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63

D. Andrew Mong, MD

Pediatric Musculoskeletal radiology

  1.  How does growing bone respond to trauma, and how is this different from mature bone?

The cartilaginous physis separates the epiphysis from the metaphysis. Pediatric ligaments and tendons are relatively 

stronger than growing bone (in contrast to adults). Given an equivalent force applied to growing and mature bone, the 

growing bone has a higher likelihood of fracture. In addition, immature bone has a propensity to bow instead of break, 

which may cause buckles in one side of the cortex (torus fractures) or greenstick fractures (fracture of one cortex and 

bowing of the other). These patterns are not seen in mature bone.

  2.  What is the significance of fractures of the physis?

The cartilaginous physis is vulnerable to injury, especially at its attachment to the metaphysis. Disruption of the physis 

may result in slower growth and premature fusion, leading to limb length discrepancy.

  3.  How are fractures of the physis classified?

Physeal injuries are classified in the Salter-Harris scheme, increasing in severity from I to V. Type I is a fracture through 

the physis. The fracture line in type II includes the metaphysis and physis. Type III fracture includes the epiphysis and the 

physis. Type IV fracture involves the metaphysis, physis, and epiphysis. Type V fracture is a crush injury of the physis. 

Follow-up for Salter-Harris fractures may include magnetic resonance imaging (MRI), which can delineate an abnormally 

fused physis in the healing phase that may need to be disrupted to allow future osseous growth (

Fig. 63-1

).

  4.  What are secondary ossification centers?

Secondary ossification centers appear and then fuse later with the primary ossification center on plain radiographs at 

predictable times during skeletal maturation. Multiple secondary ossification centers are around the elbow and appear 

at different ages. Their usual sequence can be remembered by the mnemonic C-R-I-T-O-E: capitellum (1 year), radial 

head (3 years), internal (medial) epicondyle (5 years), t rochlea (7 years), olecranon (9 years), and external (lateral) 

epicondyle (11 years) (

Fig. 63-2

).

  5.  Why are secondary ossification centers particularly important to understand in the 

setting of elbow trauma?

One important reason to understand this sequence is that a type I Salter-Harris fracture through the physis of the medial 

epicondyle may cause displacement of this ossification center into the region of the trochlea. This displacement might create 

the false impression that the trochlear ossification center is present, whereas the medial epicondylar ossification center has 

not yet appeared. Knowledge of this sequence allows 

one to identify this appearance appropriately as a 

displaced fracture.

  6.  How may subtle supracondylar 

fractures of the elbow be 

diagnosed?

Pediatric elbow fractures often occur in the 

supracondylar region, where the humerus is 

relatively flat. The anterior humeral line, drawn on 

the lateral view of the elbow along the anterior 

humerus, normally intersects the middle third of the 

capitellum. This intersection is likely to be disrupted 

in supracondylar fractures. The presence of a joint 

effusion (hemarthrosis) is also extremely helpful and 

can be assessed by the presence of an elevated 

posterior fat pad, which is displaced and visible on the 

lateral view if there is blood in the joint. Displacement 

of the anterior fat pad (“sail” sign) may also be seen 

with hemarthrosis, but this finding is less specific.

Normal

I

II

III

IV

V

Figure 63-1. 

Salter-Harris fractures of the distal femur.

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Pediatric Musculoskeletal radiology

  7.  Describe nursemaid’s elbow.

Nursemaid’s elbow is caused by radial head 

subluxation through the annular ligament of the 

elbow, resulting in abnormal positioning of the 

ligament between the radial head and capitellum. It 

is often caused by sudden traction on the forearm 

in a child 1 to 3 years old. Radiographs may 

have normal results, but are obtained to exclude 

fractures.

  8.  List risk factors for developmental 

dysplasia of the hip (DDH).

•

White race

•

Female gender

•

Torticollis

•

Clubfoot

•

Breech birth

  9.  When is DDH suspected clinically?

It is difficult to diagnose DDH in newborns 4 weeks 

old or younger because of normal joint laxity, but 

this condition is suspected in infants with leg length discrepancy and asymmetric thigh creases. The Barlow maneuver 

on physical examination dislocates the femoral head rearward, and the Ortolani maneuver reduces the recently 

dislocated hip, often with a resultant “clunk.”

