Periosteal new bone formation:
- Healing fractures
- Metabolic – scurvy, hypervitaminosis A/D, Gaucher’s disease
- Physiologic – during rapid growth
- Solid tumours
- Premature birth – prostaglandin E, physiologic, metabolic disease of prematurity
- Cleidocranial dysplasia
- Osteogenesis imperfecta
- Zellweger syndrome – autosomal recessive, seizures, metan retardation, microcystic renal disease, death in infancy
- Menkes sydnrome – males, fragile bones, abnormal copper metabolism
Most common site in children. Most distal forearm fractures are buckle or transverse of radial metaphysis/physis/epiphysis ± ulnar metaphysis. Displacement/obliteration of pronator fat pad, which is a thin line of fat with mild convex border.
Nondisplaced oblique or spiral fracture midshaft tibia when child first begins to walk, better seen on oblique views. Similar fractures in proximal ant tibia, calcaneus, cuboid.
Structural bony failure at tendon or aponeurotic insertion. Adolescents prone due to greater strength, extreme activity, immaturity and growing apophyses (more prone to injury than tendons). Displaced ossified apophysis (variable) ± periosteal new bone (may be exuberant). Chronic avulsion may cause pain or be incidental, with irregularity and periostitis.
- Common injuries at iliac crest (transversalis, internal and external obliques), ASIS (sartorius), AIIS (rectus femoris), ischial apophysis (hamstrings inc biceps femorus, gracilis, semimembranosis, semitendinosis), lesser trochanter (iliopsoas).
- Chronic avulsion of patellar tendon at patella (Sinding-Larsen-Johansson syndrome) – common 10-14yo, irregular bony fragments at inf patella with soft tissue swelling, thickened and indistict patellar tendon.
- Chronic avulsion injury patellar tendon at tibial tuberosity (Osgood-Schlatter lesion) – common active adolescent boys, bony fragmentation of tuberosity with soft tissue swelling, thickened indistict patellar tendon.
Injury from repetitive trauma, usually new or recently started intesnse activity. In paediatrics commonly tibia (proximal posterior or anterior), fibula, metatarsals, calcaneus. Transverse/oblique sclerotic band or lucent line surrounded by sclerosis or periosteal reaction. Bone scan focal uptake days to weeks prior to XR findings. MRI low T2 linear with surrounding oedema.
- Calcaneal stress fracture – common after cast removal, returning to actiity after prolonged disuse. Vertical sclerotic band paralleling the posterior cortex.
Non-Accidental Injury (NAI)
(Child abuse, battered child syndrome, shaken baby syndrome, trauma X). Most <1yo, almost all <6yo. 30% of infant fractures are due to abuse. 80% of deaths from head trauma <2yo are from abuse. If suspected, skeletal survey for legal documentation, which includes skull AP&lat, chest AP±oblique, abdo/pelvis/hips AP, spine lat, AP limbs, PA hands, AP feet. Repeat survey after ~2/52 for healing injuries not seen on initial esp if <2yo. May also do skeletal scintigraphy (if >2yo, not sensitive for skull fractures), abdo CT, MRI brain. Most common skeletal injury is long bone fracture, second is skull fracture. Immature callus first appears at 7-14/7 (as early as 4/7), remodelling of deformity begins by 3/12; prolonged by repeated injury.
- Posterior medial rib fractures adjacent to costovertebral joints (highly specific) – from squeezing of thorax. Not caused by CPR.
- Metaphyseal fracture – highly specific, through primitive spongiosa (weakest portion of bone), from forceful pulling of extremity or shaking (twisting and tension). Triangular metaphyseal corner fracture or cresenteric rim of bone tangentially (bucket-handle fracture).
- Fractured outer 1/3 of clavicle.
- Fractures of different ages, different body parts.
- Fractures of sapulae, spiral long bone in nonambulatory infant, spinous process, sternum.
- Extraskeletal manifestations include lung contusion, duodenal haematoma, organ laceration, pancreatitis, acute/chronic subdural haematomas/hygromas, cerebral oedema/infarction (asphysia), intracerebral haematoma.
DDx osteogenesis imperfecta and Menkes syndrome (both of these are associated with excessive Wormian bones and osteopenia); Scmid type metaphyseal chondrodysplasia, Langer type spondyloepiphyseal dysplasia, Caffey’s disease.
