By the end of this chapter you'll be able to…

  • 1State the three properties that distinguish a growing skeleton and their consequences
  • 2Predict which deformities remodel and which do not
  • 3Explain how form follows function in joint development and why timing dominates treatment
  • 4List the mechanical risk factors for developmental dysplasia of the hip
  • 5Explain why swaddling practice matters in South Asia
  • 6Select the correct hip examination for a given age
  • 7Choose between ultrasound and radiograph by the state of ossification
  • 8Explain why excessive abduction in a Pavlik harness causes avascular necrosis
  • 9State the current position on universal against selective hip screening
  • 10Sequence Ponseti correction using CAVE and explain why equinus is last
  • 11Explain why Ponseti relapse is a bracing failure
  • 12Explain the containment principle in Perthes disease
  • 13Recognise slipped capital femoral epiphysis and explain why reduction is avoided
  • 14Apply the Kocher criteria and justify urgency in septic arthritis of the hip
  • 15Distinguish physiological angular and torsional variants from pathology
  • 16Distinguish postural from structural scoliosis and identify atypical features
  • 17Recognise congenital muscular torticollis and its associations
  • 18Explain the orthopaedic consequences of cerebral palsy and the need for hip surveillance
  • 19Recognise osteogenesis imperfecta and achondroplasia and their principal dangers
  • 20Explain why radial club hand requires systemic investigation
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Why this chapter matters in NEET PG
Paediatric orthopaedics is not adult orthopaedics scaled down. A child's bone behaves differently, heals differently, deforms differently and corrects differently, and the reasons are structural rather than incidental. Almost every difference follows from three properties of a growing skeleton, and holding those three converts a long list of eponymous conditions into a small set of consequences. Clinically the field is dominated by timing, because a joint held in the wrong position does not merely function badly but forms badly, so the same abnormality treated at six weeks, six months and six years needs a harness, an operation and a reconstruction respectively.

Congenital & Pediatric Orthopedics

Paediatric orthopaedics is not adult orthopaedics scaled down. A child's bone behaves differently, heals differently, deforms differently and corrects differently, and the reasons are structural rather than incidental.

Almost every difference follows from three properties of a growing skeleton, and holding those three converts a long list of eponymous conditions into a small set of consequences.

1. The Growing Skeleton Is Different

PropertyConsequence
The physisLongitudinal growth, but also a weak plane and a structure that can be permanently damaged
Thick, strong periosteumFractures are often incomplete, and it acts as a hinge during reduction
Remodelling capacityAngulation near a growth plate corrects itself, and rotation does not

The physis is both the opportunity and the danger. Because a child grows, an imperfect reduction may remodel to normal. Because the physis can be injured or tethered, an insult produces progressive deformity that worsens with every year of remaining growth.

The rule that follows is used constantly. Angulation in the plane of joint movement, close to an active physis, in a young child, remodels well. Rotational malalignment does not remodel at any age.

2. Form Follows Function

The second organising idea concerns the joints rather than the bones.

A joint is moulded by its own use during development. The acetabulum deepens because a concentric femoral head presses into it. The foot achieves its shape because it is loaded in a particular position.

The consequence is that a joint held in the wrong position does not simply function badly; it forms badly, and the deformity becomes structural.

This is why paediatric orthopaedics is so preoccupied with time. The same abnormality treated at six weeks, six months and six years requires a harness, an operation and a reconstruction respectively, and the outcomes differ correspondingly.

3. Developmental Dysplasia of the Hip

The name changed from congenital dislocation because the condition is a spectrum and because it can develop after birth rather than always being present at it.

The spectrum runs from a shallow but located acetabulum, through a hip that can be dislocated, to one that is dislocated and finally to one that is irreducibly dislocated.

Risk factors are mechanical. Breech presentation, female sex, first-born status, oligohydramnios and a family history all reduce the space or the tone available for normal hip development. The left hip is affected most often, because it lies against the maternal spine in the usual fetal position.

Swaddling with the hips extended and adducted is an important and preventable cause, which matters in India and across South Asia where tight swaddling is traditional. Hip-healthy swaddling leaves the legs free to flex and abduct.

Examining the hip

Ortolani and Barlow tests work only in the first weeks. Ortolani relocates a dislocated hip with a palpable clunk, and Barlow dislocates a located but unstable one.

After about three months both become unreliable, because the soft tissues contract and the hip can no longer be moved in or out of the socket.

Limited abduction then becomes the most reliable sign, along with the Galeazzi sign of apparent femoral shortening with the hips and knees flexed, and asymmetric thigh creases, which are common in normal infants and unreliable alone.

Imaging and treatment

Ultrasound is the investigation before the femoral head ossifies, which occurs at around four to six months, and the Graf method measures the alpha angle of acetabular coverage. After ossification a plain radiograph is used, assessed with Hilgenreiner and Perkin lines, Shenton line and the acetabular index.

Treatment is by age. Under six months, a Pavlik harness holds the hips flexed and abducted, allowing the acetabulum to remodel around a reduced head. Excessive abduction must be avoided, because it compresses the femoral head against the acetabular margin and causes avascular necrosis.

Between six and eighteen months, closed reduction under anaesthesia with a hip spica is usual. Beyond that, open reduction with femoral or pelvic osteotomy is required.

Whether all infants should have ultrasound screening remains unsettled. A 2025 evidence review found that universal screening increased non-surgical intervention without a corresponding reduction in late-presenting dysplasia or in the need for surgery, so the balance against overtreatment is genuinely unclear.

4. Congenital Talipes Equinovarus

Clubfoot is a fixed structural deformity present at birth, and its components are remembered as CAVE.

ComponentDeformity
CavusHigh medial arch
AdductusForefoot turned inward
VarusHeel turned inward
EquinusAnkle plantar flexed

The order matters, because Ponseti correction follows exactly that sequence. Cavus is corrected first by supinating the forefoot to align it with the hindfoot, then adductus and varus are corrected together by abducting the foot around the talar head, and equinus is corrected last.

Correcting equinus before the other components produces a rocker-bottom foot, because the midfoot breaks rather than the ankle dorsiflexing.

The Ponseti method is weekly manipulation and casting, typically around five casts, followed by percutaneous Achilles tenotomy in the majority of feet to complete the equinus correction, then a foot abduction brace.

Indian series report excellent results. A recent tertiary centre study of 550 feet achieved full correction in 94.7 percent, required tenotomy in 77.2 percent, needed a mean of 5.18 casts, and had residual deformity in 5.3 percent.

