Types of osteomyelitis \200 \200 \200 Acute. Subacute (2 \200\2233wks duration). Chronic: bone). Bone abscesses may become surrou nded by thick, \201 brous tissue and sclerotic bone (Brodie \200\231s abscess). may develop \200\230sequestrum \200\231 (dead bone) and \200\230involucrum \200\231 (new Etiology The yield for bacterial growth from synovial \202 uid and bone aspirate is small ; therefore organisms are not always isolated. Staphylococcus aure- us is most common in ch ildren in all age groups. Other organisms seen include the following: \200 < \200 2yrs: Haemophilus in \202 uenzae (rare). > \200 2yrs: Gram +ve cocci, Pseudomonas aeruginosa. \200 Neisseria gonorrhoeae. Neonates: group B streptococcus and Gram \200\223ve enteric bacilli. Adolescents: Consider salmonella in SCD. Tuberculosis is rare. Symptoms and signs \200 \200 Neonates characteristically do not appear ill and may not have fever. Older children have p ain, limping, refusal to walk/weight bear, fever, malaise, \202 u-like symptoms. Overlyin g bone may be tender (+ warm), with/without swelling. Long bones principally affected: Tibi a > femur > humerus. Differential diagnosis This includes: \200 b p.768). \200 \200 \200 \200 \200 \200 JIA ( Lyme/post-streptococcal arthritis ( Acute leukemia ( Neuroblastoma ( Neoplasm (e.g. o steoid osteoma, osteosarcoma, Ewing \200\231s sarcoma). CRMO. LCH. b pp.244, 712). b p.658). b p.666). 20_McClure_20.indd 740 11/14/2012 3:24:04 PM INFECTIONS: OSTEOMYELITIS 741 Investigations \200 \200 Blood: X-ray of bone: visible. Late stages reveal metaphyseal rarefaction. Destructive chan ges in bone appear after 10 days. US-guided aspiration: MRI: formation, joint effusion, sub periosteal extension. Bone scans: joint involvement (seen as hot spots) and differentiate j oint from bone involvement; good for infections of pelvis, proximal femur, and spine. Open biopsy may be necessary. Consider immunological evaluation if atypical organism. FBC, ESR, CRP, blood cultures (positive in 50%). early stages may be normal; soft tissue oedema may be \200 for microscopy and culture. soft tissue assessment \200\224bone marrow involvement; abscess good for acute osteomyelitis; can identify up to 90% of \200 Treatment \200 Medical: antibiotics for 4wks. Early liaison with microbiologist required. Surgical: a sequestered abscess or collection (not accessible to antibiotics). IV antibiotics for a minimum of 2wks, followed by oral drainage and debridement if there is frank pus on aspiration or Prognosis Usually excellent if treated early. Disease recurrence/pro- gression to chronic i nfection is seen in <10%. Complications \200 \200 Systemic: Local: may include septicaemia. pathological fracture, sequestration, growth disturbance. 20_McClure_20.indd 741 11/14/2012 3:24:04 PM CHAPTER 20 Bones and joints 742 Spinal disorders General management History Pain, onset of deformity, loss of weight, night sweats, family history, disa- bility, other disorders. Examination \200 Inspection: asymmetry, scapular prominence, skin lesions (especially mid line pits and haemangiomas), caf au lait spots (associated with neuro \201 bromatosis), foot deformity, leg atrophy. Feel: Move: General: Investigations: \200 \200 \200 spinal tenderness. forward \202 exion, hamstring tightness. neurological examination. radiographs, CT, MRI, bone scan. General spinal disorders Back pain Take it seriously! More likely to be caused by signi \201 cant pathology than in adult (e.g. osteoid osteoma, eosinophilic granuloma). Beware of the following, especially in young children \200\224several weeks of symptoms; night pain; increasing symptoms; abnormal neurology; recent onset of scoliosis; night sweats. Pain may be referred from intra-abdominal or intrathoracic process. Investigate thoroughly, but rem ember 50% of children experience back pain by 15yrs of age. Discitis In \202 ammation (probably infection) of the disc space: \200 \200 Age Symptoms: pain. Symptoms may be vague. Investigations: Treatment: in \202 ammatory mar kers return to normal. Outcome: group: any age (infants and children rather than adolescents). fever; irritability; unwilling to walk; back pain, abdominal \200 bloods (i CRP and ESR); MRI; bone scan. antibiotics (according to local policy), at least until usually do well. Congenital anomalies Diastematomyelia: spinal cord is split by a central cartilaginous/bony prom- inence. \200 Signs: foot); cutaneous lesions seen in most children; positive neuro logy seen in 50%. Management: progressive. Spina bi \201 da. other abnormalities are common (e.g. scoliosis, clubfoot, cavus consider resection of spur if neurology appears/is Regional spinal disorders Cervical spine: torticollis See b pp.127, 883. Thoracic spine See Scheuermann \200\231s disease (b p.744). 