Infective and Inflammatory
Periosteal Reaction in the Newborn
Common in 1st 3/12, involving rapidly growing long bones (femur, tibia, humers). Physiologic new bone formation, TORCH infections, prostaglandin therapy, Caffey disease, metastatic neuroblastoma and abuse.
Physiological growth with periostel reaction – symmetric distribution throughout rapid growing bones, benign reaction. Up to 6/12, most 1-4/12. Single layed lines paralleling diaphyseal cortex esp long bones of femurs, tibia.
Transplacentally acquired infections (TORCH):
- Congenital Rubella syndrome – most common viral, eye abnormal, deafness, hepatosplenomegaly, aortic and pulmonary stenosis, IUGR, bony changes in 50%. Irregular fraying of long bone metaphyses with generalised lucency, ‘celery stalk’ appearance (longitudinal irregular fraying) esp 1st 3/52.
- Congenital syphilis – hepatosplenomegaly, rash, rhinorrhoea, anaemia, ascities, bony changes in 95% (may not appear until 6-8/52 after infection, but before positive serology). Nonspecific metaphyseal lucent bands, periosteal reaction of long bones, Wimberger corner sign (destruction med proximal metaphysis of tibia with irregular lucency).
Caffey disease (infantile cortical hyperostosis) – rare slef-limiting idiopathic disease, almost always <6/12. Irritability, fever. Laminated periosteal reaction, adjacent soft tissue swelling, markedly increased uptake on bone scan. Commonly mandible, clavicle, scapula, ulnar, ribs.
Most extension from adjacent metaphysis from bacterial sepis, most Staph aureus and group A streptococci. Most monoarticular, large joints esp hip then knee. Most common in infants and teenagers, but can be any age. Diagnostic delay -> joint destruction. Asymmetric widening of hip joint by >2mm on nonrotated XR (distance betw teardrop and med cortex metaphysis, Waldenström sign); not very sensitive for effusion as fluid tends to accumulate in ant recess before displacing femur laterally. Soft tisue swelling, displacement/obliteration of fat pads (obturator internus, gluteus, ilipsoas). US long anterior to joint, asymmetric widening of hypoechoic space betw proximal femur shaft and joint capsule diagnostic of an effusion. Lack of effusion does not exclude septic arthritis. Other causes of effusion includes toxic synovitis, noninfectious arthritis, Perthes disease.
Half <5yo, nonspecific presentation, raised ESR. Most haematogenous, many recent respiratory infection or otitis media. Most common Staphylococcus auerus. Metaphyses or metaphyseal equivalents, ?rich slow moving blood supply, 75% in long bones esp femur, tibia, humerus. Earliest sign is deep soft tissue swelling with displaced/obliterated fat planes. Bony changes may not be see until 10/7 with poorly defined lucency and progressive bony destruction, periosteal new bone (cf bone scan positive within 24-72hrs). If chronic -> sclerotic bony lesion. Bone scan shows focal increased activity on angiographic, soft tissue and pool phases. MRI increased T2, large areas surrounding oedema, nonehanced areas suggest necrosis or abscess.
Juvenile Rheumatoid Arthritis (JRA)
Langerhans Cell Histiocytosis (LCH)
(Histiocytosis X). Idiopathic focal, localised or systemic ?inflammatory or neoplastic proliferation of Langerhans cells. M:F 2:1, more common in whites.
- Eosinophilic granuloma (EG) – isolated to bone or lung, 70% of LCH, good prognosis. Most single site of bony invovlement. Extremely variable with lucent/sclerotic lesions, permeative or geographic, slerotic or poorly defined border. Most common skull (beveled edge from inner > outer table destruction), ribs (may be multiple, expanded), femur, pelvis, spine (verebral plana – destruction with severe collapse), mandible. Skeletal survey to identify other lesions, CXR for lung involvement, MRI/CT for local extent.
- Letterer-Siwe disease – acute disseminated LCH <1yo. Poor prognosis with mortality in 1-2yrs. Acute hepatospelnomegaly, rash, lymphadenopathy, marrow failure, lung involvement.
- Hand-Schuller-Christian disease – chronic systemic LCH, typically 3-6yo, high morbidity. Hepatosplenomegaly, diabetes insipidus, exophthalmos, dermatitis, growth retardation, most have bony involvement.
See Bone Tumours
- Epiphyseal – Chondroblastoma, osteomyelitis, histiocytosis, TB
- Metaphyseal – Osteosarcoma, osteochondroma, enchondroma, lymphoma, leukaemia, metastases
- Metadiaphyseal – Fibrous dysplasia, NOF (at muscular and ligamentous insertions), chondromyxoid fibroma.