The single most important teaching point is that relapse is a bracing problem, not a casting problem. The correction achieved by casting is reliable; what fails is brace wear, which must continue full time for around three months and then at night until the age of four or five. Families who stop early are the families whose children relapse.

5. Perthes Disease

Perthes disease is idiopathic osteonecrosis of the femoral head in a growing child, typically between four and eight years and far commoner in boys.

Presentation is a painless or minimally painful limp, and the pain, when present, is often felt at the knee, because the obturator nerve supplies both the hip joint and the medial knee.

The disease passes through necrosis, fragmentation, reossification and remodelling over two to four years, and the femoral head is soft and deformable during the fragmentation phase.

The principle of treatment is containment, meaning keeping the femoral head seated deeply within the acetabulum so that the acetabulum acts as a mould while the head is plastic. This is achieved by maintaining abduction, with bracing or with femoral or pelvic osteotomy.

Prognosis worsens with older age at onset, because there is less remaining growth in which to remodel, and with greater involvement of the lateral pillar of the femoral head.

6. Slipped Capital Femoral Epiphysis

Here the epiphysis slips off the metaphysis through the physis, and the classical patient is an overweight adolescent around the time of the growth spurt.

Hypothyroidism, growth hormone deficiency and renal osteodystrophy are recognised endocrine associations, and they should be considered particularly in a child who is younger or thinner than expected.

The presentation is again hip or knee pain with a limp, and knee pain in an adolescent must prompt hip examination.

The most useful clinical sign is obligate external rotation on hip flexion, since the slipped head forces the limb to rotate outward as the hip is flexed.

Radiographically, Klein's line drawn along the superior femoral neck should intersect part of the epiphysis, and fails to do so in a slip, and a frog-leg lateral view is essential because early slips are missed on the anteroposterior film alone.

Treatment is in situ pinning, and reduction of the slip is avoided because it disrupts the retinacular vessels and precipitates avascular necrosis. Accepting the deformity and stabilising the physis is safer than correcting it.

7. The Limping Child

The differential is organised by age and by the presence of fever, and the one diagnosis that cannot be missed is septic arthritis.

Septic arthritis of the hip is a surgical emergency, because pus under pressure in a joint with an intracapsular blood supply destroys articular cartilage within days and can infarct the femoral head.

Transient synovitis is the common mimic, following a viral illness, with a child who is systemically well and can usually still bear weight.

The Kocher criteria separate them: inability to bear weight, fever above 38.5 degrees, erythrocyte sedimentation rate above 40, and white cell count above 12,000. The probability of septic arthritis rises steeply as more criteria are met, approaching certainty when all four are present.

Aspiration is the definitive investigation, and treatment is urgent surgical drainage with antibiotics.

8. Variants That Are Not Disease

A large proportion of paediatric orthopaedic referrals are normal variants, and recognising them prevents unnecessary intervention.

Genu varum is physiological up to about two years, after which the legs pass through a valgus phase peaking around three to four years and settle by about seven.

Blount disease is the pathological version of varus, occurring in overweight children with medial metaphyseal beaking of the proximal tibia, and unlike physiological bowing it progresses.

Rickets is the other cause of pathological bowing and must be excluded biochemically.

In-toeing has three causes distinguished by age. Metatarsus adductus presents in infancy, internal tibial torsion in the toddler, and increased femoral anteversion in the older child who characteristically sits in a W position.

All three usually resolve without treatment, and the historical use of braces and special shoes has been abandoned because they do not alter the natural history.

9. Scoliosis and Torticollis

Scoliosis is a lateral curvature of the spine with rotation, and the rotation is what makes it visible.

The Adams forward bend test detects the rib hump, because bending forward removes the compensatory posture and displays the vertebral rotation as an asymmetric prominence of the rib cage.

A postural curve disappears on forward bending; a structural curve does not, and that single distinction separates the child who needs observation from the one who needs a radiograph.

The Cobb angle measures the curve on a standing radiograph, drawn between the endplates of the most tilted vertebrae at each end.

Skeletal maturity determines what happens next, because a curve progresses while growth remains. The Risser sign grades ossification of the iliac apophysis from zero to five, and a low Risser grade in a child still growing predicts progression.

Adolescent idiopathic scoliosis is the commonest form, affects girls disproportionately at the pubertal growth spurt, and is painless. Pain, a left thoracic curve, or a rapidly progressive curve in a young child are all atypical and require magnetic resonance imaging, because they suggest an underlying spinal cord abnormality such as syringomyelia or a tethered cord.

Broadly, curves under about twenty degrees are observed, moderate curves in a growing child are braced to prevent progression rather than to correct, and large curves are treated surgically.

Congenital scoliosis is different in origin and behaviour, arising from vertebral malformation such as a hemivertebra, presenting earlier, and associated with cardiac and renal anomalies that must be sought because they share an embryological window.

Congenital muscular torticollis

The sternocleidomastoid is fibrotic and shortened, so the head tilts towards the affected side and the chin turns away from it.

A firm swelling within the muscle may be palpable in early infancy. Most cases respond to stretching physiotherapy, and the associated conditions to look for are plagiocephaly from positional moulding and developmental dysplasia of the hip, which shares the intrauterine crowding mechanism.

10. Neuromuscular and Genetic Conditions

Cerebral palsy produces orthopaedic problems through muscle imbalance rather than through primary bone disease. Spastic muscles overpower their antagonists, joints are held in abnormal positions, and the bone and joint deform accordingly, which is the same form-follows-function principle stated earlier.

Hip surveillance is essential in cerebral palsy, because progressive hip displacement is common, painless until late, and far easier to prevent than to reconstruct.

Osteogenesis imperfecta results from defective type I collagen, giving fragile bones, blue sclerae, dentinogenesis imperfecta and conductive hearing loss. Bisphosphonates reduce fracture rates. It is the most important differential for non-accidental injury in a child with multiple fractures.

Achondroplasia results from a gain-of-function mutation in FGFR3, is autosomal dominant with most cases arising de novo, and produces rhizomelic shortening with a trident hand.

The danger in infancy is foramen magnum stenosis, which can cause central apnoea and sudden death, while spinal stenosis is the problem of later life.

Limb anomalies worth recognising

Radial club hand is a longitudinal deficiency of the radius, with the wrist deviated radially and the thumb hypoplastic or absent, and it is the one limb anomaly that mandates systemic investigation.

The reason is that the radius forms during the same embryological window as the heart, the kidneys and the marrow, so associations include the VACTERL group, Holt-Oram syndrome with cardiac septal defects, Fanconi anaemia and thrombocytopenia with absent radius. Finding the hand should prompt echocardiography, renal imaging and a blood count.