20_McClure_20.indd 742 11/14/2012 3:24:04 PM SPINAL DISORDERS 743 Lumbar spine: spondylolysis and spondylolisthesis \200 defect of pars interarticularis (spondylolysis). If bilateral and De \201 nition: at the s ame level may result in anterior displacement of one vertebra upon another (spondylolisthes is). Usually due to a stress fracture through a congenitally dysplastic pars. Incidence: os teopetrosis), connective tissue (e.g. Marfan \200\231s), hyperextension sports (e.g. gymnas tics). Symptoms/signs: Decreased forward \202 exion and straight leg raise. Investigation s: dog \200\231s collar \200\231. Bone scan/SPECT for occult fractures and evidence of heal ing. Management: consider short-term bracing, analgesia, hamstring stretches, and core stre ngthening. Operative intervention seldom required for stabilization. uncommon, associated with spina bi \201 da, metabolic (e.g. sudden/insidious onset of pain exacerbated by activity. X-rays \200\224lateral and oblique spinal views. Look for \200\230Scotty non-operative usually. Rest and change of activities; Sacral spine: sacral agenesis \200 De \201 nition: diabetic mothers. Signs: neurology. Management: hypoplastic/absent sacrum; most common in infants of abnormal pelvic ring affecting lower limbs with associated tailor towards severity of agenesis and neurology. 20_McClure_20.indd 743 11/14/2012 3:24:04 PM CHAPTER 20 Bones and joints 744 Spine: kyphosis \200 De \201 nition: from Greek Kyphos, a hump. Increased curvature of the spine in the sagitta l plane, visible from the side. Normally there is a 20 \200\22340 curvature of the thorac ic spine. History: neurological symptoms, family history. site, age of onset, rate of progression, associated scoliosis/pain/ Examination Assess: \200 \200 Flexibility: Ability to lie \202 at: greater severity of kyphosis). Hips for tight hamstr ings: Full respiratory (pulmonary function) and neurological examination. stand, bend forwards, bend backwards (hyperextension). associated lumbar lordosis (more pro minent with \200 limited straight leg raising. Investigation PA and lateral standing X-rays of entire spine. Diagnosis Three major causes are identi \201 ed by answers to: \200 \200 \200 Is it \202 exible? Is it painful? When did it start? Postural kyphosis (most common) Flexible, usually painless, onset <10yrs old. \200 Other poor at games. Investigations: complete correction. Treatment: for dorsal spine, educ ation, occasionally brace. Outcome: \201 ndings: tall; girls > boys; poor physical development; \202 at-footed; supine hyperextension lateral radiograph con \201 rms physiotherapy to improve posture and provide exercises corrects spontaneously by end of adolescence. Congenital kyphosis Rigid, occasionally painful, onset <10yrs old. \200 Other congenital spinal abnormality, e.g. spina bi \201 da. Cause: segmentation during the \201 rst trimester. Treatment: Outcome: \201 ndings: severe deformities recognized at birth, associated with may be secondary to failure of vertebral formation +/ \200\223 \200 brace, if progression fusion to prevent paraplegia. can progress rapidly and lead to paraplegia. Scheuermann \200\231s disease \200 Rigid, aching pain between shoulder blades; onset 10 \200\22315yrs (previously normal spine ). Incidence: Etiology: \200 unknown (up to 7 \200\2238% of population in cadaveric studies). osteochondritis. 20_McClure_20.indd 744 11/14/2012 3:24:04 PM SPINE: KYPHOSIS 745 Investigations \200 >45 kyphosis with >5 anterior AP and lateral spine X-rays: wedging at three sequential vertebrae = radiographical de \201 nition of Scheuermann \200\231s disease. May have vertebral body end-plate changes (Sc hmorl \200\231s nodes \200\224vertical herniations of the intervertebral disks into the ver tebral end-plate), spondylolysis (30 \200\22350%), scoliosis (33%). Treatment \200 \200 \200 Physiotherapy Medical: Surgical mature, with severe pain or evidence of cord involvement. (extension exercises): bracing may be considered. NSAIDs. correction: with severe kyphosis (>70 ), the patient is skeletally Outcome Little evidence that patients with kyphosis <70 experience late progres- sion, di sabling pain, or neurological compromise. 