CFB OT02 Childrens Orthopaedics And Deformities
A pediatric orthopedic subspecialty focused on the diagnosis and management of congenital, developmental, and acquired musculoskeletal deformities in children, including conditions such as clubfoot, limb length discrepancies, angular deformities, and skeletal dysplasias.
Children's Orthopaedics and Deformities
Lecture Map: The Big Idea
This lecture, delivered by Professor Michael To (Division of Paediatric Orthopaedics, HKU), is a foundational primer on how to approach musculoskeletal problems in children. The single most important take-home message is:
"Children are not small adults." [1]
Children have growth plates, remodelling potential, and a dynamically changing skeletal alignment throughout development. What looks "abnormal" to a worried parent is often a physiological variant that will self-correct. The clinician's job is to distinguish physiological from pathological deformities, and to intervene only when indicated.
- Past papers test paediatric fracture patterns (greenstick fractures, growth plate injuries) and basic principles of children's bones [2][3].
- Short stature, limb length discrepancy (LLD), intoeing, bowlegs/knock knees, and flatfoot are classic viva/SAQ topics.
- The lecture integrates with GC 232 (Paediatric Musculoskeletal Injury), GC 148 (Neurological Examination in Neonates), and CFB PAE02 (Child Growth and Development).
Core Concept: Why "Children Are Not Small Adults"
"Ossification centers and growth plates gradually increase in size and model into adult form." [1]
- At birth, much of the skeleton is cartilaginous. Secondary ossification centres appear at predictable ages (e.g., the elbow has six centres that appear and fuse in a set sequence — mnemonic: CRITOE).
- The growth plate (physis) is the engine of longitudinal bone growth. It sits between the epiphysis and metaphysis, consists of organized chondrocyte zones (reserve → proliferative → hypertrophic → calcified → ossification), and is the weakest mechanical link in a child's bone — hence Salter–Harris fractures pass through the physis rather than through ligaments. [4]
- On X-ray, the physis appears as a radiolucent line. Don't mistake it for a fracture.
Why this matters: Any injury, infection, or metabolic insult that damages the growth plate can cause physeal arrest → limb length discrepancy or angular deformity. The lecture specifically lists physeal arrest as one of the causes of short stature on the overview slide. [1]
Epiphyseal growth allows bones to increase in length and the articular surface to mature. [1]
The epiphysis is responsible for the shape of the joint surface. Conditions like Perthes disease (avascular necrosis of the femoral head epiphysis) or multiple epiphyseal dysplasia (MED) affect this region, leading to abnormal joint contour, limb malalignment, and early arthritis.
Modelling and remodelling potential is highlighted as a unique paediatric advantage. [1]
- Modelling = the process by which bone changes shape during growth (e.g., a bowed femur gradually straightens).
- Remodelling = Wolff's law — bone responds to mechanical stress by resorbing where stress is low and depositing where stress is high.
- In children, a malunited fracture can progressively correct itself through remodelling, especially if:
- The child is young (more growth remaining).
- The fracture is close to a growth plate (more active remodelling zone).
- The angulation is in the plane of motion of the adjacent joint.
- This is why many paediatric fractures can be treated conservatively with immobilisation (e.g., the greenstick radius fracture in the 2020 MCQ — answer: POP cast, not ORIF). [2][4]
"Growth is a process" — the lecture lists the five common parental concerns: short stature, intoeing, knock knees, bowlegs, flatfoot. [1]
These are developmental variants that change with age. Premature intervention (e.g., braces for intoeing) is unnecessary and ineffective.
Skeletal maturity: Female ~14, Male ~16. [1]
After skeletal maturity, the growth plates fuse and no further longitudinal growth or remodelling-based correction occurs. This is crucial for planning interventions like epiphysiodesis, which must be timed before skeletal maturity.
Slide-by-Slide High-Yield Content
Multidisciplinary approach: Paediatricians, endocrinologist, orthopaedic surgeons [1]
| Component | Details |
|---|---|
| History | Family history; Medications affecting calcium absorption (glucocorticoids, anti-epileptics); diet [1] |
| Physical Exam | Body height, limb deformities [1]; assess proportion (arm span vs height), syndromal features |
| Lab Exam | Vitamin D, calcium, alkaline phosphatase, growth hormone, thyroid and parathyroid hormones; Genetic studies [1] |
| Radiology | X-rays [1] — bone age (left wrist), limb alignment, growth plate morphology |
Why These Specific Labs?
- Vitamin D / Calcium / ALP: Rickets (nutritional or hypophosphataemic) is a major cause of pathological bowlegs. ALP is elevated in active rickets because osteoblasts are working overtime but cannot mineralise.
