PEDIATRIC MUSCULOSKELETAL RADIOLOGY
63
D. Andrew Mong, MD
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), trochlea (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
Normal III
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
IIIIVV
of the anterior fat pad ( sail sign) may also be seen
with hemarthrosis, but this finding is less specific.
Figure 63-1. Salter-Harris fractures of the distal femur.
439
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H A P T E R
440 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
Figure 63-2. Frog-leg view of the left hip shows open physis with
inferior displacement of the femoral capital epiphysis compared with the
9. When is DDH suspected clinically?
metaphysis. (Courtesy of Richard Markowitz, MD, Children s Hospital of
It is difficult to diagnose DDH in newborns 4 weeks
Philadelphia.)
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).
PEDIATRIC RADIOLOGY 441
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.
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
Figure 63-3. Markedly increased anteroposterior diameter from
of the brain through the squamosal, anterior sagittal,
premature closure of sagittal suture, creating a boat-shaped skull, or
and metopic sutures.
scaphocephaly.
442 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
Figure 63-4. Frontal plain film of the hand shows cupping and fraying
of the vertebral bodies, with squarelike
of metaphyses (arrows) from rickets. (Courtesy of Richard Markowitz,
depressions seen in the superior and inferior end MD, Children s Hospital of Philadelphia.)
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).
PEDIATRIC RADIOLOGY 443
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?
Figure 63-5. Sagittal T1-weighted MR image of the brain shows
widening of the diploic space (arrows) of the skull from marrow
Dense metaphyseal bands may be a normal
expansion in a patient with sickle cell anemia. This finding is not specific
variant, so it is important to look at areas that do
for sickle cell anemia and may be found in other severe anemias, such
not have a lot of bone turnover to see whether they
as thalassemia or iron deficiency anemia.
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.
BIBLIOGRAPHY
[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.
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