20_McClure_20.indd 745 11/14/2012 3:24:05 PM CHAPTER 20 Bones and joints 746 Spine: scoliosis Idiopathic scoliosis \200 ) +/ \200\223 rotation deformity of the spine without Lateral curvature (>10 an identi \201 able cause. Description of curvature based on direction of apical convexity. There are 3 types. Infantile plagiocephaly (skull \202 attening), hip dysplasia, and other congeni tal defects. May be s to underlying spinal abnormality. Juvenile risk of curve progression (70% require treatment with 50% needing brace and 50% surgery). Adolescent: (<3yrs old): left > right side; males > females; associated (3 \200\22310yr olds): may be s to underlying spinal abnormality; high most common in 11 \200\22316-yr-olds. Females > male. Incidence \200 \200 \200 , 2% incidence. , 0.2% incidence. Curves >10 Curves >30 Right thoracic curves > double major (right thoracic and left lumbar) > left lumbar > right lumbar. Risk factors Positive family history; daughters of affected mothers more likely to be affec ted, Marfans, neuro \201 bromatosis. Disease progression Risk factors for curve progression: age <12yrs; skeletal immaturity; fe male; curve magnitude >20 ; spine at greatest risk of curve progression during puberty. Na tural history after skeletal maturity is curves < 30 unlikely to progress, if >50 2/3 w ill progress. Severe curves (Cobb angle >100 ) associated with pulmonary dysfunction, earl y mortality, pain, poor self- image. Symptoms Onset of symptoms, rate of progression, Is it painful? (in \202 ammatory or neopl astic.) Ask about respiratory and neurological symptoms. Signs \200 \200 Inspect child standing. Describe scoliosis as the side to which the spine is convex (should er on convex side is elevated). Inspect: trunk shift; spinal deformity; rib rotational defo rmity (rib hump). Bend \200\224touch toes. Adam \200\231s forward test: bending. If scolios is disappears: postural (80% of scoliosis). Full neurological examination including abdomin al re \202 exes. Lower limb examination (other causes of postural scoliosis: unilateral mu scle spasm; unequal leg length). pelvic height \200\224limb length difference; waistline asymmetry; \200 Is it \201 xed? asymmetry of the posterior chest wall on forward \200 True idiopathic scoliosis Painless, convex to the right in the thoracic spine, not associat ed with any neurological changes. 20_McClure_20.indd 746 11/14/2012 3:24:05 PM SPINE: SCOLIOSIS 747 Investigations \200 \200 Standing PA and lateral X-rays full spine. MRI if pain, neurological changes, rapidly progr essive curve, excessive kyphosis, left thoracic/thoracolumbar curves, considering surgery. Treatment Based on maturity of patient, magnitude of deformity, and curve progres- sion. Th e aim is to prevent further progression. Non-operative \200 \200 ). Close observation (6-monthly X-rays for curves <25 Bracing is controversial. May slow/halt curve progression \200\224the more it \200\231s worn, the more effective it is. Consider fo r children with curves <40 . Manipulation and casting for young children with more severe curves Operative \200 Anterior/posterior spinal fusion with instrumentation for severe deformities (>45 ). Poste rior instrumentation without fusion Vertebral expanding prosthetic titanium rib \200 Congenital scoliosis Most common congenital spinal disorder. Etiology Abnormal vertebral development in the \201 rst trimester. Associations Can be isolated deformity or associated with other con- genital abnormalities: Spinal (40%)> genitourinary (20%) > heart disease (10 \200\22315%), also associated with s yndromes, e.g. VACTERL (b p.848). Disease progression Risk of progression dependent on morp hology and growth potential of vertebrae. Greatest risk during periods of rapid growth (<2y rs and >10yrs old). Treatment Early diagnosis; often need surgery. Scoliosis secondary to neuromuscular disorders Symptoms and signs Progresses more rapidly a nd may continue after maturity; longer curves involving more vertebrae and less likely to h ave compensatory curves. Associations \200 Skeletal: \200 Pulmonary: \200 Neurological: \200 Upper degenerat ion, syringomyelia, spinal cord tumor/trauma, tethered cord, diastematomyelia. Lower (myopa thic: DMD). Syndromes pelvic obliquity, bony deformities, cervical involvement. more frequent, d lung function an d pneumonia. brainstem, proprioception, Klippel \200\223Feil syndrome. motor neuron disease: cerebral pa lsy, spina bi \201 da, spinocerebellar motor neuron disease: poliomyelitis, spinal muscular atrophy, : neuro \201 bromatosis, Marfan \200\231s. 20_McClure_20.indd 747 11/14/2012 3:24:05 PM CHAPTER 20 Bones and joints 748 Hip disorders: developmental dysplasia of the hip Previously known as \200\230congenital d islocation of the hip \200\231. Disorder of hip joint development resulting in hip instabil ity/subluxation/dislocation 9 ac- etabular dysplasia. \200 Incidence: spontaneously stabilize by 9wks). Risk racial predilection, breech presentation. Etiology: oestrogens), decreased intrauterine volume (breech position, \201 rst born, ol igohydramnios). Associations: adductus (10%), talipes calcaneovalgus, teratologic dislocati on, Down \200\231s syndrome. Teratologic with neuromuscular syndromes (e.g. myelodysplasia, arthrogryposis, chromosomal abnormalities, lumbosacral agenesis, diastrophic dwar \201 sm ). The hip is dislocated before birth. It is more dif \201 cult to treat. 