Sprengel deformity is congenital failure of scapular descent, leaving a small high scapula that limits abduction, sometimes tethered to the cervical spine by an omovertebral bar.

Polydactyly and syndactyly are the commonest congenital hand anomalies, and the practical point is timing: separation of fused digits is undertaken early enough to prevent the growing bones deviating around one another.

11. Worked Examples

Example 1. A 5-month-old girl born breech has limited abduction of the left hip and apparent shortening of the left femur on the Galeazzi test. What imaging and treatment?

Developmental dysplasia of the hip. At five months the femoral head may not yet be ossified, so ultrasound is appropriate, with a radiograph if ossification has occurred. Ortolani and Barlow tests are unreliable at this age because the soft tissues have contracted, which is why limited abduction is the more useful sign. A Pavlik harness is used under six months, avoiding excessive abduction, which causes avascular necrosis.

Example 2. A newborn has bilateral clubfeet. The parents ask why the ankle deformity is corrected last.

Because correcting equinus first breaks the midfoot rather than dorsiflexing the ankle, producing a rocker-bottom deformity. The Ponseti sequence follows CAVE: cavus is corrected first by supinating the forefoot to align it with the hindfoot, then adductus and varus together by abducting the foot around the talar head, and equinus last, usually assisted by percutaneous Achilles tenotomy. Relapse afterwards is almost always a failure of brace wear rather than of casting.

Example 3. A 13-year-old obese boy has knee pain and a limp. Hip flexion produces obligate external rotation. What is the diagnosis and why is reduction avoided?

Slipped capital femoral epiphysis. Knee pain in an adolescent must prompt hip examination, because the obturator nerve refers hip pain to the medial knee. Obligate external rotation on flexion is the characteristic sign, and a frog-leg lateral radiograph is required since early slips are missed on the anteroposterior view. Treatment is in situ pinning; forceful reduction disrupts the retinacular blood supply and causes avascular necrosis.

Example 4. A 4-year-old cannot bear weight, has a temperature of 39 degrees, an erythrocyte sedimentation rate of 60 and a white cell count of 15,000. Diagnosis and management?

All four Kocher criteria are met, so septic arthritis of the hip is near certain. This is a surgical emergency, because pus under pressure destroys articular cartilage within days and can infarct the femoral head through its intracapsular vessels. Urgent aspiration confirms the diagnosis and surgical drainage with antibiotics follows. Transient synovitis would present in a systemically well child who can usually still bear weight.

Summary

The growing skeleton differs by three properties: a physis, a thick periosteum and remodelling capacity.

Angulation near an active physis remodels; rotation never does.

Form follows function, so a joint held wrongly forms wrongly, which is why timing dominates treatment.

Developmental dysplasia is a spectrum with mechanical risk factors, and tight swaddling with extended hips is a preventable cause.

Ortolani and Barlow work only in the first weeks; limited abduction is the later sign.

Ultrasound before ossification, radiograph after, and avoid excessive abduction in a Pavlik harness.

Clubfoot corrects in the CAVE order, and equinus last to avoid a rocker-bottom foot.

Ponseti relapse is a bracing failure, not a casting failure.

Perthes is treated by containment, using the acetabulum as a mould while the head is plastic.

Knee pain in a child can be hip disease, through the obturator nerve.

Slipped epiphysis is pinned in situ, because reduction causes avascular necrosis.

Four Kocher criteria make septic arthritis near certain, and the hip is a surgical emergency.

Bowing before two and knock knees at three are normal; Blount disease progresses.

Adams forward bending separates postural from structural scoliosis, and pain or a left thoracic curve requires magnetic resonance imaging.

Congenital muscular torticollis tilts the head towards the lesion and turns the chin away, and it accompanies hip dysplasia and plagiocephaly.

Radial club hand demands a heart, a kidney and a blood count, since the radius forms in the same window as all three.

Osteogenesis imperfecta is the key differential for non-accidental injury.

In achondroplasia the infant danger is foramen magnum stenosis.

Key formulas & results

Everything to memorise for the exam hall, in one card. Screenshot this for revision.

