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
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.
Learning Objectives (Directly from Slides)
Core Concept: Why "Children Are Not Small Adults"
1. Growth Plates (Physes) and Ossification Centres
"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 and contains organised chondrocyte zones (reserve → proliferative → hypertrophic → provisional calcification/ossification). It is vulnerable to trauma, infection, ischaemia and metabolic disease; physeal injury can produce a Salter-Harris fracture and later partial or complete growth arrest. [4]
How to read the serial elbow/hip radiographs: unossified cartilage is invisible on plain X-ray, so a young joint can look “incomplete” without being abnormal. Identify the expected ossification centres for age, compare sides when appropriate, and check alignment; do not call every lucent physis or absent-yet-unossified centre a fracture/dislocation.
Each long bone grows more from one end than the other. This determines which physeal injuries carry the greatest impact on final limb length. [1]
| Bone | Proximal Physis | Distal Physis |
|---|---|---|
| Humerus | 80% | 20% |
| Radius | 25% | 75% |
| Ulna | 80% | 20% |
| Femur | 30% | 70% |
| Tibia | 55% | 45% |
| Fibula | 60% | 40% |
Clinical relevance: A physeal injury at the distal femur (70% of femoral growth) or proximal humerus (80% of humeral growth) has far greater potential for limb length discrepancy than injury at the opposite end. This also guides epiphysiodesis site selection — the growth plate that contributes more can be tethered for a larger correction effect.
- On X-ray, the physis appears as a radiolucent line. Don't mistake it for a fracture.
The image-heavy overview is not a list of equivalent diagnoses. It contrasts normal developmental shape with several different mechanisms of deformity:
| Appearance in the montage | Mechanism to recognise |
|---|---|
| Symmetrical bowing in an infant | Often physiological, but interpret against age and progression |
| Short or angulated segment after injury/infection | Local physeal arrest; expect asymmetry or progressive LLD/angular change |
| Spondyloepiphyseal dysplasia (SED) | Trunk and epiphyseal involvement; disproportion may be short-trunk |
| Multiple epiphyseal dysplasia (MED) | Multiple abnormal epiphyses, malalignment and early joint disease |
| Mucopolysaccharidosis | Multisystem disorder with dysostosis multiplex |
| Achondroplasia | Rhizomelic disproportion from an activating FGFR3 variant |
The visual discriminator is therefore not simply “bowed versus straight”: ask whether the pattern is age-appropriate, symmetric, proportionate, progressive and accompanied by systemic or syndromic features.
Why this matters: Any injury, infection, ischaemic or metabolic insult that damages the growth plate can cause physeal arrest → segmental shortening, limb length discrepancy or angular deformity. Local physeal arrest does not usually cause generalised proportional short stature.
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]
Limits of the remodelling image: the serial humeral radiographs show dramatic correction because the child has growth remaining and the deformity is favourably placed. Do not generalise that result to rotational deformity, intra-articular displacement, major translation/shortening or angulation poorly aligned with the neighbouring joint's plane of motion; those remodel much less predictably.
"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.
Lecture rule of thumb: Female ~14, Male ~16. [1]
These ages are a planning approximation, not a biological cut-off for an individual child. Pubertal timing and bone age vary, so surgical planning uses serial height/limb measurements, sexual maturity and often a left-hand/wrist bone-age assessment rather than chronological age alone. After physeal closure there is no further longitudinal growth, and growth-modulation procedures can no longer work. [9]
Slide-by-Slide High-Yield Content
Multidisciplinary approach: Paediatricians, endocrinologist, orthopaedic surgeons [1]
| Component | Details |
|---|---|
| History | Serial growth, gestation/birth size, nutrition and chronic illness; family and pubertal history; pain/function; trauma/infection; medicines (including glucocorticoids and some anti-seizure drugs) [1][10] |
| Physical exam | Accurate height/weight plotted serially; growth velocity; mid-parental target; pubertal stage; arm span and upper:lower segment; gait, rotational profile and limb deformity; dysmorphic/systemic features [10] |
| Laboratory tests | Targeted, not automatic. The slide's examples include vitamin D, calcium, ALP, thyroid/parathyroid testing and genetic studies; suspected growth failure may instead require CBC/CMP, ESR/CRP, TSH/free T4, coeliac screen, IGF-1/IGFBP-3 or genetics according to the phenotype [1][10] |
| Imaging | Use the question to choose imaging: left-hand/wrist bone age for growth assessment; standing long-leg radiographs for pathological alignment/LLD; site-specific films for suspected focal disease [8][9] |
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]
Do not use the slide as a blanket test panel
One low height percentile is less informative than the trajectory. A healthy child tracking a low centile with normal growth velocity may need observation rather than every test on the slide. Falling across centiles after age 3, height below the 3rd centile, height far below genetic potential, absent catch-up after fetal growth restriction, abnormal proportions or syndromic features should prompt targeted evaluation/referral. [10]
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 |
The slide groups these visually, but the mechanisms differ: achondroplasia is a generalised skeletal dysplasia, whereas fibular hemimelia is a segmental congenital limb deficiency that primarily produces lower-limb shortening/LLD rather than a classic whole-body short-stature syndrome.