- Diaphyseal – Ewing sarcoma, histiocytosis, neuroblastoma.
- Central – UBC
- Eccentric – ABC
- Cortical – osteoid osteoma
Permeative lesions are agressive inflammatory or neoplastic lesions with ill-defined borders, wide zone of transition, multiple small irregular holes centrally. DDx if <5yo osteomyelitis, LCH, neuroblastoma mets; if >5yo Ewing sarcoma, lymphoma/leukaemia, osteomyelitis, LCH.
Variable appearance, lytic or sclerotic, expansile or nonexpansile. Classically smudged ‘ground-glass’ opacity, more dense centrally. Periosteal reaction only if pathological fracture.
McCune-Albright syndrome – polyostotic fibrous dysplasia, skin pigmentation abnormalities, endocrine abnormalities (esp precocious puberty in girls). Esp facial bones, pelvis, spine, proximal humeri. Tend to be unilateral. Many have pathological fracture by 10yo. No malignant potential.
(Cortical avulsive injury, cortical irregularity syndrome). Slef-limiting, typically adolecents (11% of 10-15yo), M>F. May be asymptomatic/incidental or cause pain. Often bilateral. ?Chronic avulsive injury of adductor magnus causing posterior medial distal femoral metaphyseal iregularity. Irregular cortical margin (but still intact) and lucency, scoop-like defect. MRI high T2 adjacent to the defect. No associated soft tissue mass.
Variable apophyseal appearances, may be fragmented, mimic periosteal reaction, mixed sclerosis and lucency esp tibial tuberosity, ischeal tuberosity, ischeopubic synchondrosis, posterior calcaneal apophysis.
Fibrous Cortical Defect
Nonossifying fibroma if large. 40% of children, common 5-6yo, around knees esp distal femur. Lucent, eccentric, well-defined, thin sclerotic cortical rim, round or oval. Over time -> increased sclerosis -> resolves.
Common, most adolescents, M>F. Pain worse at night, relieved by NSAIDS/aspirin. ?Benign neoplasm or inflammatory lesion. Cortex of metadiaphyses or diaphysis of lower limb long bones. Lucent cortical nidus <15mm surrounded by reactive sclerosis, occasional central punctate density (target sign). CT to demonstrate nidus and cortical location. Bone scan ‘double-density sign’ of increased uptake by nidus surrounded by less intense uptake of sclerotic bone. Osteoblastoma is a large osteoid osteoma.
(Osteogenic sarcoma). Most common primary bone malignancy, esp 10-15yo, M>F. Occasionally associated with hereditary retinoblastoma, previous radiotherapy. Very malignant with aggressive osteoid and bone formation. Medullary (most), periosteal or paraosteal. 90% metaphysis of long bones esp areas of rapid growth with 40% distal femur, 20% proximal tibia, 15% proximal humerus. Usually large at presentation. Lucent bony destruction with aggressive periosteal reaction, pooly defined borders. Tumour bone formation in >90%, differentiating from other malignancies; cloudlike density, extending beyond expected confines of bony shaft. Poorly differentiated, aggressive lesions are nonspecific, may not have tumoral bone. MRI for extent of marrow abnormal, soft tissue mass, cortical destruction; all bony T2 signal assumed tumour involvement rather than peritumoral marrow oedema for sake of planning purposes. May have skip lesions hence whole length of bone needs to be imaged. Tx surgery (limb salvage in 80%) and chemotherapy, 5-yr survival 77%. Mets to lungs, bones (in 15%), assesed with lung CT and bone scan.
Second most common after osteosarcoma. Very aggressive, small round blue cells. Younger adolescents, <5yo vary rare. Common in femur and pelvis (2/3 of cases), tibia, humerus, ribs. PNET and Askin tumour (chest wall) are the same as Ewing sarcoma, and now classified as Ewing sarcoma family of tumours. Variable appearances. 45% metaphysis, 33% diaphysis (much more common than other tumours). Soft tissue mass in 80%, usually dominant. Most aggressive with lucent lesion, poorly defined borders, permeative appearance, saucerization, aggressive periosteal reaction (spiculated/hair-on-end, onion skin, Codman triangle). Predominantly sclerotic in 15%. MRI destructive bony mass with soft tissue component. 5-yr survival 70% if localised, 30% if mets.