2:1000 (but up to 20:1000 newborn hips are unstable; 90% factors: family history (1:5), female > male (5:1), Left > right (1.5:1), capsular laxity (increased type III collagen, maternal other \200\230packaging \200\231 disorders: torticollis (20%), metatarsus dislocation: a distinct form of hip dislocation associated Disease progression Capsular laxity + shallow acetabulum l instability/subluxation/dislocat ion l muscle contracture l progressive acetabular dysplasia with a \201 bro- fatty substa nce \201 lling the acetabulum (pulvinar); femoral head becomes hypoplastic. History Usual ly uneventful pregnancy; parents may notice delayed walk- ing, painless limp, prone to fall s. DDH may be incidental \201 nding. Examination All newborn infants should be screened for DDH before discharge and then again at 6wks. High-risk infants are selected for ultrasound screening. Still controversy over se lective v universal screening program. Neonate \200 Is hip dislocated? If so, is it reducible? Ortolani \200\231s test (O for out). Gently elev ate (anteriorly) and abduct the dislocated hip to reduce it (clunk of reduction). If not di slocated, can I dislocate it (i.e. dislocatable)? Barlow \200\231s test. Gently adduct and depress (posteriorly) femur; vulnerable hip dislocates. These 2 provocation maneuvers become unreliable after age 6 \200\2238wks. \200 asymmetric gluteal folds, limited abduction, leg length Infant: discrepancy. Galeazzi sign \200\224 \202 ex knees with feet together; +ve sign = a ffected femur appears short due to dislocated hip joint. (Note. Also +ve if femur is congen itally short; \200\223ve with bilateral DDH). 20_McClure_20.indd 748 11/14/2012 3:24:05 PM HIP DISORDERS: DEVELOPMENTAL DYSPLASIA OF THE HIP 749 Older child: may walk with limp; positive Trendelenburg test. With bilateral dislocations, the only sign may be an exaggerated lumbar lordosis and limited hip abduction. Investigations \200 \200 Age >6mths: acetabular index, and hypoplastic femoral head in superolateral position is dem onstrated. Shenton \200\231s line broken. <6mths: hip US (before ossi \201 cation; operator-dependent). AP pelvis radiograph. A shallow acetabulum with increased Treatment Depends on age of child (see Box 20.1). An urgent referral to a paedi- atric orth opedic surgeon is needed in order to start treatment as soon as possible. The aim is to ach ieve and maintain concentric hip reduction to encourage early acetabular development to red uce the risk of future degenerative joint disease. Box 20.1 Treatment at different ages Age <6mths Pavlik harness (maintain hip in \202 exed position with some hip abduc- tion) Age 6 \200\22318mths \200 Manipulation and closed reduction (+/ \200\223 adductor tenotomy) + hip spica plaster cast Open reduction (medial approach if <12mths old; anterior approach if >12mths old) + hip spi ca plaster cast Age 18 \200\22324mths \200 \200 Trial of closed reduction Open reduction (anterior approach) +/ \200\223 pelvic osteotomy + hip spica plaster cast Age 2 \200\2236yrs \200 Open reduction (anterior approach) +/ \200\223 femoral shortening +/ \200\223 pelvic osteot omy + hip spica plaster cast Complications \200 \200 \200 Early: Intermediate: Late: inadequate reduction and redislocation. residual acetabular dysplasia; avascular necrosis. early osteoarthritic changes. Prognosis Any residual acetabular dysplasia may be treated with a pelvic osteotomy as a sec ondary procedure. Long-term acetabular dysplasia is likely to lead to early degenerative ch anges in the hip. 20_McClure_20.indd 749 11/14/2012 3:24:05 PM CHAPTER 20 Bones and joints 750 Hip disorders: Perthes \200\231 disease Also known as Legg \200\223Calve \200\223Perthes di sease. It is due to an idiopathic osteonecrosis (avascular necrosis) of the femoral head of unknown aetiol- ogy. Incidence: 1:10,000 Risk factors Boys > girls (4:1); age 4 \200\22310yrs. <20% bilateral (usually staged + asym - metric), 10% family history, low birth weight, 4% children with transient synovitis, dela yed skeletal maturity. Etiology Unknown, although several risk factors lead to avascular necrosis: trauma, endocri ne (e.g. hypothyroidism, renal disease, steroids), metabolic, coagu- lability (blood dyscra sia, protein C or S de \201 ciency, thrombophilia). Differential diagnosis \200 \200 \200 \200 \200 \200 \200 \200 b p.767). b p.767). Multiple epiphyseal dysplasia ( Spondyloepiphyseal dysplasia ( Hypo \201 brinolysis. Slipp ed upper femoral epiphysis (SUFE) ( b p.772). Septic arthritis ( TB of hip. Trauma. SCD. b p.752). Pathological stages \200 \200 Avascular: Fragmentation: severe fragmentation and loss of height. Remodeling: Healed: hip appears sclerotic with minimal loss of epiphyseal height initially \201 