through the evolution of healing of the epiphysis Containment: - containment of the femoral head in the normal acetabulum during repair process may lead to a more sperical head and congruous joint - containment is not clearly defined but generally implies 80 % coverage - prevents extrusion and compression by acetabular rim - bracing or surgery can achieve containment Contained “ healed” Perthes Long Term Consequences: - coxa magna - coxa plana - coxa breva - hinged abduction: - occurs when an enlarged femoral head is laterally extruded and impinges against the acetabular rim when the hip is abducted Slipped Capital Femoral Epiphysis ETIOLOGY: - slip of the captial femoral epiphysis occurs with in a narrow window of physiologic maturity of the growing child - arises from mechanical and constitutional factors - position of growth plate of proximal femur normally changes from horizontal to to oblique during preadolescence and adolescence - wt increase that occurs during adolescent growth spurt puts extra strain on the growth plate Clinical Findings: - it occurs most often in boys 10-17 yrs of age (avg 12 yrs) - in females, the average age is 12 years - bilateral involvement in about 1/3 of pts, NB *** - remember that bilateral involvement is occurs in over 25% of patients - often within 6 months of the other side, therefore need to watch for symptoms in opposite hip - pts may have underlying endocrine disease (such as hypothyroidism or delayed puberty & bone age) ****- patients who are on or below the 10 percentile for height at the time of presentation should be screened for hypothyroidism by measuring thyroid-stimulating hormone and free thyroxine as a preliminary screening test; - most common presentation is chronic slip (60 % of cases) - may cause pain refered to hip, distal medial thigh, or knee - on exam, look for loss internal rotation, which may be manifested by observing the extended hip move into external rotation as hip is flexed - restricted abduction is found w/ severe slips Radiographic Findings in SCFE AP View: - normal hip shows epiphysis of femoral head projecting above & lateral to the superior border of the femoral neck - affected hip shows widening and irregularity of growth plate Klein's Line: - line drawn along superior border of femoral neck should cross at least a portion of the femoral epiphysis - slip must be suspected if a straight line drawn up lateral surface of femoral neck does not touch the femoral head KLEIN’S LINE Lateral View: ***NOTE- AP view may not reveal initial slip, which explains need for a true lateral lateral which will detect a posteriorly directed slip - w/ an acute slip, a frog leg lateral may be contraindicated since it can increase the slip therefore always order a shoot through lateral - the most sensitive indicator of a mild slip is the loss of lateral overhang of the femoral epiphysis; Classification: Grade I: displacement of epiphysis less than 30% of width of femoral neck Grade II: slip between 30%-60% Grade III: includes slips of greater than 60% the width of neck; SEVERE SCFE Treatment - is designed to fuse epiphysis on femoral neck which prevents further slipping - this usually involves insertion of one screw into anterior aspect femoral neck (depending on degree of slip) to enter center of epiphysis - this is achieved w/ care to avoid penetration into the hip joint which can lead to chondrolysis ****No Reduction of the Slip is carried out. The hip is pinned in situ - to avoid osteonecrosis of the femoral head GROWTH PLATE CLOSED - no further risk of slip Complications: 1) avascular necrosis: - risk factors: - severity of slip - reduction of slip - location of pins ( need to avoid anterolateral cortex) **** risk of AVN is approx 20-50% w/ attempted reduction vs. less than 5% w/o reduction; 2) Chondrolysis: - need to monitor for irritation of the hip and loss of joint space post op