- Growth Hormone / Thyroid / Parathyroid: Endocrine causes of proportional short stature (GH deficiency, hypothyroidism) or metabolic bone disease (hyperparathyroidism → subperiosteal resorption).
- Genetic studies: For skeletal dysplasias (e.g., FGFR3 mutation in achondroplasia). [5]
Short stature: Proportional vs Disproportional [1]
| Type | Examples | Key Features |
|---|---|---|
| Proportional | Familial, Endocrine [1] | Normal body proportions; plot on growth chart; check parental heights and mid-parental height; bone age may be delayed (constitutional delay) or appropriate (familial) |
| Disproportional | Achondroplasia, Fibular hemimelia [1] | Abnormal upper:lower segment ratio or arm span:height ratio |
Achondroplasia (Key Example from Slides + Senior Notes)
- Genetics: AD inheritance, ~50% de novo; FGFR3 mutation [5]
- Clinical: Disproportionate short stature with rhizomelic shortening (proximal limbs affected most), macrocephaly, frontal bossing, flat nasal bridge, thoracolumbar kyphosis (gibbus), trident hand [5]
- Management: GH replacement, limb lengthening surgery [5]
- The lecture slide specifically shows clinical photos of achondroplasia patients alongside other skeletal dysplasias (MED, SED, mucopolysaccharidosis). [1]
Exam Trap: Proportional vs Disproportional
A common MCQ trap: Turner syndrome (45,XO) causes proportional short stature, NOT disproportional. The 2025 MCQ Q77 tests Turner syndrome recognition with webbed neck, cubitus valgus, shield chest — distinct from achondroplasia's rhizomelic shortening. [3]
Commonly asked questions — this slide is a clinical reasoning framework: [1]
| Concern | Key Questions to Ask |
|---|---|
| Short stature | Percentile? Height of parents? Proportion of body? Syndromal features? Skeletal dysplasia? |
| Bowlegs / Knock knees / LLD | Age? Unilateral? History of injury? Infection? |
| Intoeing gait | Symmetrical? Which level? Neuromuscular problems? Gait pattern? |
| Flatfoot | Flexible? Rigid? |
Why these questions matter:
- Age: Physiological bowlegs are normal under age 2; physiological knock knees peak at age 3–4. Persistence beyond expected ages = pathological.
- Unilateral: Bilateral symmetrical deformity → likely physiological or systemic. Unilateral → think injury, infection, tumour, or localised growth disturbance.
- History of injury/infection: Physeal damage → asymmetric growth arrest → progressive deformity.
- Flexible vs Rigid (flatfoot): The single most important distinction. A rigid flatfoot is never physiological.
D. Limb Length Discrepancy (LLD)
LLD: About 20–30% normal subjects have LLD between 0.5–2 cm. Usually compensated well if LLD < 2.5 cm. Treatment not usually needed. [1]
This is a critical threshold to remember: < 2.5 cm → usually no treatment needed.
| Category | Examples |
|---|---|
| Congenital | Proximal femoral focal deficiency (PFFD), fibular hemimelia, hemihypertrophy [1] |
| Developmental | Physeal injury or infection, Ollier's disease, poliomyelitis [1] |
- PFFD: Congenital hypoplasia/aplasia of the proximal femur. Results in severe LLD and hip instability.
- Fibular hemimelia: Congenital absence/hypoplasia of the fibula. Most common congenital long bone deficiency.
- Hemihypertrophy: One side of the body grows larger → associated with Wilms tumour and hepatoblastoma (Beckwith–Wiedemann syndrome).
- Ollier's disease: Multiple enchondromas → asymmetric growth → LLD.
- Perthes disease: Mentioned on slides — AVN of femoral head → abnormal gait as a result of LLD. [1]
Multiplier method: based on children's age and LLD to predict the ultimate LLD. [1]
Worked example from slide:
- 7-year-old boy with current LLD = 6.3 cm
- Multiplier for 7-year-old male = 1.57
- LLD at maturity = 6.3 × 1.57 = 9.9 cm [1]
This predicted LLD guides treatment planning: if the predicted LLD at maturity is significant (e.g., > 2.5 cm), surgical intervention is warranted.