Achondroplasia (Key Example from Slides + Senior Notes)
- Genetics: Autosomal dominant; an activating FGFR3 pathogenic variant. About 80% of affected people have average-stature parents because the variant is de novo; absence of family history does not exclude the diagnosis. [11]
- Clinical: Disproportionate short stature with rhizomelic shortening (proximal limbs affected most), macrocephaly, frontal bossing, flat nasal bridge, thoracolumbar kyphosis (gibbus), trident hand [5]
- Management: Multidisciplinary surveillance focuses on craniocervical junction compression, sleep-disordered breathing, hearing/otitis, kyphosis, genu varum, spinal stenosis and weight. Growth hormone is not “replacement” unless GH deficiency exists. Current targeted options include C-type natriuretic peptide-pathway therapy for eligible children with open physes; extended limb lengthening is a major shared decision with substantial burdens and risks. [11]
- 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 painful or truly rigid foot is not the usual benign flexible variant and needs assessment for an underlying cause.
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]
Treat those figures as the lecture's screening heuristic, not a universal treatment rule. Small differences are common and often tolerated; management depends on symptoms, cause, hip/knee/foot stability, predicted discrepancy at maturity and the child's priorities. A standing block test levels the pelvis and estimates functional LLD; calibrated standing long-leg imaging separates femoral from tibial contribution when precision matters. [8]
| 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 / lateralised overgrowth: One side or body region is larger. Tumour surveillance is relevant when this is part of an overgrowth syndrome, but it should not be inferred from every apparent LLD without a genetics/paediatric assessment.
- Ollier's disease: Multiple enchondromas → asymmetric growth → LLD.
- Perthes disease: The slide pairs it with an abnormal-gait image. Perthes classically causes a painful or painless limp, restricted hip abduction/internal rotation and later femoral-head/neck deformity; shortening can contribute, but an apparent short-leg gait is not synonymous with a true fixed LLD. [1]
The lecture slide illustrates the normal gait cycle alongside the abnormal gait caused by LLD: [1]
- Stance phase (~60% of gait cycle): Initial contact → Loading response → Midstance → Terminal stance → Preswing
- Swing phase (~40% of gait cycle): Initial swing → Midswing → Terminal swing
LLD disrupts symmetry between limbs. Compensation may include pelvic obliquity, toe-walking on the shorter side, knee flexion on the longer side or circumduction/hip hiking for clearance. A Trendelenburg sign instead points to hip-abductor insufficiency; do not use it as a synonym for short-leg gait. [8]
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 helps guide treatment planning, but no single numerical result makes surgery automatic.