The organising tool
A GROWING SKELETON HAS THREE PROPERTIES AN ADULT SKELETON LACKS. THE PHYSIS gives LONGITUDINAL GROWTH BUT ALSO A WEAK PLANE AND A STRUCTURE THAT CAN BE PERMANENTLY DAMAGED. A THICK STRONG PERIOSTEUM makes FRACTURES OFTEN INCOMPLETE AND ACTS AS A HINGE DURING REDUCTION. REMODELLING CAPACITY means ANGULATION NEAR A GROWTH PLATE CORRECTS ITSELF.
THE PHYSIS IS BOTH THE OPPORTUNITY AND THE DANGER. Because a child grows, AN IMPERFECT REDUCTION MAY REMODEL TO NORMAL. Because the physis can be injured or tethered, AN INSULT PRODUCES PROGRESSIVE DEFORMITY THAT WORSENS WITH EVERY YEAR OF REMAINING GROWTH.
The remodelling rule
ANGULATION IN THE PLANE OF JOINT MOVEMENT, CLOSE TO AN ACTIVE PHYSIS, IN A YOUNG CHILD, REMODELS WELL. ROTATIONAL MALALIGNMENT DOES NOT REMODEL AT ANY AGE.
This is used constantly in deciding what degree of residual deformity is acceptable after reduction, and the rotational exception is the one candidates forget, because it feels as though a growing bone should correct everything.
Form follows function
A JOINT IS MOULDED BY ITS OWN USE DURING DEVELOPMENT. THE ACETABULUM DEEPENS BECAUSE A CONCENTRIC FEMORAL HEAD PRESSES INTO IT. A JOINT HELD IN THE WRONG POSITION DOES NOT SIMPLY FUNCTION BADLY; IT FORMS BADLY, AND THE DEFORMITY BECOMES STRUCTURAL.
This is why paediatric orthopaedics is SO PREOCCUPIED WITH TIME. THE SAME ABNORMALITY TREATED AT SIX WEEKS, SIX MONTHS AND SIX YEARS REQUIRES A HARNESS, AN OPERATION AND A RECONSTRUCTION RESPECTIVELY, AND THE OUTCOMES DIFFER CORRESPONDINGLY.
The dysplasia spectrum and its risk factors
The spectrum runs from A SHALLOW BUT LOCATED ACETABULUM, through A HIP THAT CAN BE DISLOCATED, to ONE THAT IS DISLOCATED and finally ONE THAT IS IRREDUCIBLY DISLOCATED. RISK FACTORS ARE MECHANICAL: BREECH PRESENTATION, FEMALE SEX, FIRST-BORN STATUS, OLIGOHYDRAMNIOS AND FAMILY HISTORY.
THE LEFT HIP IS AFFECTED MOST OFTEN, BECAUSE IT LIES AGAINST THE MATERNAL SPINE IN THE USUAL FETAL POSITION. SWADDLING WITH THE HIPS EXTENDED AND ADDUCTED IS AN IMPORTANT AND PREVENTABLE CAUSE, which matters IN INDIA AND ACROSS SOUTH ASIA WHERE TIGHT SWADDLING IS TRADITIONAL.
Examining the hip by age
ORTOLANI AND BARLOW TESTS WORK ONLY IN THE FIRST WEEKS. ORTOLANI RELOCATES A DISLOCATED HIP WITH A PALPABLE CLUNK; BARLOW DISLOCATES A LOCATED BUT UNSTABLE ONE. AFTER ABOUT THREE MONTHS BOTH BECOME UNRELIABLE, BECAUSE THE SOFT TISSUES CONTRACT. LIMITED ABDUCTION THEN BECOMES THE MOST RELIABLE SIGN.
The GALEAZZI SIGN of APPARENT FEMORAL SHORTENING WITH HIPS AND KNEES FLEXED supports it, and ASYMMETRIC THIGH CREASES ARE COMMON IN NORMAL INFANTS AND UNRELIABLE ALONE. Choosing the test by age is what the examiner is testing.
Imaging and treatment of dysplasia
ULTRASOUND IS THE INVESTIGATION BEFORE THE FEMORAL HEAD OSSIFIES, AT AROUND FOUR TO SIX MONTHS, using the GRAF ALPHA ANGLE. AFTER OSSIFICATION A PLAIN RADIOGRAPH IS USED, with HILGENREINER AND PERKIN LINES, SHENTON LINE AND THE ACETABULAR INDEX. UNDER SIX MONTHS: PAVLIK HARNESS. SIX TO EIGHTEEN MONTHS: CLOSED REDUCTION AND SPICA. BEYOND: OPEN REDUCTION WITH OSTEOTOMY.
EXCESSIVE ABDUCTION IN THE HARNESS MUST BE AVOIDED, BECAUSE IT COMPRESSES THE FEMORAL HEAD AGAINST THE ACETABULAR MARGIN AND CAUSES AVASCULAR NECROSIS. The harness works by HOLDING THE HIPS FLEXED AND ABDUCTED SO THE ACETABULUM REMODELS AROUND A REDUCED HEAD.
The screening question
WHETHER ALL INFANTS SHOULD HAVE ULTRASOUND SCREENING REMAINS UNSETTLED. A 2025 EVIDENCE REVIEW FOUND THAT UNIVERSAL SCREENING INCREASED NON-SURGICAL INTERVENTION WITHOUT A CORRESPONDING REDUCTION IN LATE-PRESENTING DYSPLASIA OR IN THE NEED FOR SURGERY.
The balance AGAINST OVERTREATMENT IS GENUINELY UNCLEAR, and the honest position is that the relative benefit of universal over selective screening remains unproven. This POSTDATES MOST REVISION MATERIAL, which tends to assert one position or the other.
CAVE and the Ponseti sequence
CAVUS, ADDUCTUS, VARUS, EQUINUS. PONSETI CORRECTION FOLLOWS EXACTLY THAT ORDER: CAVUS FIRST BY SUPINATING THE FOREFOOT TO ALIGN IT WITH THE HINDFOOT, THEN ADDUCTUS AND VARUS TOGETHER BY ABDUCTING THE FOOT AROUND THE TALAR HEAD, AND EQUINUS LAST.
CORRECTING EQUINUS BEFORE THE OTHER COMPONENTS PRODUCES A ROCKER-BOTTOM FOOT, BECAUSE THE MIDFOOT BREAKS RATHER THAN THE ANKLE DORSIFLEXING. This is the reason the order is not arbitrary and is examined directly.
Ponseti outcomes and the relapse rule
WEEKLY MANIPULATION AND CASTING, TYPICALLY AROUND FIVE CASTS, FOLLOWED BY PERCUTANEOUS ACHILLES TENOTOMY IN THE MAJORITY OF FEET, THEN A FOOT ABDUCTION BRACE. An Indian tertiary series of 550 FEET achieved FULL CORRECTION IN 94.7 PERCENT, TENOTOMY IN 77.2 PERCENT, A MEAN OF 5.18 CASTS, AND RESIDUAL DEFORMITY IN 5.3 PERCENT.
THE SINGLE MOST IMPORTANT TEACHING POINT IS THAT RELAPSE IS A BRACING PROBLEM, NOT A CASTING PROBLEM. Brace wear must continue FULL TIME FOR AROUND THREE MONTHS AND THEN AT NIGHT UNTIL THE AGE OF FOUR OR FIVE, and FAMILIES WHO STOP EARLY ARE THE FAMILIES WHOSE CHILDREN RELAPSE.
Perthes disease
IDIOPATHIC OSTEONECROSIS OF THE FEMORAL HEAD IN A GROWING CHILD, TYPICALLY BETWEEN FOUR AND EIGHT YEARS AND FAR COMMONER IN BOYS. Presentation is A PAINLESS OR MINIMALLY PAINFUL LIMP, and THE PAIN WHEN PRESENT IS OFTEN FELT AT THE KNEE. Stages: NECROSIS, FRAGMENTATION, REOSSIFICATION, REMODELLING over two to four years.
Knee pain occurs BECAUSE THE OBTURATOR NERVE SUPPLIES BOTH THE HIP JOINT AND THE MEDIAL KNEE. PROGNOSIS WORSENS WITH OLDER AGE AT ONSET, because THERE IS LESS REMAINING GROWTH IN WHICH TO REMODEL, and with GREATER INVOLVEMENT OF THE LATERAL PILLAR.
The containment principle
KEEP THE FEMORAL HEAD SEATED DEEPLY WITHIN THE ACETABULUM SO THAT THE ACETABULUM ACTS AS A MOULD WHILE THE HEAD IS PLASTIC. Achieved by MAINTAINING ABDUCTION, with BRACING OR FEMORAL OR PELVIC OSTEOTOMY.
This is the form-follows-function principle applied therapeutically: the head is SOFT AND DEFORMABLE DURING THE FRAGMENTATION PHASE, so the shape it ends up with depends on WHAT IT IS PRESSED AGAINST WHILE IT REOSSIFIES.
