"Congenital & Pediatric Orthopedics" — Practice

Question 1

Which sign is most reliable for developmental dysplasia of the hip in a six-month-old?

Accepted Answer

C

Question 2

In the Ponseti method, which deformity is corrected last?

Accepted Answer

D

Question 3

A 13-year-old obese boy has knee pain and obligate external rotation on hip flexion. What is the treatment?

Accepted Answer

B

Question 4

A 4-year-old cannot bear weight, has a temperature of 39, an ESR of 60 and a white cell count of 15,000. What is the management?

Accepted Answer

C

Question 5

A 3-year-old has knock knees. Parents are anxious. What is the correct advice?

Accepted Answer

B

Question 6

Explain why paediatric orthopaedic treatment is so dominated by timing, using developmental dysplasia of the hip as the example.

Accepted Answer

Because a developing joint is shaped by the forces acting on it, so a period of abnormal position is not merely lost function but altered anatomy.

The acetabulum at birth is shallow. It deepens over the following months and years because a concentric femoral head presses into it, and the depth achieved depends on that pressure being applied in the right place. This is the form-follows-function principle.

If the head is dislocated or subluxed, the acetabulum receives no central stimulus. It stays shallow, the roof becomes oblique, and a false acetabulum may form where the head actually sits. Meanwhile the soft tissues adapt: the capsule becomes hourglass-shaped, the ligamentum teres hypertrophies, the psoas tendon indents the capsule, and the adductors and iliopsoas shorten.

The treatment required therefore escalates with each of these changes. In the first weeks, holding the hip reduced in flexion and abduction with a Pavlik harness is enough, because the acetabulum will then mould itself normally.

By six to eighteen months, contracture prevents simple positioning, so reduction under anaesthesia and a spica cast are needed, and even then the acetabulum may not fully remodel.

Beyond that, the obstacles to reduction must be removed surgically, and the acetabulum is often too deformed to correct itself, so a pelvic osteotomy is added to redirect it.

The same logic operates in clubfoot, in Perthes disease where containment must occur while the head is plastic, and in cerebral palsy hip surveillance. In each case the treatment window is defined by remaining growth.

Question 7

Why is a slipped capital femoral epiphysis fixed in situ rather than reduced, when a displaced fracture elsewhere would be reduced?

Accepted Answer

Because of the blood supply to the femoral head and the way it is arranged around the physis.

The femoral head in a child and adolescent is supplied almost entirely by the retinacular vessels, principally the lateral epiphyseal branches of the medial circumflex femoral artery. These run along the femoral neck beneath the reflected capsule and cross the physis to enter the epiphysis.

In a slip, the epiphysis displaces posteriorly and inferiorly relative to the metaphysis, but it does so gradually in the chronic form, and the retinacular vessels stretch and accommodate. They are usually intact even in a substantial slip, which is why chronic slips do not routinely become avascular.

Forceful reduction moves the epiphysis rapidly back onto the neck, and those same accommodated vessels are kinked, stretched acutely or torn. The reported rate of avascular necrosis after reduction is substantially higher than after in situ fixation, and avascular necrosis in this age group destroys the hip.

The trade-off is therefore explicit. In situ pinning leaves a residual deformity, with a cam-shaped proximal femur that can cause impingement and, in the long term, osteoarthritis. But the deformity is compatible with decades of function and partially remodels, whereas avascular necrosis is not.

An unstable acute slip, in which the child cannot bear weight at all, is a different situation with a much higher intrinsic risk of avascular necrosis, and management there is more contentious.

The general principle worth carrying is that accepting a deformity is correct whenever correcting it threatens the blood supply of the fragment.

Question 8

Explain why the Ponseti method succeeds where extensive surgery had failed, and where it still fails.

Accepted Answer

Because it works with the biology of connective tissue rather than against it.

Clubfoot is not a dislocation to be repositioned but a three-dimensional deformity in which the tarsal bones are malaligned and the medial soft tissues are contracted. The historic surgical approach released those tissues extensively, and the results were poor in the long term: stiff, painful, scarred feet that often needed further operations in adolescence and adulthood.

Ponseti recognised that ligament and tendon respond to sustained gentle stretch by remodelling, and that the tarsal bones themselves reshape as they are held in a corrected position. Weekly manipulation with a cast maintaining the correction achieves progressive change without cutting anything, and the foot ends supple rather than scarred.

The sequence follows the anatomy. The forefoot is supinated first to correct cavus and bring it into line with the hindfoot. The foot is then abducted around the head of the talus, which corrects adductus and varus together because the calcaneus rotates under the talus as a unit. Equinus is corrected last, and because the Achilles tendon consists of dense collagen that responds poorly to stretch, a percutaneous tenotomy is required in most feet. It heals within three weeks in a cast.

Where the method fails is afterwards. The corrected foot has a strong tendency to recur while the child grows, and the foot abduction brace is what prevents it, worn full time for about three months and then at night until four or five.

Compliance is therefore the rate-limiting step, and relapse correlates far more closely with brace wear than with any aspect of the casting.

Question 9

A 7-year-old girl has a painful left thoracic scoliosis that has progressed over six months. Why is this not managed as adolescent idiopathic scoliosis?

Accepted Answer

Because every feature listed is atypical, and each one independently raises the probability of an underlying neurological or structural cause.

Adolescent idiopathic scoliosis is, by definition, a diagnosis of exclusion in an adolescent. It typically begins at the pubertal growth spurt, affects girls disproportionately, and is painless. The curve is most often a right thoracic curve.

This child is seven, which is too young. The curve is painful, which idiopathic curves are not. It is left thoracic, which is the opposite of the usual pattern. And it is progressing rapidly.

Each of these is a recognised red flag, and together they make an underlying cause likely. The commonest are intraspinal abnormalities such as syringomyelia, Chiari malformation, a tethered cord or a spinal cord tumour, all of which distort the neural axis and produce scoliosis secondarily.

Magnetic resonance imaging of the whole spine is therefore mandatory before any treatment decision, because bracing or operating on a curve caused by a syrinx addresses the deformity while leaving the cause to progress.

A full neurological examination is equally important and is frequently abnormal, with asymmetric abdominal reflexes being a classically sensitive early sign of a syrinx.

The other differential is congenital scoliosis from a vertebral malformation such as a hemivertebra, which also presents early and progresses. It carries its own investigation requirement, since the vertebrae form alongside the heart and kidneys and cardiac and renal anomalies are associated.

Only once those are excluded does the question of Cobb angle, Risser grade and bracing arise.

Practice — "Congenital & Pediatric Orthopedics"

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