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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.)

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Pediatric Musculoskeletal radiology

441

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.)

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443

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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.


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