Slipped capital femoral epiphysis
THE EPIPHYSIS SLIPS OFF THE METAPHYSIS THROUGH THE PHYSIS, classically in AN OVERWEIGHT ADOLESCENT AROUND THE GROWTH SPURT. HYPOTHYROIDISM, GROWTH HORMONE DEFICIENCY AND RENAL OSTEODYSTROPHY are endocrine associations. THE MOST USEFUL CLINICAL SIGN IS OBLIGATE EXTERNAL ROTATION ON HIP FLEXION.
Endocrine causes should be considered PARTICULARLY IN A CHILD YOUNGER OR THINNER THAN EXPECTED. Presentation is again HIP OR KNEE PAIN WITH A LIMP, and KNEE PAIN IN AN ADOLESCENT MUST PROMPT HIP EXAMINATION.
Imaging and treating the slip
KLEIN'S LINE DRAWN ALONG THE SUPERIOR FEMORAL NECK SHOULD INTERSECT PART OF THE EPIPHYSIS, AND FAILS TO DO SO IN A SLIP. A FROG-LEG LATERAL VIEW IS ESSENTIAL BECAUSE EARLY SLIPS ARE MISSED ON THE ANTEROPOSTERIOR FILM ALONE. TREATMENT IS IN SITU PINNING, AND REDUCTION OF THE SLIP IS AVOIDED.
Reduction DISRUPTS THE RETINACULAR VESSELS AND PRECIPITATES AVASCULAR NECROSIS, so ACCEPTING THE DEFORMITY AND STABILISING THE PHYSIS IS SAFER THAN CORRECTING IT. This is counterintuitive and is examined for that reason.
The limping child and Kocher
KOCHER CRITERIA: INABILITY TO BEAR WEIGHT, FEVER ABOVE 38.5 DEGREES, ERYTHROCYTE SEDIMENTATION RATE ABOVE 40, AND WHITE CELL COUNT ABOVE 12,000. THE PROBABILITY OF SEPTIC ARTHRITIS RISES STEEPLY AS MORE CRITERIA ARE MET, APPROACHING CERTAINTY WHEN ALL FOUR ARE PRESENT.
SEPTIC ARTHRITIS OF THE HIP IS A SURGICAL EMERGENCY, BECAUSE PUS UNDER PRESSURE IN A JOINT WITH AN INTRACAPSULAR BLOOD SUPPLY DESTROYS ARTICULAR CARTILAGE WITHIN DAYS AND CAN INFARCT THE FEMORAL HEAD. TRANSIENT SYNOVITIS IS THE COMMON MIMIC, following a viral illness, with A SYSTEMICALLY WELL CHILD WHO CAN USUALLY STILL BEAR WEIGHT.
Normal variants
GENU VARUM IS PHYSIOLOGICAL UP TO ABOUT TWO YEARS, after which the legs pass through A VALGUS PHASE PEAKING AROUND THREE TO FOUR YEARS AND SETTLE BY ABOUT SEVEN. IN-TOEING has three causes by age: METATARSUS ADDUCTUS IN INFANCY, INTERNAL TIBIAL TORSION IN THE TODDLER, AND INCREASED FEMORAL ANTEVERSION IN THE OLDER CHILD WHO SITS IN A W POSITION.
ALL THREE USUALLY RESOLVE WITHOUT TREATMENT, and THE HISTORICAL USE OF BRACES AND SPECIAL SHOES HAS BEEN ABANDONED BECAUSE THEY DO NOT ALTER THE NATURAL HISTORY. BLOUNT DISEASE IS THE PATHOLOGICAL VERSION OF VARUS, in OVERWEIGHT CHILDREN with MEDIAL METAPHYSEAL BEAKING, and unlike physiological bowing IT PROGRESSES. RICKETS must be excluded biochemically.
Scoliosis
A LATERAL CURVATURE WITH ROTATION, AND THE ROTATION IS WHAT MAKES IT VISIBLE. THE ADAMS FORWARD BEND TEST DETECTS THE RIB HUMP. A POSTURAL CURVE DISAPPEARS ON FORWARD BENDING; A STRUCTURAL CURVE DOES NOT. THE COBB ANGLE MEASURES THE CURVE. THE RISSER SIGN GRADES ILIAC APOPHYSEAL OSSIFICATION FROM ZERO TO FIVE.
A LOW RISSER GRADE IN A CHILD STILL GROWING PREDICTS PROGRESSION, because A CURVE PROGRESSES WHILE GROWTH REMAINS. Broadly, CURVES UNDER ABOUT TWENTY DEGREES ARE OBSERVED, MODERATE CURVES IN A GROWING CHILD ARE BRACED TO PREVENT PROGRESSION RATHER THAN TO CORRECT, AND LARGE CURVES ARE TREATED SURGICALLY.
Atypical scoliosis
ADOLESCENT IDIOPATHIC SCOLIOSIS AFFECTS GIRLS DISPROPORTIONATELY AT THE PUBERTAL GROWTH SPURT AND IS PAINLESS. PAIN, A LEFT THORACIC CURVE, OR A RAPIDLY PROGRESSIVE CURVE IN A YOUNG CHILD ARE ALL ATYPICAL AND REQUIRE MAGNETIC RESONANCE IMAGING.
Those features suggest AN UNDERLYING SPINAL CORD ABNORMALITY SUCH AS SYRINGOMYELIA OR A TETHERED CORD. CONGENITAL SCOLIOSIS arises from VERTEBRAL MALFORMATION SUCH AS A HEMIVERTEBRA, PRESENTS EARLIER, and is ASSOCIATED WITH CARDIAC AND RENAL ANOMALIES THAT MUST BE SOUGHT BECAUSE THEY SHARE AN EMBRYOLOGICAL WINDOW.
Congenital muscular torticollis
THE STERNOCLEIDOMASTOID IS FIBROTIC AND SHORTENED, SO THE HEAD TILTS TOWARDS THE AFFECTED SIDE AND THE CHIN TURNS AWAY FROM IT. A FIRM SWELLING WITHIN THE MUSCLE MAY BE PALPABLE IN EARLY INFANCY. MOST CASES RESPOND TO STRETCHING PHYSIOTHERAPY.
The associated conditions to look for are PLAGIOCEPHALY FROM POSITIONAL MOULDING AND DEVELOPMENTAL DYSPLASIA OF THE HIP, WHICH SHARES THE INTRAUTERINE CROWDING MECHANISM. The direction rule - TILT TOWARDS, CHIN AWAY - is examined directly.
Cerebral palsy
PRODUCES ORTHOPAEDIC PROBLEMS THROUGH MUSCLE IMBALANCE RATHER THAN THROUGH PRIMARY BONE DISEASE. SPASTIC MUSCLES OVERPOWER THEIR ANTAGONISTS, JOINTS ARE HELD IN ABNORMAL POSITIONS, AND THE BONE AND JOINT DEFORM ACCORDINGLY. HIP SURVEILLANCE IS ESSENTIAL.
This is THE SAME FORM-FOLLOWS-FUNCTION PRINCIPLE stated at the start of the chapter, applied to a neurological cause. PROGRESSIVE HIP DISPLACEMENT IS COMMON, PAINLESS UNTIL LATE, AND FAR EASIER TO PREVENT THAN TO RECONSTRUCT, which is the entire justification for scheduled radiographic surveillance.
Osteogenesis imperfecta and achondroplasia
OSTEOGENESIS IMPERFECTA results from DEFECTIVE TYPE I COLLAGEN, giving FRAGILE BONES, BLUE SCLERAE, DENTINOGENESIS IMPERFECTA AND CONDUCTIVE HEARING LOSS; BISPHOSPHONATES REDUCE FRACTURE RATES. ACHONDROPLASIA results from A GAIN-OF-FUNCTION MUTATION IN FGFR3, is AUTOSOMAL DOMINANT WITH MOST CASES DE NOVO, and produces RHIZOMELIC SHORTENING WITH A TRIDENT HAND.
OSTEOGENESIS IMPERFECTA IS THE MOST IMPORTANT DIFFERENTIAL FOR NON-ACCIDENTAL INJURY in a child with multiple fractures. In achondroplasia THE DANGER IN INFANCY IS FORAMEN MAGNUM STENOSIS, WHICH CAN CAUSE CENTRAL APNOEA AND SUDDEN DEATH, while SPINAL STENOSIS IS THE PROBLEM OF LATER LIFE.
Radial club hand
A LONGITUDINAL DEFICIENCY OF THE RADIUS, with THE WRIST DEVIATED RADIALLY AND THE THUMB HYPOPLASTIC OR ABSENT. IT IS THE ONE LIMB ANOMALY THAT MANDATES SYSTEMIC INVESTIGATION: ECHOCARDIOGRAPHY, RENAL IMAGING AND A BLOOD COUNT.
The reason is that THE RADIUS FORMS DURING THE SAME EMBRYOLOGICAL WINDOW AS THE HEART, THE KIDNEYS AND THE MARROW, so associations include the VACTERL GROUP, HOLT-ORAM SYNDROME WITH CARDIAC SEPTAL DEFECTS, FANCONI ANAEMIA AND THROMBOCYTOPENIA WITH ABSENT RADIUS. SPRENGEL DEFORMITY is CONGENITAL FAILURE OF SCAPULAR DESCENT, sometimes tethered by an OMOVERTEBRAL BAR.
⚠️