Most commonly from small round blue cell tumours. Neuroblastoma esp <3yo where it is more common than 10 bone tumour. Leukaemia/lymphoma -> metaphyses, bony destruction, irregular ill-defined lucent metaphyseal bands (leukaemic lines); primary bone lymphoma rare.
Developmental Dysplasia of the Hip (DDH)
(Congenital hip dislocation CDH). M:F 1:6 (increased sensitivity of maternal hormones), 1:1000, bilateral in 1/3, higher risk in whites, breech, oligohydramnios, firstborn (unstretched uterus), LBW, FHx, papoosing/swaddling, torticollis, scloliosis, Ehlers-Danlos, neuromuscular imbalance. Asymmetric gluteal folds, limited abduction, positive click on Ortolani (relocation) or Barlow (dislocation) maneuvers. Teratogenic/pathologic dislocation if associated with Chiari II, arthrogryposis. Abnormal ligament laxity -> decentering of femoral head -> acetabular dysplasia (wider and shallower) to accommodate ROM -> vicious cycle. Pulvinar (fibrofatty tissue) may fill the acetabulum. Inverted limbus – acetabular labrum may flip inferiorly against med femoral head. Hourglass configuration of joint capsule – tight psoas tendon stretched across medial to displaced femoral head. Adductor muscles shorten. Ligamentum teres elongates and becomes redundant. Pseudoacetabulum – broad shallow depresion in lat ilium. If untreated dysplasia may progress to significant dysplasia, dislocation, early osteoarthritis.
US best to wait until 4-6/52 old due to physiologic ligamentous laxity in 1st few days, can’t use after ~9-12/12 due to shadowing of capital femoral epiphysis obscuring acetabulum. At least 5MHz, scan both hips leaving stress views until last (delaying upsetting baby). Leave harness in situ if present and don’t perform stress maneuvers unless instructed by surgeon (may be difficult to relocate). Centre femoral head by maximising its diameter. Place hypoechoic triradiate cartilage at centre (which is slighly ant to centre of acetabulum with slightly longer ischium post (on axial view).
- Coronal images (standard plane) – supine or lateral decubitus with hip in neutral position (20deg flexed). Straight iliac cortex parallel to transducer, clear acetabular roof, centred femoral head on R of image, incl triradiate cartilage and ant labrum (to see if it is flipped). If ilium concave then too far post, if flares lat (towards transducer) then too far ant. Need to document coronal image at least twice for alpha angle reproducibility. Superior echogenic line of iliac bone should cover at least 50% of femoral head. Acetabular roof should be gently concave; straight is indeterminate, wavy is abnormal. Overlying the femoral head is the labrum, then capsule, then glutenous minimus/medius.
- Alpha angle – straight part of iliac bone to acetabular roof. Normal >60deg (55deg in newborns); reduced/shallow in DDH.
- Beta angle – lateral ilium to inf labrum. Normal <55deg.
- Transverse/axial images extends through centre of femoral head and triradiate cartilage with pubic bone ant and longer ischium post. If too flexed may include greater trochnater ± femoral shaft. Modified Barlow maneuver with hip flexed and adducted, post force. Subluxation causes post-lateral displacement, a normal hip will move by up to 1-2mm.
- If hip is subluxed or dislocated, need to determine if alignment is improved with altering position of femur.
XR only useful when femoral heads start to ossify at ~3/12, should be nonrotated with symphysis pubis and coccyx superimposed. Asymmetrically small ossified epiphysis is nonspecific.
- Hilgenreiner (Y-Y) line extends between acetabular triradiate cartilages.
- Acetabular angle/index between Y-Y line and line from AIIS and triradiate cartilage. Normal <30deg at bith and <22deg at 1yo. Increased with DDH and neuromuscular disorders, decreased with <1yo Down syndrome and skeletal dysplasias.
- Perkins line is perpendicular to Y-Y traversing sup-lat corner of acetabulum. Femoral head should lie medially (and <2-3mm different to contralateral side) or bisect mid 1/3 of metaphysis.
- Reimer’s migration index (usually for hip dysplasia in CP, not DDH) – percentage of transverse ossified capital femoral epiphysis lateral to Perkins line.
- Centre-edge angle measures subluxation, between Perkin’s line and line from AIIS and centre of capital femoral epiphysis. Normal 20deg in infancy, 26-30deg in adolescence.
- Shenton arc should be smooth between medial proximal metaphysis of femur and inferior sup pubic ramus.