ssures appear in epiphysis, followed by more \200 regeneration, new bone formation, and head remodeling no avascular bone visible on radiographs Symptoms Mild/intermittent anterior thigh/groin/referred knee pain with limp; classical \200\230painless limp \200\231. Note: Knee pain: beware hip pathology. Special signs \200 Look: antalgic gait common (see b pp.34, 752). Feel: Move: internal rotation) with muscle s pasm. proximal thigh atrophy, mild short stature, limp/Trendelenburg/ \200 effusion (from synovitis), groin/thigh tenderness. decreased hip range of movement (especially abduction and 20_McClure_20.indd 750 11/14/2012 3:24:05 PM HIP DISORDERS: PERTHES \200\231 DISEASE 751 Investigations \200 many different classi \201 cations, but most AP and lateral pelvic X-rays: useful is later al pillar classi \201 cation. The femoral head is divided into thirds. Group A no loss of height of lateral 1/3, B up to 50% loss of height, group C >50% loss of height. MRI may hel p diagnosis especially in the early stages. Technetium 99 bone scan: poor vascular supply. Dynamic arthrography to delineate hip joint and plan surgery. \200 decreased uptake in femoral epiphysis due to Prognosis This is a local self-healing disorder. Prognosis depends on bone age and X-ray ap pearances. Poor prognostic indicators are: \200 heavy child; d range of movement; adduction contracture; Clinical: \202 exion into abduction, female and older age at presentation (> 6yrs). Radio logical: lateral calci \201 cation; whole head involvement; metaphyseal cysts; lateral pil lar group C hips. Gage \200\231s sign; lateral subluxation of femoral head with Treatment is controversial The aims are to relieve symptoms and signs by eliminating hip ir ritability and maintaining hip range of movements. This is achieved by: \200 \200 \200 Maintaining sphericity of femoral head. Containing femoral head in acetabulum whilst remode ling occurs. Preventing epiphyseal collapse and secondary osteoarthritis. Non-operative treatment Observation and activity modi \201 cation, includ- ing bed rest an d walking aids. NSAIDs, physiotherapy. Bracing is controversial. Operative treatment Femoral/pelvic osteotomies to contain femoral head in acetabulum. 20_McClure_20.indd 751 11/14/2012 3:24:05 PM CHAPTER 20 Bones and joints 752 Hip disorders: slipped upper femoral epiphysis Displacement of the upper femoral epiphysis on the metaphysis through the hypertrophic zone of the growth plate. The femoral neck displ aces anteriorly and the head remains in the acetabulum. \200 Incidence: 25 \200\22360% bilateral. Risk positive family history, puberty, boys (12 \200 \22316yrs) > girls (10 \200\22314yrs). Etiology: \200 \200 \200 the most common adolescent hip disorder (3:100 000); factors: African American, >50% obese (weight >95th percentile), unknown, but associated with the following: Endocrine \200\224 Mechanical \200\224 Other \200\224 hypothyroidism, hypogonadism, renal osteodystrophy; retroversion of femoral neck or vertica l growth plate; Down syndrome, radiotherapy/chemotherapy. Symptoms and signs Groin, thigh, or knee pain. Antalgic gait, limited hip \202 exion and abduction, \202 exion into external rotation, and thigh atrophy. Always consider hip pathology in a child presenting with knee pain. Presentation Characterized by 2 broad types of children. \200 Obese maturation bone age. Tall thin, often boys, post growth spurt (younger age in girls): overabundance of growth hormones. hypogonadal (low circulating sex hormones): delayed skeletal Diagnostic classi \201 cation This is based on duration of symptoms. \200 Preslip: seen on contralateral hip. Acute trauma; pain so severe child unable to weight bea r; usually unstable. Acute on chronic: acute slip on pre-existing chronic slip; usually hav e previous symptoms (pain, limp, out toe gait) for several months; unable to weight bear; u sually unstable. Chronic: worsen as slip progresses; child able to walk with mildly antalgi c externally rotated gait. Usually stable. Slips may be further sub-classi \201 ed into st able or unstable (Loder): unstable slip \200\231 child unable to weight bear, even with cru tches, and cannot do straight leg raise actively. These have increased risk of AVN. wide epiphysis; mild discomfort, but normal examination; often slip: mild symptoms <3wks, then sudden slippage usually without most common type; history for several months; symptoms in an 20_McClure_20.indd 752 11/14/2012 3:24:06 PM HIP DISORDERS: SLIPPED UPPER FEMORAL EPIPHYSIS 753 Investigations \200 X-Ray: intersects lateral capital epiphysis on AP. MRI: Endocrine tests: AP pelvis and frog lateral hips. Widening of physis, Klein \200\231s line \200 useful in pre-slip diagnosis, and evidence of AVN. if appropriate, e.g. thyroid function. Treatment