Treatment: Shoe raise; Limb length equalisation surgery — Epiphysiodesis (stop the growth of longer bone); Lengthening (lengthen the shorter bone) [1]
| Treatment | Indication | How It Works |
|---|---|---|
| Shoe raise | Mild LLD (2–3 cm) | Non-surgical; compensates functionally |
| Epiphysiodesis | Moderate LLD; must be timed correctly before skeletal maturity | Stop the growth of the longer bone by ablating/tethering the growth plate; requires accurate prediction of remaining growth |
| Lengthening | Large LLD or when epiphysiodesis alone is insufficient | Lengthen the shorter bone using distraction osteogenesis (Ilizarov or motorised intramedullary nails); lecture shows cases of limb lengthening for PFFD [1] |
High Yield: Epiphysiodesis Timing
Epiphysiodesis is a permanent procedure — once you destroy the growth plate, growth stops irreversibly. You must use growth prediction charts (e.g., Green–Anderson, Paley multiplier) to time the procedure so that both limbs end up the same length at skeletal maturity. If done too early → over-correction (the previously longer leg becomes short). If done too late → under-correction.
In normal skeletally mature young adults, hip, knee and ankle should be in a straight line (mechanical axis). Any significant deviation = Malalignment. [1]
- Mechanical axis: Line from centre of femoral head to centre of ankle joint. Should pass through the centre of the knee.
- Anatomical axis: Line along the shaft of the femur. Normally makes ~6° valgus angle with the mechanical axis.
Physiological Angular Development of the Knee
| Age | Normal Alignment |
|---|---|
| Birth – 18 months | Genu varum (bowlegs) — physiological |
| 18 months – 3 years | Transitions from varus to valgus |
| 3–4 years | Genu valgum (knock knees) — peaks, physiological |
| 7–8 years | Gradually corrects to adult alignment (~7° valgus in females, ~5° in males) |
Clinical pearl: If a parent brings a 2-year-old with bowlegs, the appropriate response is usually reassurance and observation — this is normal physiology. However, if bowlegs are:
- Unilateral → think pathological (Blount disease, physeal bar, tumour)
- Progressive after age 2 → think pathological
- Associated with rickets features (widened metaphyses, rachitic rosary) → investigate
F. Limb Malalignment: Management
The lecture shows a beautiful case series of bowlegs corrected by guided growth control: [1]
| Stage | Findings |
|---|---|
| Pre-op | Genu varum 18° |
| 20 months post-op | Full correction achieved |
| Continued observation | Over-correction 4° (intentional slight over-correction expected) |
| After plate removal | Rebound after plate removal → 2° valgus (final acceptable alignment) |
How guided growth works: A plate is placed on one side of the growth plate (the medial side for varus, lateral side for valgus). This tethers one side while the other continues to grow → gradual angular correction. When alignment is correct (or slightly over-corrected), the plate is removed. There is typically rebound toward the original deformity, so slight over-correction is planned.
Why "rebound"? After plate removal, the previously tethered growth plate resumes more rapid growth (catch-up growth) and the mechanical forces that caused the original deformity may still be present.
- Inherited disorder of type 1 collagen → bone fragility, bowing, frequent fractures [5]
- Type I (most common): AD, fractures + blue sclerae ± hearing loss [5]
- Type II: Lethal form, multiple fractures in utero [5]
- Management: Bisphosphonates (↓ fracture rate), intramedullary rodding for deformity correction [5]
- Lecture shows a patient with MED with bilateral valgus malalignment requiring reconstruction [1]
- MED affects multiple epiphyses → irregular joint surfaces → malalignment + early OA
Intoeing gait or walking with an excessively inward foot-progression angle is very common in children. [1]
Three Levels of Intoeing
| Level | Cause | Typical Age | Natural History |
|---|---|---|---|
| Hip | Increased femoral anteversion | 3–10 years [1] | 80– > 95% resolve spontaneously [1] |
| Tibia | Increased internal tibial torsion [1] | Infancy – 3 years | Usually resolves by age 4–5 |
| Foot | Metatarsus adductus [1] | Newborn | Most resolve by age 1; flexible → observation; rigid → serial casting |
"Braces or shoe modification has no effect in speeding up the modelling" [1]
High Yield: Intoeing — Reassurance Is Key
This is a common parental anxiety. The lecture emphatically states that braces and shoe modifications do NOT speed up resolution. The vast majority of intoeing resolves spontaneously. Only refer if there are neuromuscular signs (e.g., cerebral palsy), asymmetry, or functional impairment persisting beyond expected age.
How to assess femoral anteversion clinically:
- Child lies prone with knees flexed to 90°. Internally and externally rotate the hip. In increased femoral anteversion, internal rotation is markedly greater than external rotation.
- The heel bisector test (shown on slides) evaluates forefoot alignment: normally the heel bisector passes through the 2nd–3rd toe. If it passes more laterally → metatarsus adductus. [1]
H. Flatfoot (Pes Planus)
Flatfoot: Loss of normal medial longitudinal arch, forefoot abduction, excessive hindfoot valgus. [1]
Staheli et al 1987 — 882 feet of children and adults with no musculoskeletal problems: Flatfoot is usual in infants and common in children. [1]
The medial longitudinal arch develops spontaneously during the 1st decade of life. Most young children have flat feet simply because of the fat pad under the arch and ligamentous laxity.