Important limitation: the multiplier method assumes a particular growth pattern and is especially convenient for congenital, proportionate discrepancies. Developmental discrepancies after physeal injury or infection may not progress proportionally. Predictions should be checked against serial measurements, skeletal age and other methods (Moseley straight-line or Green-Anderson) rather than treated as exact. The slide's 9.9 cm is a worked teaching calculation, not a stand-alone operative plan. [9]
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 |
|---|---|---|
| Observation / shoe lift | Small or well-tolerated discrepancy; lift height is individualised | Levels the pelvis and can improve gait or fatigue without changing bone length |
| Epiphysiodesis | Commonly considered for a predicted 2–6 cm discrepancy in a growing child [9] | Permanent ablation stops a selected physis; implant-based techniques may slow growth temporarily. Timing and symmetry are crucial |
| Shortening | Selected skeletally mature patients with a moderate discrepancy | Acutely shortens the longer bone, avoiding reliance on remaining growth |
| Lengthening | Larger discrepancy or complex limb deficiency | Distraction osteogenesis lengthens the shorter segment; external fixation is shown in the PFFD slide. It requires prolonged rehabilitation and carries neurovascular, joint, bone-healing and infection risks [1][9] |
High Yield: Epiphysiodesis Timing
Classic drill/burr epiphysiodesis is permanent; staple/plate/screw growth modulation may be designed to be temporary. In either case, compare predicted LLD at maturity using serial data, skeletal age and more than one prediction method when possible. If permanent arrest is done too early, the previously longer leg can become short; if too late, residual discrepancy remains. [9]
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: On a standing hip-to-ankle radiograph, draw a line from the centre of the femoral head to the centre of the ankle mortise. It should cross the central portion of the knee (often near the medial tibial spine); lateral passage indicates valgus and medial passage indicates varus. [12]
- Anatomical axis: Line down the intramedullary shaft. The femoral anatomical axis is oblique because the femoral head is offset from the shaft, whereas the tibial anatomical and mechanical axes are much closer.
- Read the whole film: first locate the mechanical-axis deviation, then identify whether the deformity is femoral, tibial or both (e.g., using mLDFA and MPTA). A cropped knee film cannot answer that reliably. [12]
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) |
This table is the textual reading of the slide's curve: varus at birth moves through neutral at roughly 18–24 months, reaches maximum physiological valgus at 3–4 years, then settles toward about 5–7° valgus by around age 7. There is a broad normal range; the trend, symmetry and symptoms matter more than one angle. [12]
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° (the selected target in this case) |
| After plate removal | Rebound after plate removal → 2° valgus (final acceptable alignment) |
How guided growth works: A plate is placed on the convex side of the deformity: usually lateral tethering for varus and medial tethering for valgus. The tethered side grows more slowly while the opposite side continues to grow, producing gradual correction. It requires an open physis and enough growth remaining. Standing long-leg films localise the deformity and serial review (often every 3–4 months during correction) detects overcorrection, hardware problems or an unintended sagittal/rotational change. [12]
Reading the sequence: the lecture case progresses from 18° varus → neutral at 20 months → 4° intentional overcorrection → 2° valgus after implant removal. This illustrates that rebound can occur, not that every child should automatically be overcorrected. Slight overcorrection may be considered in younger children at higher rebound risk; the decision and timing are individualised. [12]
- Acute correction (osteotomy) — the lecture shows a case of unilateral genu valgum measured at 19.2°, corrected with osteotomy and internal fixation [1]. Unilateral/asymmetric deformity is a red flag for pathology, but it is not by itself an automatic indication for surgery. Osteotomy is used when immediate correction is required or growth modulation is no longer possible; the correction level should match the deformity analysis. [12]
- Intramedullary rodding — shown for osteogenesis imperfecta (OI) [1]
- The slide shows a 5-year-old boy with osteogenesis imperfecta with multiple fractures and bowing, managed with telescoping intramedullary rods [1]
- Genetically heterogeneous bone-fragility disorder; the classic and most common forms involve type I collagen genes (COL1A1/COL1A2) → fractures, bowing and variable extraskeletal features [5]
- Type I (most common): AD, fractures + blue sclerae ± hearing loss [5]
- Type II: Usually perinatally lethal, with severe skeletal fragility and fractures in utero [5]
- Management: Specialist bisphosphonate therapy can improve vertebral shape/bone density and mobility in selected children; intramedullary rodding supports long bones and corrects deformity [5]
The slide's operative sequence shows multiple osteotomies with intramedullary support, followed by functional recovery. Rodding straightens and supports long bones but does not cure the collagen disorder; fracture care, rehabilitation, mobility, pain, hearing/dental/respiratory needs and specialist medical treatment remain part of longitudinal care.