The aim is to prevent further \200\230slippage \200\231 and to minimize complica tions. Operative Usually pin in situ (to encourage the proximal femoral epiphysis to close, hence preventing further slippage); usually not reduced as manipulation may increase the incidenc e of avascular necrosis. Prophylactic pinning of opposite hip is controversial. It is recom mended in younger children and those with endocrinopathy. Complications \200 Chondrolysis narrowed joint space, pain, decreased motion): associated with more severe slips; occurs more frequently among African American children and females ; associated with pins protruding out of the femoral head. Osteonecrosis/avascular necrosis (higher incidence in unstable hips): due to injury to retinacular vessels (at time of slip or manipulation) or compression from intracapsular haematoma. Commonly leads to degenerati ve joint disease. Avascular necrosis uncommon in stable slips. (degeneration of the articular cartilage of the hip with 20_McClure_20.indd 753 11/14/2012 3:24:06 PM CHAPTER 20 Bones and joints 754 Knee disorders Anterior knee pain Common in the growing child and is usually due to overuse . Pain is worse with load-bearing, going downstairs, and prolonged sitting with knee \202 exed. Common causes include the following: Osteochondroses: Sinding \200\223Larsen \200\223Johans son disease: Bipartite patellae: usually bilateral and a normal variant of ossi \201 catio n. There is a risk of developing an avulsion fracture; thus the child should rest, stop spo rts, and the knee should be splinted. NSAIDs may help. Once resolved, a gradual return to a ctivities is possible. Patella maltracking: several causes including dysplasia of the femor al condyles, malalignment of the quadriceps mechanism with relatively weak vastus medialis, genu valgum, tibial torsion, increased laxity. Presents with vague anterior knee pain, ins tability, +/ \200\223 episodes of patella dislocation. Treatment is physiotherapy, but some may need surgery. Chondromalacia patellae: progress to osteoarthritis (X-rays may be norma l) Treatment physio strengthening and stretches. \200 \200 Osgood \200\223Schlatter \200\231s disease (see b p.761). see b p.761. softening of the articular cartilage, which may Genu recurvatum Congenital hyperextension \200 \200 \200 Commonest in breech presentations. Associated with arthrogryposis, spina bi \201 da, DDH, talipes equinovarus. Severity varies from mild hyperextension to dislocation. Management: l ook for other abnormalities (e.g. DDH). Gentle stretching, serial casting, quadriceps lengt hening at 1 \200\2233mths if necessary. Acquired recurvatum \200 Physiological \200\230curved \200\231 knee occurring in girls due to joint laxity. May be familial and predispose to sprains or patella instability. Consider neurological causes if not bilateral. Clinical features include a hyperextended knee, generalized lax joints. May be caused by trauma to the proximal anterior tibial physis causing a progressive deformity with growth. \200 \200 Genu valgum (knock knees) De \201 ned by position of knees such that, when standing with k nees to- gether, the medial malleoli are not touching (therefore it is a frontal plane defo rmity). Commonly observed between ages 2 and 7yrs. Causes Bilateral \200 \200 \200 Physiological: Metabolic: Skeletal dysplasia: most common. renal osteodystrophy, rickets, hypophosphataemia. Kniest \200\231s syndrome, congenital dislocation of patella. 20_McClure_20.indd 754 11/14/2012 3:24:06 PM KNEE DISORDERS 755 Hematological: myelodyplasia. Unilateral Asymmetric growth \200\224trauma/infection/tumor/epiphyseal dysplasia to tibia o r femur. Presentation Child is noticed to walk knock-kneed. Establish rate of pro- gression, diet, a nd family history. Examination \200 General: dysmorphic features. Full lower limb examination (standing and lying); often accompanied by \202 at feet (pes planus); measure knee angle and intermalle olar distance. Speci \201 c the long axis of tibia bisects the long axis of femur can be m easured clinically and radiologically. Widened intermalleolar distance (distance between me dial malleoli of ankles). height and body proportions. May be overweight or have signs. Tibiofemoral angle assessment. The angle at which Investigations No X-ray required until >18mths age; then AP and lateral standing full leg l ength views. Treatment \200 \200 Non-operative: Operative: medial side tibia. If skeletally mature corrective osteotomy mainstay for physiological genu valgum. reversible epiphysiodesis (physeal stapling or eight plate) of Prognosis 95% physiological valgus resolves with growth achieving normal adult alignment by 7 \200\2238yrs. Genu varum (bowed knees) Bowing of the knees if patient stands with ankles together. Normal