Tx harness or spica cast holding hips in flexion, mild abduction and mild external rotation, keeping femoral heads within centre of acetabulum, which will deepen after a few months. Varus osteotomy of the proximal femur enhances hip reduction, which may be fixed with blade plate. Additional derotation osteotomy corrects excesive anteversion. Acetabular osteotomiess increase coverage. Any procedure has risk of AVN.
Chronic Hip Subluxation
Progressive hip subluxation/dislocation in patients with neuromuscular disorders (eg cerebral palsy). XRs to evaluate bony acetabulum coverage (%), degree of coxa valga and presence of dislocation.
Proximal Focal Femoral Deficiency (PFFD)
Congenital hypoplasia/aplasia of proximal femur with shortening, usually centered at intertrochanteric region. Most severe form also has absent acetabulum, femoral head and proximal femur. Varus deformity common. Associated with ipsilateral fibular hemimelia (absent fibula), foot deformity.
Congenital Coxa Vara and Valga
Normal femoral neck shaft angle 150deg at birth, 125deg in adults.
- Congenital coxa vara – limb bud insult, usually stable over time. May be associated with PFFD.
- Infantile/developmental coxa vara – progresses with growth causing limb-length discrepancy. Bilateral in 50%, otherwise usually isolated.
- Acquired coxa vara – from trauma to proximal femoral physis (esp SUFE), metabolic conditions (esp rickets, osteomalacia), tumours, skeletal dysplasias, fibrous dysplasia, Pagets.
- Coxa valga usually from reduced tone of muscles and reduced ambulation, esp cerebral palsy.
Slipped Upper Femoral Epiphysis (SUFE)
(Slipped capital femoral epiphysis, SCFE). Idiopathic SH1 fracture through proximal femoral epihysis with head displaced post-med. 12-15yo, M:F 2.5:1, African Americans, obese, renal osteodystrophy. Period of rapid growth in body weight, muscle strength and femoral neck varus angulation, increasing shear loading. Bilateral in 1/3, but don’t usually present at same time. Frog-leg eiphysis displaced post like icecream falling off the cone. Southwick method angle on frog leg lat between line perpendicular to epiphyseal axis and line along axis of femoral neck to assess tilt. Line of Klein on AP along lat cortex metaphysis should bisect part of the epiphysis. Asymmetric widening of physis, indistinct metaphyseal border of physis, post acetabulum does not overlay medial metaphysis. Tx 3 point pin fixation to prevent further slippage without reduction, causing short and broad femoral neck in varus deformity. Cx avascular necrosis (10%), acute chondrolysis (rare), early OA. May elect to pin contralateral hip to prevent SUFE and maintain symmetric growth.
(Legg-Calve-Perthes disease, LCP). Idiopathic avascular necrosis of the proximal femoral epiphysis. M:F 4:1, whites, 5-8yo. Bilateral in 10%. Associated with skeletal immaturity. Joint effusion -> relatively small ossified femoral epiphysis -> mixed sclerosis and lucencies -> subchondral linear lucency (crescent sign, best seen on frog-leg view, represents fracture through necrotic bone) -> fragmentation and flattening, metaphyseal irregularity and lucent cysts -> short wide femoral neck (coxa magna), flattening and irregularity of acetabulum, physeal arrest, intra-articular bodies -> reduced ROM, early OA. MRI shows high T2 marrow oedema, loss of marrow signal on T1, asymmetric reduced enhancement. Bone scan asymemtric lack of uptake. Prognosis worse with age at diagnosis (less time to remodel), >50% of femoral head involvement, incomplete coverage of femoral head ossification centre by acetabular roof. Tx usually conservative with femoral/acetabular osteotomies if problems develop.
DDx Meyer’s dysplasia – delayed irregular/fragmented ossification of capital femoral epiphysis, 2-4yo, usually bilateral. From hypothyroidism, sickle cell, Gaucher’s disease, epiphyseal dysplasias.
(Toxic synovitis). Most common acute hip pain 3-10yo. Nonspecific inflammation and hypertrophy of the synovium, sterile joint effusion. M:F 2:1. ?From trauma, virus or post-vaccine/drug reaction. Controversial association with Perthes disease. Symptoms subside with rest. Diagnosis of exclusion.
Constitutional disorders of bone (developmental abnormalilty) – diffuse skeletal abnormality including skeletal dysplasias, mucopolysaccharidoses, osteogenesis imperfecta.