Traps NEET PG sets — and how to dodge them

These are the exact option-traps and misreads that cost marks under negative marking.

WATCH OUT
Assuming all paediatric deformity remodels with growth
Angulation in the plane of joint movement close to an active physis in a young child remodels well, but rotational malalignment does not remodel at any age. Accepting a rotational deformity because the child is young is a permanent error.
WATCH OUT
Performing Ortolani and Barlow tests on a six-month-old
Both depend on the hip being movable in and out of the socket, and after about three months soft tissue contracture prevents that. Limited abduction becomes the most reliable sign, supported by the Galeazzi sign of apparent femoral shortening.
WATCH OUT
Requesting a hip radiograph in a two-month-old
The femoral head does not ossify until around four to six months, so the radiograph shows little. Ultrasound with the Graf method is the investigation before ossification, and a radiograph becomes useful only after it.
WATCH OUT
Maximising abduction in a Pavlik harness to hold the hip reduced
Excessive abduction compresses the femoral head against the acetabular margin and causes avascular necrosis. The harness holds the hip flexed and in safe abduction, allowing the acetabulum to remodel around a reduced head rather than forcing it.
WATCH OUT
Asserting that universal hip ultrasound screening is clearly superior
A 2025 evidence review found that universal screening increased non-surgical intervention without reducing late-presenting dysplasia or the need for surgery. The relative benefit remains unproven, and overtreatment is a genuine cost.
WATCH OUT
Correcting equinus early in clubfoot casting
Dorsiflexing the ankle before the cavus, adductus and varus are corrected breaks the midfoot instead, producing a rocker-bottom foot. The CAVE order exists for this reason and is not an arbitrary mnemonic.
WATCH OUT
Attributing clubfoot relapse to inadequate casting
Casting correction is reliable, and relapse is almost always a failure of brace wear. The foot abduction brace must be worn full time for about three months and then at night until four or five, and families who stop early are the ones whose children relapse.
WATCH OUT
Investigating knee pain in a child without examining the hip
The obturator nerve supplies both the hip joint and the medial knee, so hip pathology refers to the knee. Perthes disease and slipped capital femoral epiphysis both present this way, and missing them costs the hip.
WATCH OUT
Reducing a slipped capital femoral epiphysis before fixation
Forceful reduction disrupts the retinacular vessels supplying the femoral head and precipitates avascular necrosis. In situ pinning accepts the deformity and stabilises the physis, which gives a far better long-term result.
WATCH OUT
Excluding a slipped epiphysis on a normal anteroposterior radiograph
Early slips displace posteriorly and are frequently invisible on the frontal view. A frog-leg lateral is essential, and Klein's line along the superior femoral neck should intersect the epiphysis and fails to do so in a slip.
WATCH OUT
Observing a febrile child who cannot bear weight
Septic arthritis of the hip destroys cartilage within days and can infarct the femoral head. With inability to bear weight, fever above 38.5, raised inflammatory markers and leucocytosis, the diagnosis is near certain and urgent aspiration and drainage are required.
WATCH OUT
Bracing a toddler for in-toeing or bowing
Metatarsus adductus, internal tibial torsion and femoral anteversion all resolve spontaneously, as does physiological genu varum before two years. Braces and special shoes were abandoned because they do not alter natural history.
WATCH OUT
Treating all bowing as physiological
Blount disease occurs in overweight children, shows medial metaphyseal beaking of the proximal tibia and progresses rather than resolving. Rickets is the other pathological cause and must be excluded biochemically.
WATCH OUT
Managing a painful scoliosis as adolescent idiopathic disease
Adolescent idiopathic scoliosis is painless. Pain, a left thoracic curve or rapid progression in a young child all suggest an underlying cord abnormality such as syringomyelia or a tethered cord and require magnetic resonance imaging.
WATCH OUT
Waiting for hip pain before imaging a child with cerebral palsy
Progressive hip displacement in cerebral palsy is painless until it is advanced, and by then reconstruction rather than prevention is required. Scheduled radiographic hip surveillance is standard for exactly this reason.
WATCH OUT
Treating a radial club hand as an isolated limb anomaly
The radius forms in the same embryological window as the heart, kidneys and marrow, so echocardiography, renal imaging and a blood count are mandatory. Holt-Oram syndrome, Fanconi anaemia and thrombocytopenia with absent radius are all in the differential.