 10.  Name the potential complications of untreated DDH.

•

Leg length discrepancy

•

Osteoarthritis

•

Pain

•

Gait disturbance

•

Decrease in agility

 11.  How is DDH diagnosed radiographically?

Traditionally, plain films have been used to diagnose DDH. Although the femoral head begins to ossify during the 

first year (usually between 3 and 6 months), its location must be inferred in infants. The acetabulum is divided 

into quadrants by the horizontal Hilgenreiner line, drawn through both triradiate cartilages, and the vertical 

Perkin line, drawn through the lateral rim of the acetabulum. A normal femoral head should fall within the inner 

lower quadrant of these intersecting lines, whereas a femoral head in DDH would be displaced superolaterally. 

The acetabular angle should also be evaluated, drawn between Hilgenreiner line and a line connecting the 

superolateral ridge of the acetabulum with the triradiate cartilage. This angle should be less than 30 degrees in 

neonates.

 12.  How is DDH diagnosed on ultrasound (US)?

US is now the preferred method of diagnosing DDH in children younger than 1 year old. The hip is studied in the coronal 

plane. The alpha angle is measured between the straight lateral margin of the ilium and a line from the inferior point of 

the ilium tangential to the acetabulum. This is a measure of acetabular depth and should be greater than 60 degrees.  

At least half of the femoral head should be seated within the acetabulum.

 13.  What is Legg-Calvé-Perthes disease?

Legg-Calvé-Perthes disease refers to idiopathic osteonecrosis of the femoral head, usually affecting children 3 

to 12 years old with a mean age of 7 years. Plain radiographic findings include a small femoral head epiphysis, 

which may become fragmented, and widening of the articular space, which may be due to an associated joint 

effusion.

 14.  Describe slipped capital femoral epiphysis (SCFE).

SCFE is a hip disease of early adolescence (10 to 15 years old), characterized by idiopathic posterior and inferior 

slippage of the capital femoral epiphysis on the femoral neck metaphysis. Complications include avascular necrosis 

of the femoral head or chondrolysis. Anteroposterior and frog-leg views of both hips should be obtained because the 

condition can be bilateral in 40% of cases. On the frog-leg view, a normal epiphysis projects superior to Klein line, 

which is drawn along the superior surface of the femoral neck. In early SCFE, the epiphysis is flush with this line  

(see 

Fig. 63-2

).

Figure 63-2. 

Frog-leg view of the left hip shows open physis with 

inferior displacement of the femoral capital epiphysis compared with the 

metaphysis. (Courtesy of Richard Markowitz, MD, Children’s Hospital of 

Philadelphia.)

Pediatric Musculoskeletal radiology

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Pediatric radiology

 15.  How is SCFE treated?

Treatment goals include the prevention of further slippage and physeal plate closure. SCFE may be treated with internal 

fixation, bone graft, osteotomy, and cast immobilization. There is no attempt to reduce the slip because this may cause 

avascular necrosis.

 16.  What are coxa vara and coxa valga?

Coxa vara and coxa valga are abnormalities of the femoral shaft-to-neck ratio. The normal ratio is 150 degrees at birth, 

decreasing to 120 to 135 degrees in adults. Coxa vara is an angle less than 120 degrees and may be secondary to 

trauma, tumor, SCFE, or a congenital abnormality. Coxa valga (>150 degrees) is usually neuromuscular in origin but may 

also be seen in blood dyscrasias such as thalassemia.

 17.  Describe Blount disease.

Blount disease is a varus deformity of the knee (i.e., the tibia is abnormally directed medially compared with the femur), 

resulting from growth disturbance of the medial aspect of the proximal tibial metaphysis. This deformity may occur in 

infants, in which case it is often bilateral, or in adolescents. Tibial osteotomy may be required for treatment because 

growth disturbance may result from abnormal tibial bowing.

 18.  What is Osgood-Schlatter disease?

Osgood-Schlatter disease is a common cause of knee pain in adolescence (11 to 14 years old) that is thought to 

result from repetitive traction through the patellar tendon onto the developing tibial tubercle. This traction can lead to 

partial avulsion through the ossification center and heterotopic bone formation. Although the diagnosis may be made 

clinically, radiographs may aid in the exclusion of other etiologies of knee pain. Lateral radiographs may reveal irregular 

ossification of the proximal tibial tubercle, calcification and thickening of the patellar tendon, and soft tissue swelling.