Recurrent bleeding into joint -> debilitating arthropathy esp knee, elbow, ankle. Haemosiderin deposits in synovium (dark on T2), hypertrophy, destruction of underlying cartilage. Epiphyseal overgrowth, severe bony irregularity, narrowing of joint spaces, squaring of patella margin, widening of intracondylar notch. Recurrent haematoma may lead to pseudotumours, usually in soft tissues, may cause pressure necrosis and lucency of adjacent bone.
Severe anaemias (sickle cell anaemia, thalassaemia) may cause marrow expansion. Thinning of cortex, coarsened trabeculae, bony remodelling, widened ribs. Widened diploic space of skull with hair-on-end appearance (esp thalasaemia). Sickle cell anaemia may cause bone infarction with sclerotic or lucent lesions; may indent vertebral endplates (‘Lincoln log’/H-shaped appearance). Other features incldue cardiomegaly, gallstones, splenomegaly (or autoinfarction with small calcified spleen in sickle cell), extramedullary haematopoiesis, predisposition to osteomyelitis.
Relative or absolute insufficiency of vitamin D or derivatives from malabsorption, renal disease, or lack of end-organ response. Insufficient conversion of cartilage to mineralised bone, most prominent in rapidly growing bones (esp knees, wrists). Metaphyseal fraying, cupping, physeal margin irregularity, widened physes (provisional zone of calcification). Osteomalacia with unsharp/smudged trabecular markings. Insufficiency fractures (Looser zones), SUFE.
Consumption eg old paint chips, usually <2yo. Broad sclerotic metaphyseal bands (lead lines) in areas of rapid growth (eg knee). DDx normal variant, but this usually spares the proximal fibula.
Indications for evaluating skeletal maturity include short stature, growth hormone deficiency, premature/postmature puberty, preoperative evaluation for surgery (scoliosis, leg length discrepancy). Maturation follows orderly progression, even when accelerated or delayed. Maturation is faster in African descent and girls.
- For <1yo the method of Sontag, Snell and Anderson tabulates number of ossifying secondary growth centres in AP view of 1 upper and 1 lower limb.
- Elgenmark method is similar, utilising only unilateral carpal and tarsal bones.
- Risser tehnique of spines in adolescents utilises iliac crest apophysis which start to ossify lat->med at 4yo; stage 0 no ossification, stage 1 lat 1/4, stage 2 lat 1/2, stage 3 lat 3/4, stage 4 whole apophysis, stage 5 fusion (coninciding with spinal skeletal maturity).
- Single view of L hand with comparison to image standards (Greulich and Pyle study of children of European descent in 1930s) epiphyseal ossification esp distal physes of fingers.
(Radial ray syndrome). Variable hypoplasia/aplasia of radius ± 1st metatarsal or thumb. May be associated with VATER, Holt-Oram syndrome (UL dysplasia, CHD), Fanconi pancytopaenia, thrombocytopaenia-absent radius syndrome.
Idiopathic excessive medial bowing of tibia (tibia vara), usually during infancy ?excessive pressure on medial metaphysis of tibia with physeal injury ?osteochondrosis. Genu varum further incresaes pressure and exacerbation. Irregularity, fragmentation and beaking of medial tibial metaphysis (cf physiological bowing).
- Infantile tibia vara (most common) – toddlers, often bilateral, painless. Normal physiological bowing worsens with weight-bearing (esp early walkers). ?Persistent microtrauma causing fragmentation.
- Adolescent tibia vara – unilateral, painful, milder deformity. ?Trauma or infection causing bony bridging of medial growth plate.
Congenital Foot Deformities
Angles should be evaluated with AP and lateral weight-bearing views.
- Hindfoot equinus/calcaneus – calcaneus usually dorsiflexed; plantarflexed in hindfoot equinus (clubfoot, congenital vertical talus), excessively dorsiflexed in hindfoot calcaneus (pes cavus, spastic deformities).
- Calcaneal pitch – angle between base calcaneus and calcaneus to inf 5th MT, normal 20-30deg.
- Calcaneal-tibial angle – longitudinal axis of tibia and calcaneus normal 60-90deg.
- Hindfoot varus and valgus – talus assumed fixed to tibia, with calcaneus rotated internally (varus) or externally (valgus).
- AP talocalcaneal angle – between longitudinal axes, normal 15-40deg (30-50deg newborns). Midtalar line usually passes through/slightly medial to 1st MT (lat in hindfoot varus and vice versa). Midcalcaneal line through base 4th MT.