"Orthosis for flexible flatfoot cannot modify foot arch" [1]
High Yield: Flexible Flatfoot Does NOT Need Orthotics
This is a major teaching point. Parents often buy expensive arch support insoles. The lecture explicitly states these do NOT change the natural arch development. Money wasted. Only rigid flatfoot requires investigation and possible intervention.
Tip-toeing test: Observe hindfoot valgus [1]
| Feature | Flexible Flatfoot | Rigid Flatfoot |
|---|---|---|
| Arch on tip-toe | Arch reconstitutes (hindfoot inverts to varus) | No arch restoration (hindfoot stays in valgus) |
| Significance | Normal — physiological variant | Abnormal — investigate |
| Common cause | Ligamentous laxity, fat pad | Tarsal coalition (shown on slides [1]) |
| Management | Reassurance, observation | CT/MRI to confirm coalition → surgical excision or fusion if symptomatic |
Why does the tip-toe test work? When standing on tip-toes, the peroneus longus and tibialis posterior contract, pulling the hindfoot into inversion and reconstituting the arch. In tarsal coalition, the bones are abnormally bridged (e.g., calcaneo-navicular or talo-calcaneal bar), preventing this normal motion.
"The growth is different in everyone" — lecture shows side-by-side comparison of hypophosphataemic rickets and normal variance. [1]
- Hypophosphataemic rickets (X-linked dominant): Defective phosphate reabsorption in the proximal tubule → hypophosphataemia → defective mineralisation → rickets. Distinguished from nutritional rickets by persistent hypophosphataemia despite treatment. [6]
- On X-ray: widened, frayed, cupped metaphyses; bowing of weight-bearing bones.
- The lecture point is: don't label every bowlegged child as having rickets — you need lab confirmation.
"Children are not small adults. They are very unique physiologically and anatomically. 'Deformity' is common and may be due to physiological development. Surgery should be reserved for those pathological and symptomatic ones." [1]
Integration with Related Material
"The bone deformities in children after fracture have the ability to remodel. There are unique fracture patterns in children due to their special bone property. Treatment strategies could be different from adults." [4]
The remodelling potential discussed in this lecture directly explains why paediatric fractures are managed more conservatively. A greenstick fracture in a child's radius (2020 MCQ Q14) is treated with POP cast, not ORIF, because the bone will remodel.
| Condition | Key Point from Senior Notes | Integration |
|---|---|---|
| Developmental Dysplasia of Hip (DDH) | Clinical screening at birth (Barlow/Ortolani); USS before 6 months [7] | Not in this lecture but important differential for abnormal gait |
| Perthes Disease | AVN of femoral head; age 4–8; male > female [7] | Lecture mentions Perthes as cause of abnormal gait as a result of LLD [1] |
| SCFE | Slipped capital femoral epiphysis; obese pre-teen; knee/hip pain [7] | Not in this lecture but important in paediatric hip DDx |
| Scoliosis | Lateral curvature > 10° Cobb angle; idiopathic most common [7] | Not in this lecture |
Exam Intelligence
| Format | Example Stem |
|---|---|
| MCQ | "A 2-year-old presents with bilateral bowlegs. What is the most appropriate management?" → Reassurance and observation |
| MCQ | "Which of the following features suggests pathological rather than physiological flatfoot?" → Rigid hindfoot on tip-toe test |
| SAQ | "A 7-year-old boy has LLD of 5 cm. The multiplier for his age is 1.57. Calculate predicted LLD at maturity and outline management." |
| SAQ | "List 3 causes of disproportional short stature in children." → Achondroplasia, SED, MED/fibular hemimelia |
| Minicase | "A child with osteogenesis imperfecta presents with progressive bowing. Describe the management principles." |
| MCQ | "A mother asks about arch support insoles for her 3-year-old with flat feet. What do you advise?" → Not effective; arch develops naturally |
| Trap | Correct Approach |
|---|---|
| Treating physiological bowlegs/knock knees with braces | Observation — these self-correct |
| Ordering X-rays for a normal variant (e.g., bilateral symmetric bowlegs in a 1-year-old) | Clinical assessment first; X-ray only if features suggest pathology |
| Confusing proportional and disproportional short stature | Proportional = familial/endocrine; Disproportional = skeletal dysplasia |
| Recommending orthotics for flexible flatfoot | Orthotics do NOT modify the arch — reassure |
| Performing epiphysiodesis after skeletal maturity | Growth plates are fused → epiphysiodesis is useless; need osteotomy |
| Forgetting to check if flatfoot is rigid vs flexible | Always do the tip-toe test |
| Feature | Physiological | Pathological |
|---|---|---|
| Laterality | Bilateral, symmetric | Unilateral or asymmetric |
| Age-appropriateness | Within normal developmental range | Outside expected age range |
| History of injury/infection | Absent | Present |
| Associated syndromal features | Absent | Present |
| Progression | Self-correcting | Progressive |
-
"A 3-year-old child presents with bilateral knock knees. What would you advise the parents?"