 19.  What is the difference between a triplane fracture and a juvenile Tillaux fracture  

of the ankle?

Both fractures occur after partial closure of the distal tibial physis. On frontal radiographs, a triplane fracture appears 

as a Salter III fracture through the epiphysis, and on the lateral radiograph, it appears as a Salter II fracture through the 

metaphysis. A juvenile Tillaux fracture is simply a Salter III fracture that occurs at the anterolateral aspect of the distal 

tibia. The physis fuses from medial to lateral, leaving the lateral aspect more vulnerable to injury.

 20.  What is Freiberg infraction?

Freiberg infraction is an idiopathic osteochondrosis of the head of a metatarsal bone (usually the second), which results 

in flattening and osteosclerosis of the metatarsal head. It is usually seen in adolescents (13 to 18 years old).

 21.  What are craniosynostoses?

A craniosynostosis represents premature closure of 

a suture of the skull. This premature closure results 

in cessation of growth of the skull perpendicular to 

the suture line and abnormal compensatory growth 

along the axis of the closed suture. For this reason, 

sagittal craniosynostosis results in an elongated skull 

in the anteroposterior dimension (scaphocephaly) 

(

Fig. 63-3

). Plagiocephaly results from premature 

closure of one coronal suture, resulting in abnormal 

bulging on the opposite forehead. Premature closure 

of the metopic suture results in trigonocephaly, 

which appears as a triangular keel-shaped forehead. 

Cloverleaf skull (kleeblattschädel) results from 

premature closure of the coronal, lambdoid, and 

posterior sagittal sutures, with bulging of the vertex 

of the brain through the squamosal, anterior sagittal, 

and metopic sutures.

Key Points: Characteristic Ages of Pediatric Hip Disorders

1.  Developmental dysplasia is a disorder of infants.

2.  Legg-Calvé-Perthes disease occurs in children 3 to 12 years old.

3.  SCFE occurs in children 10 to 15 years old. This disorder cannot occur after 

the physes have fused.

Figure 63-3. 

Markedly increased anteroposterior diameter from 

premature closure of sagittal suture, creating a boat-shaped skull, or 

scaphocephaly.

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Pediatric Musculoskeletal radiology

 22.  Give the differential diagnosis for vertebra plana.

Flattening of a vertebral body (vertebra plana) in a child should first bring to mind the diagnosis of Langerhans cell 

histiocytosis. Other diagnostic possibilities in pediatric patients include leukemia, lymphoma, metastatic disease, 

infection, and storage diseases.

 23.  When and where do pediatric primary tumors of bone occur?

Ewing sarcoma and osteosarcoma are the most common primary pediatric bone tumors and typically occur 

between ages 10 and 25 years. The most common sites are the pelvis, thigh, lower leg, upper arm, and ribs, but soft 

tissue may also be the primary site of involvement. Ewing sarcoma typically does not have a matrix and appears 

as a permeative aggressive lesion, often with associated periosteal reaction. Most osteosarcomas occur in the 

metaphysis, typically around the knee. Although the appearance of osteosarcomas is variable, they often produce a 

characteristic fluffy osteoid matrix.

 24.  How should a suspected osteoid osteoma be evaluated?

Osteoid osteoma is a benign neoplasm with a nidus of osteoid-rich tissue that typically causes an intense sclerotic 

reaction in surrounding bone. An osteoid osteoma may occur in the cortical, cancellous, or periosteal regions of 

any bone (or rarely in adjacent soft tissues). Most patients are between ages 10 and 30 years and often give a 

typical history of night pain relieved by aspirin. Radionuclide bone scan may point to the abnormality before any 

changes are apparent on plain film and should be performed on any patient with a painful scoliosis in whom 

osteoid osteoma in the spine is the working diagnosis. If plain films do not reveal the lucent nidus surrounded by 

sclerotic bone, a computed tomography (CT) scan is the preferred next step because intracortical tumors may be 

missed on MRI.

 25.  What is rickets?

Rickets is a relative or absolute deficiency in vitamin D, which causes a decrease in ossification. It is almost exclusively 

seen in children younger than 2 years.

 26.  How does rickets appear 

radiographically?