ly genu varum (15 ) at birth progresses to physiological genu valgum by 4 \200\2235yrs. Ge nu varum is common in children <3yrs (especially obese children who start walking <1yrs old ) Causes \200 Physiological: appearance due to: \200 \200 Structural: Metabolic: hypophosphataemia (b pp.444 \200\223445), calcium de \201 ciency. dysplasia: metaphyseal dysplasia, achondropl asia, Skeletal enchondromatosis (b p.766). Local asymmetric growth: Blount \200\231s diseas e (abnormal growth of medial aspect of proximal tibial epiphysis), osteochondromas, physeal injury (e.g. trauma, infection), dysplasia. in utero (curled up) fetal position results in a bowed a tight posterior hip capsule which causes external rotation of the hips; internal tibial t orsion. \200 osteogenesis imperfecta (b p.762). vitamin D de \201 ciency (nutritional rickets)/resistan t rickets, History Parents notice child is walking bowlegged/in toeing of feet. Establish developmenta l milestones and rate of progression, family history, diet, social history, etc. 20_McClure_20.indd 755 11/14/2012 3:24:06 PM CHAPTER 20 Bones and joints 756 Examination General examination including height and weight; full lower limb examina- tion including rotational pro \201 le, widened intercondylar distance (distance between medial femoral condyles). Investigations Weight-bearing AP and lateral lower leg views Symmetrical physiological bowi ng, \202 aring of tibia and femur. Can also mea- sure tibiofemoral angle, metataphyseal \200\223diaphyseal angles. Treatment Severe physiological genu varum may be treated by guided growth (re- versible epi physiodesis) using staples or eight plates. Blounts disease may require corrective osteotom es. Refer to orthopedic pediatric surgeon Prognosis 95% of cases of physiological varus resolve with age. Osteochondritis dissecans of the knee Occurs when an area of subchondral bone becomes avasc ular and frag- ments and separates from the underlying bone. May involve the overlying cart ilage, leading to mechanical problems (e.g. loose bodies) and joint in- congruity. Most com monly involves the lateral aspect of the medial femo- ral condyle. It may progress to early degenerative osteoarthritis. \200 Risk trauma, ischaemia, abnormal epiphyseal ossi \201 cation. Clinical Knee swelling after activities, but no history of acute trauma or injury. May be tender over affected articula r cartilage of medial femoral condyle if knee is fully \202 exed. Disease progression: th e overlying articular cartilage is usually intact in younger children and the bone heals as revascularization occurs. The risk of articular fracture with separation and loose body fo rmation increases with increasing age, larger lesions, and a weight-bearing location. factors: adolescents (10 \200\22315yrs). Boys > girls. Often secondary to features: non-speci \201 c knee pain, +/ \200\223 locking and +/ \200\223 stiffness. Investigations X-rays of knee in AP, lateral, and notch views to assess femoral condyles. M RI may be useful for determining integrity of articular cartilage and de \201 ning whether synovial \202 uid is behind the lesion. Treatment Depends on patient age, size, and stability of fragment. Usually a short treatmen t with rest, anti-in \202 ammatory drugs, and splintage will suf \201 ce. However, it may require surgery: \200 as above, including observation with periodic X-rays Non-operative: and MRIs to assess degr ee of healing. Bracing and restricted weight- bearing/activities if signi \201 cant growth remaining. Operative: adolescent with minimal growth left/loose lesion \200\224 arthroscop ic assessment with possible debridement and microfracture through subchondral plate to prom ote revascularization and healing. Fixation of large fragments. 20_McClure_20.indd 756 11/14/2012 3:24:06 PM KNEE DISORDERS 757 Prognosis Worse with large lesions in lateral femoral condyle in older children. Note: Osteochondritis dessicans may occur in other major joints in- cluding the elbow (capi tellum) and less often the lateral condyle of the patella. 20_McClure_20.indd 757 11/14/2012 3:24:06 PM CHAPTER 20 Bones and joints 758 Orthopedic trauma Trauma is the most common cause of childhood deaths. It is often due to f alls especially in the home environment (home> sports > school > road traf \201 c accident ). Road traf \201 c accident is the leading cause of death. NAI should be con- sidered (see b pp.527, 923, 1000). Fractures Generally boys > girls with a peak incidence at 12yrs of age, although speci \201 c injuries peak at different ages, e.g. NAI at 1yr, femoral fractures at 3yrs, pedestr ian vs car at 6yrs, lateral condyle/supracondylar fractures at 7yrs, physeal injury at 11 \200\22312yrs. 4% are multiple fractures. Children \200\231s fractures usually are