- Lateral talocalcaneal angle (Kite’s angle) – angle between long axis of talus and base of calcaneus, normal 25-45deg (50deg newborns). In hindfoot varus the talus cannot be as plantarflexed, reducing this angle; and vice versa.
- Forefoot varus and valgus – On AP normal MTs converge proximally with slight overlap at bases. On lat 2nd MT usually most dorsal, 5th most plantar.
- Forefoot varus/inversion (usually with supination) – On AP forefoot narrowing and increased proximal convergence. On lat ladder-like appearance with 1st MT most dorsal.
- Forefoot valgus/eversion (usually with pronation) – On AP broadening and reduced MT overlap at the bases. On lat MTs more superimposed and 1st MT most plantar.
- Clubfoot (congenital talipes equinovarus, CTEV) – Hindfoot equinus, hindfoot varus and forefoot varus. Most common (1:1000), M:F 2-3:1. ?From ligamentous laxity, muscle imbalance, intrauterine position deformity.
- Rocker bottom foot (congenital vertical talus, talipes equinovalgus) – Hindfoot equinus, hindfoot valgus and forefoot valgus with dorsiflexion, extreme plantarflexion of talus with dorsally dislocated navicular. Rigid flat foot. May be isolated or associated with syndromes (eg myelomeningocoele).
- Flexible flatfoot (pes planovalgus) – Hindfoot valgus and forefoot valgus, no equinus. Physiologic in those <3yo. Common (4%), flexible only seen on weight-bearing radiographs and reduced with non-weightbearing views. DDx apparant flatfoot from genu valgum.
- Pes cavus (high arched foot, congenital claw foot) – Hindfoot calcaneus with compensatory forefoot plantarflexion. May be associated with upper motor neuron lesions (Freidreich’s ataxia), lower motor neuron lesions (polio), vascular ischaemic (Volkmann’s contracture) or peroneal muscular dystrophy (Charcot-Marie-Tooth disease).
- Metatasus adductus – Forefoot adduction/varus with normal hindfoot. Very common, usually bilateral, F>M.
- Acquired bunion most commonly from 1st MT varus and hallux valgus. F>>M, usually from ill-fitting shoes.
Abnormal fibrous (syndesmosis), cartilaginous (synchondrosis) or bony (synostosis) connection between tarsal bones, if not osseous there is close approximation of bones with irregular cortical margins, bone deformity, slcerosis, adjacent marrow oedema. Talar beak – large dorsal osteophyte distal talus, from excess compensatory motion at talonavicular joint. 2% of pop, may have chronic foot pain or propensity for ankle injury, usually presenting in adolescence. Bilateral in 50%. Most isolated due to failure of segmentation in utero; rarely associated with hereditary symphalangism, Apert’s syndrome, hand-foot-uterus syndrome. Tx surgical excision of coalition, casting, arthrodesis.
- Calcaneonavicular coalition – best seen on oblique view with anterior process of calcaneus elongated to navicular (resembling anteater’s nose) with osseous coalition or fragmented slcerotic abnormal joint. Tip of anteior process is squared (normally pointed). Reverse anteater sign with elobgated navicular.
- Talocalcaneal/subtalar coalition – usualy of middle subtalar joint (rarely post facet if more extensive), with fusion of sustentaculum tali of calcaneus to middle subtalar facet. Talar beaking more prominent due to more movement restriction. Poor visualisation of joint space, prominent C-shaped band of overlapping bone over calcaneus (on lat, unreliable), irregularity and sclerosis of middle facet and sustentaculum tali, joint may be dysplastic and orientated obliquely. Better seen on Haris/skier’s view of calcaneus or coronal CT.
If multiple fusions may develop ball-and-socket ankle with spherical talar dome allowing inversion and eversion.
Endothelial malformations divided into haemangiomas and vascular malformations depending on natural history, cellular turnover and histology. Infantile haemangiomas exhibit cellular proliferation, small/absent at birth, rapid growth in infancy and involute during childhood. Vascular malformations are composed of dysplastic vessels, present and birth and grow proportionally with the child, persisting throughout life; categorised into low flow (lymphatic, capillary, venous, mixed vascular malformations) or high flow (arteriovenous malformations and arteriovenous fistula). Tend to infiltrate without respecting fascial planes, often involve multiple tissue types.