Bone density is overall decreased. More specific 

signs include loss of the zone of provisional 

calcification within the metaphysis of long bones; 

this leads to metaphyseal irregularity, cupping, and 

fraying with an associated widened physis. These 

changes are seen best in the distal radius, which 

is why films of the wrists are ordered to evaluate 

rickets (

Fig. 63-4

). Another classic appearance is 

the “rachitic rosary,” which is enlargement of the 

costochondral joints in the chest.

 27.  Describe the bony changes of sickle 

cell anemia.

Sickle cell anemia is secondary to a disorder 

of “sickling” of red blood cells resulting from 

abnormal hemoglobin molecules. Clumped, 

sickled cells form venous (and sometimes 

arterial) thromboses, affecting multiple organs. 

Osseous manifestations include patchy sclerotic 

changes in bone from infarctions. A more 

specific sign includes a “Lincoln log” appearance 

of the vertebral bodies, with squarelike 

depressions seen in the superior and inferior end 

plates on a lateral spine film. Avascular necrosis 

of the hips may also be seen. Affected patients 

are prone to osteomyelitis from Staphylococcus aureus and Salmonella. On MRI, it can be difficult to distinguish 

infarction from osteomyelitis because both may produce signal abnormalities in marrow (bright T2 signal) along 

with adjacent soft tissue changes. Dactylitis is a nonspecific term referring to inflammation of a digit, which may 

also be seen in sickle cell anemia and be secondary to infarction or infection. Finally, because of the chronic 

anemia, patients with sickle cell anemia have an increased red-to-yellow marrow ratio, which may be inferred on 

a lateral skull radiograph by the widening of the diploic space (

Fig. 63-5

).

Figure 63-4. 

Frontal plain film of the hand shows cupping and fraying 

of metaphyses (arrows) from rickets. (Courtesy of Richard Markowitz, 

MD, Children’s Hospital of Philadelphia.)

Pediatric Musculoskeletal radiology

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Pediatric radiology

28.   What is the most common type 

of dwarfism, and what are its 

manifestations?

 

 The most common type of dwarfism is 

achondroplasia. This is a rhizomelic (shortening 

of the proximal bones) autosomal dominant 

disorder. Typical characteristics include a large 

head with frontal bossing, a trident configuration 

of the hands, genu varum (bowed legs), and 

an exaggerated lumbar lordosis (with posterior 

scalloping of the vertebral bodies). On a frontal 

radiograph of the lumbosacral spine in a normal 

patient, the distance between the pedicles 

gradually widens from L1 to L5, whereas an 

achondroplastic dwarf shows a decrease in the 

interpedicular distance of the caudal spine. Other 

radiographic findings include a notchlike sacroiliac 

groove and metaphyseal flaring of the long bones.

29.   What is the differential diagnosis 

for dense metaphyseal bands? 

How does one know when they are 

abnormally dense?

 Dense metaphyseal bands may be a normal 

variant, so it is important to look at areas that do 

not have a lot of bone turnover to see whether they 

are affected as well. Specifically, the metaphyses 

of the fibula are good areas to check. A major 

concern is heavy metal poisoning (specifically lead intoxication). Lead poisoning can be diagnosed by noting not 

only the metaphyseal bands, but also the radiopaque lead chips seen on a frontal plain view of the abdomen floating 

in the child’s intestines. Other etiologic factors include stress lines, treated rickets, scurvy, hypervitaminosis D, or 

treated leukemia.

B

iBliography

[1]  S.P. England, S. Sundberg, Management of common pediatric fractures, Pediatr. Clin. North Am. 43 (1996) 991–1012.

[2]  S.C. Kao, W.L. Smith, Skeletal injuries in the pediatric patient, Radiol. Clin. North Am. 35 (1997) 727–746.

[3]  E. Lemyre, E.M. Azouz, A.S. Teebi, et al., Bone dysplasia series: achondroplasia, hypochondroplasia and thanatophoric dysplasia: review 

and update, Can. Assoc. Radiol. J. 50 (1999) 185–197.

[4]  R.E. Lins, R.W. Simovitch, P.M. Waters, Pediatric elbow trauma, Orthop. Clin. North Am. 30 (1999) 119–132.

Figure 63-5. 

Sagittal T1-weighted MR image of the brain shows 

widening of the diploic space (arrows) of the skull from marrow 

expansion in a patient with sickle cell anemia. This finding is not specific 

for sickle cell anemia and may be found in other severe anemias, such 

as thalassemia or iron deficiency anemia.