Exam-pattern practice

PYQ-style questions with full solutions. Work through them as a readiness check — mark yourself honestly and get your gap report at the end.

Readiness check

Are you exam-ready for "Congenital & Pediatric Orthopedics"?

9 problems from this chapter. Try each one, reveal the worked solution, mark yourself honestly — get your gap report at the end.

9 questions~6 min

5-minute revision

The whole chapter, distilled. Read this the night before the exam.

  • Three properties: physis, thick periosteum, remodelling capacity.
  • Angulation near an active physis remodels; rotation never does.
  • Form follows function, so position during growth determines shape.
  • Timing determines whether treatment is a harness or a reconstruction.
  • Dysplasia risk factors are mechanical: breech, female, first-born, oligohydramnios.
  • The left hip is most often affected.
  • Tight swaddling with extended hips is a preventable cause.
  • Ortolani relocates; Barlow dislocates.
  • Both are unreliable after about three months.
  • Limited abduction is the reliable later sign.
  • Galeazzi shows apparent femoral shortening.
  • Ultrasound before ossification, radiograph after.
  • Graf alpha angle measures acetabular coverage.
  • Pavlik harness under six months, avoiding excess abduction.
  • Excess abduction causes avascular necrosis.
  • Closed reduction six to eighteen months, open reduction beyond.
  • Universal screening has unproven benefit over selective.
  • CAVE: cavus, adductus, varus, equinus.
  • Ponseti corrects in that order, equinus last.
  • Early equinus correction gives a rocker-bottom foot.
  • About five casts, then tenotomy in most feet.
  • Indian series: 94.7 percent correction, 77.2 percent tenotomy.
  • Relapse is a bracing failure, not a casting failure.
  • Brace full time three months, then nights to age four or five.
  • Perthes is idiopathic osteonecrosis at four to eight years.
  • Hip pain refers to the knee via the obturator nerve.
  • Containment uses the acetabulum as a mould.
  • Older age at onset worsens Perthes prognosis.
  • Slipped epiphysis: obese adolescent at the growth spurt.
  • Consider endocrine causes if younger or thinner than expected.
  • Obligate external rotation on flexion is the key sign.
  • Klein's line fails to intersect the epiphysis.
  • A frog-leg lateral is essential.
  • Pin in situ; do not reduce.
  • Kocher: non-weight bearing, fever, ESR over 40, WBC over 12,000.
  • Septic arthritis of the hip is a surgical emergency.
  • Transient synovitis follows a viral illness in a well child.
  • Varus is normal to two years, valgus peaks at three to four.
  • Blount disease progresses and shows metaphyseal beaking.
  • In-toeing has three causes distinguished by age.
  • Braces and special shoes do not change natural history.
  • Adams forward bend separates postural from structural curves.
  • Cobb angle measures, Risser sign predicts progression.
  • Painful or left thoracic scoliosis needs MRI.
  • Congenital scoliosis carries cardiac and renal associations.
  • Torticollis tilts the head towards and turns the chin away.
  • Torticollis accompanies plagiocephaly and hip dysplasia.
  • Cerebral palsy deforms joints through muscle imbalance.
  • Hip surveillance in cerebral palsy is essential and scheduled.
  • Osteogenesis imperfecta is defective type I collagen.
  • It is the key differential for non-accidental injury.
  • Achondroplasia is FGFR3 gain-of-function, mostly de novo.
  • Foramen magnum stenosis is the infant danger.
  • Radial club hand needs echocardiography, renal imaging and a blood count.

NEET PG question blueprint

How this topic is asked, tier by tier — so you can prep to the pattern.

Typical weightage: Each NEET PG question is worth +4/-1; congenital and paediatric orthopaedics contributes 5-7 questions per attempt and overlaps with Paediatrics and Anatomy

Question styleMarks eachTypical countWhat it tests
The growing skeleton4~1The three properties, the remodelling rule and the form-follows-function principle
Developmental dysplasia4~1-2Risk factors, age-appropriate examination, imaging choice, harness use and the screening debate
Clubfoot4~1CAVE components, the Ponseti sequence, tenotomy and the bracing relapse rule
Perthes disease4~1Age, referred knee pain, the stages and the containment principle
Slipped epiphysis4~1The typical patient, endocrine associations, Klein's line, the frog-leg view and in situ pinning
The limping child4~1Kocher criteria, septic arthritis urgency and transient synovitis as the mimic
Normal variants4~1Physiological varus and valgus, in-toeing by age, Blount disease and rickets
Scoliosis4~1Adams test, Cobb angle, Risser sign, atypical features and congenital associations
Genetic and neuromuscular4~1Cerebral palsy hip surveillance, osteogenesis imperfecta, achondroplasia and radial club hand
Prep strategy
  • First pass: fix the age-linked conditions and the pure recall items - CAVE, Kocher criteria, the hip examination sequence and the imaging thresholds.
  • Second pass: understand the two organising ideas properly, because form follows function and the femoral head blood supply between them explain most of the management rules.
  • Final pass: drill the counterintuitive answers - pin the slip rather than reducing it, correct equinus last, avoid excessive abduction in the harness, and offer no brace at all for in-toeing.

Exam-hall strategy

Battle-tested tips from mentors and toppers for this topic under the sectional clock.

  1. Read the age first, since it drives the entire differential here.
  2. In a child with knee pain, examine and consider the hip.
  3. Choose the hip test by age: Ortolani and Barlow only in the first weeks.
  4. Fever with inability to bear weight means Kocher and urgent drainage.
  5. For a slipped epiphysis, the answer is in situ pinning.
  6. Reject braces and special shoes for in-toeing or physiological bowing.
  7. Painful or left thoracic scoliosis means imaging, not bracing.
  8. With NEET PG's +4/-1 marking, CAVE, the Kocher criteria and the hip examination sequence are high-certainty recall worth banking early.
  9. Under the 5-group, 42-minute time-bound format, clear those fast and spend the time on the timing and blood supply reasoning, since a closed group cannot be reopened.