Most common tumour of childhood, in 12%. Two-stage progression and regression. At birth usually small/inconspicuous with 60% not visualised. Rapid proliferation lasting up to several months then involution at ~10/12 with 50% resolved completely at 5yo. Mostly in skin esp face/scalp (larger lesiosn are port wine stains). May be associated with VHL. Complications include Kasabach-Merritt syndrome (consumptive coagulopathy), compression of vital sturctures (airway, orbit), fissures, ulceration and bleeding. Imaging usually not required, but may be used for characterisation and extent. Discrete lobular mass, high T2, isointense T1, prominent draining veins (central and peripheral high flow vessels), diffuse enhancement. Proliferative phase has prominent flow voids. Involutional phase has fibrofatty tissue (high T1) and less enhancement. DDx fibrosarcoma, rhabdomyosarcoma.
Dysplalias of small and large venous channels. May cause pain, reduced range of motion, deformity, tend to increase in late childhood or early adulthood. Tx elastic compression, percutaneous sclerosis, surgical excision. Serpentine slow-flowing sturctures, high T2, intermediate T1, phleboliths, enhance.
Chyle-filled cysts lined with endothelium. Most present at birth. Tx percutaneous sclerotherapy or surgical excision. Cystic structures of various sizes (macrocystic to microcystic) with high T2, multiloculated, no central enhancement, fluid-fluid levels.
- Lymphangiomas – hamartomatas or neoplastic. Most in the neck (75%, cystic hygroma) or axilla (25%), other areas mediastinum, retroperitoneum. Tend to increase in size after birth, when they may encroach on other structures.
- Lymphangiectasias – dilated preexisting lymph channels. Usually diffuse swelling of part/all of an extremity, is not progressive.
Direct connections between arterial and venous systems. Exacerbated during puberty and pregnancy, may cause CHF, embolism, pain, bleeding, ulceration. Less common than low-flow malformations. Tangle of multiple flow voids on MR with high flow on gradient echo. Usually no focal discrete soft tissue mass, but may have surrounding oedema or fibrofatty stroma. Arterial doppler waveforms in adjacent venous structures. Tx transarterial embolisation.
Soft Tissue Disorders
Most tumours are benign including vascular, neurogenic, fibroblastic or pseudotumours (haematomas, fat necrosis, lymph nodes). Malignant features include size >50mm, pain, rapid growth, location deep to deep fascia.
Autoimmune disease involving skeletal muscle (esp anterior compartment of thigh, muscles surrounding hip) and skin. Weakness and rash. Increased T2 in involved muscles, myofascial planes and subcutaneous tissues. Typically rapid resolution after therapy. Chronic dermatomyositis -> soft tissue calcifications.
Soft Tissue Malignancy
Primary malignancies are uncommon in children. Infants generally fibrosarcoma, older children rhabdomyosarcoma. Others incldue primitive neruoectodermal tumours (extraskeletal Ewings sarcoma), synovial sarcomas (smooth, well-defined borders)
- Aggressive fibromatosis – fibroproliferative disorder, locally agressive but doesn’t metastasize, usually older children in deep soft tissues; high T2, tend to recur along proximal resection margin.
- Rhabdomyosarcoma – 50% of paediatric soft tissue malignancies. Subtypes include embryonal (younger children, pelvis and neck) or alveolar (adolescents, trunk and extremities). Anywhere in body esp posterior to aorta, vagina, bladder, prostate. DDx Burkett lymphoma which has very rapid doubling time (down to 24hrs).
Benign mass in sternocleidomastoid in neonates with torticollis. Asymmetric fusiform thickening of SCM, heterogeneous echogenicity, asymmetric, variable echogenicity. Most symptoms resolve with stretching exercises.
Typically tender soft tissue mass, ?organising haematoma. Nonspecific enhancing soft tissue mass. Soft tissue calcifications seen after 2-6/52 as sharply circumscribed peripheral egg-shell.
Posttraumatic Fat Necrosis
Minor trauma may cause fat necrosis in subcutaneous tissue. After months there is a firm mass with scar formation. Commonly regions of thin subcutaneous tissue esp anterior tibia, buttocks. MRI linear high T2 with enhancement confined to SC tissues with associated volume loss, no discrete soft tissue mass.
- Subcutaneous granuloma annulare – involves SC tissues anterior to tibia ?related to trauma, with soft tissue mass related to granulation tissue.
Chronic Foreign Body
Palpable, granulation tissue surrounding foreign body. Typically in regions predisposed to trauma including plantar foot, anterior knee, buttocks. Typically low T1 foreign body surrounded by enhancing tissue.