more fre quent in summer than in winter. Principles of management \200 \200 b Chapter 4). Stabilize according to resuscitation principles (see Full history (including nature of injury, left/right handedness) and examination. Is the fracture open/closed? Is t he limb neurovascularly intact? Is there a compartment syndrome? Is the associated joint di slocated? Splint limb for comfort; analgesia; elevate. X-ray affected bone +/ \200\223 join t above and below. Liaise with orthopedic team. \200 \200 \200 \200 \200 Complications Early \200 Neurovascular radius fractures, median/ulnar nerve paraesthesia with supracondylar fracture s, radial nerve in humeral shaft fractures, common peroneal nerve with proximal \201 bula fractures. Compartment mid-shaft tibia fractures. problems: e.g. median nerve paraesthesia with distal syndrome: especially associated with closed low energy Intermediate \200 \200 stiffness: especially fractures around the elbow. Joint Malunion: may be compensated in younger children with remodeling. usually well tolerated if malunion is within plane of motion; Late \200 Overgrowth: hyperaemia). Femoral fractures in children may overgrow by 1 \200\2233cm. Defor mity: deformity several months later. Require long-term follow-up Non-union: occurs in long bones due to physeal stimulation (from if epiphysis is damaged, child may develop progressive rarely shaft of tibia/ulna. 20_McClure_20.indd 758 11/14/2012 3:24:06 PM orthopedic TRAUMA 759 Common fracture patterns The most common fracture pattern is a complete fracture of both co rtices (e.g. spiral, transverse, oblique, multifragmentary). However, the following fractur es are speci \201 c to children. \200 Buckle/torus outstretched hand (causing compression of one cortex resulting in \200\230buc kle \200\231 on the X-ray) resulting in a metaphyseal distal radius fracture. Inherently st able. Treatment immobilize in plaster of Paris/backslab; fracture clinic follow-up within 2 \200\2233 days. Remove plaster in 3 \200\2234wks and mobilize. Plastic but insuf \201 cie nt energy to produce a fracture. No fracture seen on X-ray (limb may appear \200\230bent \200\231). Commonly ulna (look out for radial head dislocation); occasionally \201 bula. Treat as for torus fracture. If severe bowing or dislocation require manipulation under ane sthetic. Greenstick fractures: like bending a young twig, the cortex will break on the tens ion side and bend on the compression side. The energy is insuf \201 cient to result in com plete bicortical fracture. It may require manipulation under anesthesia. Salter \200\223Har ris involve the physis (most commonly the distal radius). It is usually extra-articular, bu t fractures in the proximal femur/humerus, radial neck, distal \201 bula may be intra-art icular. fractures: children <10yrs. Usually caused by a fall on an deformation or bend fractures: traumatic bending/bowing of bone, fractures (physeal injuries): 20% of all children \200\231s fractures Some fractures may indicate NAI (b pp.527, 1000), e.g. spinal fracture or femoral shaft fra cture in the non-ambulant, rib fractures, two separate fractures at different stages of hea ling. These children should be referred for full investigation. 20_McClure_20.indd 759 11/14/2012 3:24:06 PM CHAPTER 20 Bones and joints 760 Osteochondroses A spectrum of conditions primarily affecting the epiphyses , but may also i nvolve cartilage and bone. Despite the term \200\230osteochondritis \200\231, the con- dit ion is not always due to in \202 ammation and may be due to trauma or over-usage, vascular irregularities, or may be a normal variation. The af- fected devascularized bony region un dergoes spontaneous healing with revascularization, resorption, and re-ossi \201 cation. S ymptoms are usually worse with activity and relieved with rest. It is usually a self-limiti ng con- dition with clinical outcomes ranging from normal to serious disability. Investigat ions include radiographs of the affected region, which may dem- onstrate fragmentation/coll apsed sclerotic bone. An MRI scan will con \201 rm the diagnosis. The conditions can be cl assi \201 ed anatomically. \200\230Physeal \200\231 (growth plate) osteochondroses Often require treatment. \200 Madelung deformity (distal radius): defect in the volar and ulna side of the distal radial physis resulting in a shortened tilted distal radius and a prominent ulna. Occurs in teenag e girls and features include pain, decreased range of movement, and abnormal wrist joint. T reated with analgesia and surgery. Scheuermann \200\231s Blount \200 disease (vertebra): see b p.744. disease: tibial physis. Articular osteochondroses Great potential for disability. \200 Freiberg in teenagers (females > males), presenting with pain on running and dancing. Joint