Beyond the exam

Where this skill shows up in the job you're competing for — and in life.

Checking abduction at every baby visit

Limited hip abduction is the sign that catches dysplasia after the neonatal tests stop working, and it takes seconds during any routine examination.

Counselling about swaddling

Teaching families to swaddle with the legs free to flex and abduct prevents a proportion of hip dysplasia outright, which no amount of later screening can achieve.

Following up the clubfoot brace

The determinant of a good clubfoot outcome four years later is whether the family kept using the brace, so follow-up and supply matter more than casting technique.

Examining the hip of a child with knee pain

Referred pain through the obturator nerve means Perthes disease and slipped epiphysis are routinely missed by clinicians who examine only the joint the child points to.

Where else this topic is tested

Prepare once, score in every exam that asks it.

FMGE / NExTVery high overlap — hip dysplasia, clubfoot, slipped epiphysis and the limping child are examined at identical depth and weighted heavily
USMLE Step 2 CKHigh overlap — dysplasia, Perthes, slipped epiphysis, septic arthritis and scoliosis are shared almost exactly, with minor differences in screening practice
MS Orthopaedics and DNB entranceFoundational — assumed working knowledge, with osteotomy planning, deformity correction and gait analysis examined far more deeply

Questions aspirants ask

Pulled from the Q&A community and mentor sessions.

Because the two deformities are corrected by different mechanisms, and only one of them exists in a growing bone. Angular remodelling happens at the physis and along the shaft together. A growth plate adjacent to an angular deformity responds to the altered mechanical loading by growing asymmetrically, laying down more bone on the concave side, which progressively realigns the joint surface with the mechanical axis. Simultaneously, the shaft undergoes appositional remodelling, with periosteal bone formation on the concave side and resorption on the convex side, which straightens the bone itself. Both processes are driven by loading, and both require an open physis, which is why remodelling potential is greatest in a young child with a fracture close to a fast-growing plate and in the plane of movement of the adjacent joint. Rotation has no such mechanism. There is no biological process by which a bone twists back around its long axis, because growth plates add length rather than rotating the segments they separate, and appositional remodelling changes contour rather than orientation. A malrotated femur or tibia stays malrotated permanently, and the compensation the patient develops is postural rather than skeletal. This is why intraoperative assessment of rotation is emphasised so heavily in paediatric fracture surgery even when generous angulation is accepted.

Because its blood supply is precarious in three separate ways that coincide in the growing child. First, the femoral head is largely intracapsular, so the vessels supplying it must travel along the femoral neck beneath the capsular reflection rather than entering directly. Any process that raises intracapsular pressure, such as pus in septic arthritis or blood after a fracture, compresses those vessels against bone. Second, the physis acts as a barrier to vascular anastomosis between the metaphyseal and epiphyseal circulations while it is open, so the epiphysis depends almost entirely on the retinacular vessels and has no significant collateral supply. This is precisely the arrangement that fails in Perthes disease, and it is why avascular necrosis of the femoral head is a childhood problem in a way that avascular necrosis of most other epiphyses is not. Third, the vessels can be injured mechanically by anything that moves the epiphysis relative to the neck, which is the reason a slipped capital femoral epiphysis is pinned in situ rather than reduced, and the reason excessive abduction in a Pavlik harness causes necrosis by compressing the head against the acetabular margin. Every major treatment caution in paediatric hip disease traces back to one of these three.

Because the benefit that screening was meant to deliver has proved difficult to demonstrate, while the cost in overtreatment is measurable. The rationale was straightforward: dysplasia detected in the first weeks can be treated with a harness, whereas dysplasia detected at walking age needs surgery, so finding every case early should reduce late presentations and operations. Universal ultrasound certainly finds more abnormality, and that is part of the problem. Neonatal hips are physiologically immature, and a substantial proportion of hips reported as dysplastic at birth normalise spontaneously within weeks without any treatment. Screening therefore generates a large group of infants who are harnessed unnecessarily, which is not harmless, since the harness itself carries a risk of avascular necrosis and femoral nerve palsy and imposes considerable burden on families. A 2025 evidence review found that universal screening increased rates of non-surgical intervention without a corresponding reduction in the incidence of late-presenting dysplasia or in the need for surgery, which is the outcome that matters. The honest position is therefore that the relative benefit remains unclear. Selective screening based on clinical examination and risk factors, with a low threshold for imaging, remains defensible, and clinical examination at every well-child visit continues to matter more than any single scan.

Because casting corrects the deformity and does nothing about the tendency that produced it. Clubfoot is not simply a position that the foot has fallen into; it reflects abnormal muscle balance and connective tissue behaviour that persists after the bones and ligaments have been realigned. The medial soft tissues have been stretched into a corrected length, but they retain a strong tendency to contract again, and the tibialis anterior and posterior continue to pull the foot into supination and adduction. Growth amplifies this, because the child adds length continuously to structures that are already inclined to shorten relatively. The foot abduction brace holds the feet in external rotation and dorsiflexion for the hours the child is not weight-bearing, which maintains the stretch and allows the corrected alignment to become the position in which the foot grows. It is worn full time for about three months and then at night until four or five, and relapse rates correlate closely with how faithfully that is done. This has an important consequence for practice, particularly in high-volume Indian programmes: the clinical skill that determines outcome is not casting technique but the counselling, follow-up and brace supply that keep families adherent for four years after the child looks completely normal.

Read the age first and let it drive the differential, because the conditions in this chapter have unusually tight age distributions. A neonate suggests dysplasia, clubfoot or torticollis. A toddler with a limp suggests transient synovitis, septic arthritis or a toddler's fracture. Four to eight years with a limp suggests Perthes. An overweight adolescent with hip or knee pain suggests a slipped epiphysis. A pubertal girl with an asymmetric back suggests idiopathic scoliosis. Then check for the specific hooks. Knee pain in a child means examine the hip. Fever with inability to bear weight means Kocher and septic arthritis. Limited abduction in an infant means dysplasia regardless of what the creases look like. Painful or left thoracic scoliosis means magnetic resonance imaging. Three management rules recur and are worth having ready. In situ pinning for a slipped epiphysis, never reduction. Equinus last in clubfoot. And no braces or special shoes for in-toeing or physiological bowing, because any option offering them is testing whether you know they were abandoned. Finally, if a stem gives an age and a treatment option that belongs to a different age band, such as a Pavlik harness in a two-year-old, that is the distractor.
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