- Markscheme: Physiological genu valgum is normal at age 3–4; peaks at this age and corrects by age 7–8. Reassure parents. No treatment needed. Follow-up if progressive, unilateral, or persists beyond age 8.
-
"Describe the multiplier method for predicting LLD at skeletal maturity."
- Markscheme: Multiply current LLD by the age-appropriate multiplier factor. Example: 7-year-old boy, LLD 6.3 cm, multiplier 1.57 → predicted LLD at maturity = 9.9 cm. Used to plan timing and type of surgical intervention.
-
"List 3 treatment options for limb length discrepancy in children and their indications."
- Markscheme: (1) Shoe raise — mild LLD (~2–3 cm); (2) Epiphysiodesis — moderate LLD, timed before skeletal maturity; (3) Limb lengthening — large LLD or when epiphysiodesis insufficient.
-
"How do you distinguish flexible from rigid flatfoot on clinical examination?"
- Markscheme: Tip-toe test — in flexible flatfoot, the medial longitudinal arch reconstitutes and hindfoot inverts to varus on standing on tiptoes. In rigid flatfoot, the arch does not reconstitute and hindfoot remains in valgus. Rigid flatfoot warrants investigation for tarsal coalition.
-
"A mother brings a 4-year-old boy with intoeing. What level should you assess, and what is the natural history?"
- Markscheme: Assess at three levels — hip (femoral anteversion), tibia (internal tibial torsion), foot (metatarsus adductus). At age 4, most common cause is increased femoral anteversion (typical age 3–10). Natural history: 80–95% resolve spontaneously. Braces and shoe modifications do not speed resolution.
High Yield Summary
-
Children are not small adults — they have growth plates, remodelling potential, and changing skeletal alignment throughout development.
-
Skeletal maturity: Female ~14, Male ~16.
-
Short stature: Proportional (familial, endocrine) vs Disproportional (achondroplasia, skeletal dysplasia).
-
LLD: 20–30% of normal people have 0.5–2 cm LLD; treatment usually not needed if < 2.5 cm. Use the multiplier method to predict LLD at maturity. Treatment options: shoe raise, epiphysiodesis, limb lengthening.
-
Bowlegs/knock knees: Physiological varus → valgus → neutral progression. Worry if unilateral, progressive, or associated with rickets/injury/infection.
-
Intoeing: Three levels — femoral anteversion (3–10 y), internal tibial torsion (infancy–3 y), metatarsus adductus (newborn). 80–95% resolve spontaneously. Braces/orthotics are ineffective.
-
Flatfoot: Common and normal in young children. Arch develops in the 1st decade. Orthotics for flexible flatfoot do NOT modify the arch. The critical test is flexible vs rigid (tip-toe test). Rigid flatfoot → investigate for tarsal coalition.
-
Guided growth: Tension band plating across the growth plate corrects angular deformity gradually. Slight over-correction is planned due to expected rebound after plate removal.
-
Evaluation: Multidisciplinary (paediatrics, endocrine, ortho). Labs: Vitamin D, calcium, ALP, GH, thyroid/parathyroid hormones, genetic studies. Imaging: X-rays.
-
Surgery is reserved for pathological and symptomatic deformities — not physiological variants.
Active Recall - Lecture Notes
[1] Lecture slides: CFB (OT02) Childrens Orthopaedics and Deformities.pdf (all pages) [2] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q14) [3] Past papers: 2025 Fourth Summative MCQ.pdf (Q77) [4] Lecture slides: GC 232. Paediatric Musculoskeletal Injury [Updated in 2025].pdf (p22, p32) [5] Senior notes: Adrian Lui Pediatrics Notes.pdf (p457 — Genetic Skeletal Conditions) [6] Senior notes: Block A - Electrolyte and Acid-Base Disorders.pdf (p11 — Fanconi syndrome and hypophosphataemic rickets) [7] Senior notes: Maksim Surgery Notes.pdf (p279 — Paediatric Orthopaedics)
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