- Lecture shows a patient with MED with bilateral valgus malalignment requiring reconstruction [1]
- MED affects multiple epiphyses → irregular joint surfaces → malalignment + early OA
G. Intoeing
Intoeing gait or walking with an excessively inward foot-progression angle is very common in children. [1]
| 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]
The slide's “80 → 95%” figure conveys the direction of natural history, not a precisely reproducible probability for every child. Most idiopathic femoral anteversion and internal tibial torsion improve with growth; braces, twister cables and corrective shoes do not accelerate this. Imaging is usually unnecessary for a typical symmetric presentation. [13]
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.
| Observation/test | What it localises |
|---|---|
| Foot-progression angle during gait | Net in/out direction of each foot; also watch patellar direction and symmetry |
| Prone hip rotation, knees at 90° | Internal rotation much greater than external rotation supports increased femoral anteversion |
| Thigh-foot angle / transmalleolar axis | Internal or external tibial torsion |
| Heel-bisector line | Forefoot shape: normally exits near the second toe; progressively more lateral exit supports metatarsus adductus |
The “W-sitting” photograph is an associated posture, not a cause that parents must prevent. Refer/investigate when intoeing is painful, progressive, markedly asymmetric, causes major functional limitation, lies well outside the age-adjusted range, or is accompanied by weakness, spasticity, regression or other neuromuscular signs. Derotation osteotomy is rarely considered for severe persistent functional/cosmetic deformity after about age 8; the radiographic angle alone is not the indication. [13]
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: Orthoses Do Not Build a Permanent Arch
Orthoses do not create a permanent arch or alter natural arch development in an asymptomatic flexible flatfoot. That does not mean every insert is useless: an inexpensive off-the-shelf arch support may reduce pain or fatigue in a symptomatic flexible flatfoot, and stretching is useful when the heel cord is tight. Custom devices have little routine advantage. [14]
Tip-toeing test: Observe hindfoot valgus [1]
| Feature | Flexible Flatfoot | Rigid Flatfoot |
|---|---|---|
| Arch on tip-toe / Jack test | Arch reconstitutes and hindfoot inverts; great-toe dorsiflexion also recreates the arch | Arch does not reconstitute and subtalar motion is restricted |
| Significance | Usually a normal variant when bilateral and painless | Painful rigidity needs a cause identified |
| Causes | Ligamentous laxity; apparent flattening accentuated by infant fat pad; sometimes tight Achilles | Tarsal coalition (shown on slides [1]); also congenital vertical talus, inflammatory/neuromuscular or post-traumatic causes |
| Management | Reassure if painless; activity/footwear advice, heel-cord stretching or simple orthosis for symptoms | Weight-bearing radiographs first when painful; CT/MRI only when the clinical question requires it. Surgery is for selected persistent symptomatic pathology, not every rigid-looking foot [14] |
Why do the tip-toe and Jack tests work? Heel rise activates the triceps surae and tibialis posterior, while the windlass mechanism tensions the plantar fascia; a flexible hindfoot moves from valgus toward varus and the arch reappears. Passive dorsiflexion of the great toe (Jack test) similarly tensions the plantar fascia. A coalition can block subtalar motion, so the heel fails to invert.
The Staheli figure uses an arch index (A/B): A is the narrow midfoot print and B is heel width. A larger ratio means a flatter footprint. The broad scatter is as important as the mean curve — infant flatfoot is common, the arch develops through childhood, and footprint appearance alone does not diagnose painful pathology. [1]
"The growth is different in everyone" — lecture shows side-by-side comparison of hypophosphataemic rickets and normal variance. [1]
- X-linked hypophosphataemia (XLH) is the commonest inherited hypophosphataemic rickets, caused by a PHEX pathogenic variant with excess FGF23 activity. This reduces renal phosphate reabsorption and inappropriately suppresses active vitamin D, impairing mineralisation. Other inherited and acquired causes of renal phosphate wasting also exist. [15]
- Visual/radiographic pattern: short stature with progressive lower-limb bowing; widened, frayed and cupped metaphyses at rapidly growing sites. Confirm renal phosphate wasting biochemically rather than diagnosing from appearance alone.
- Current specialist treatment may use burosumab (anti-FGF23) or conventional divided oral phosphate with active vitamin D. Phosphate alone is unsafe because it can worsen secondary hyperparathyroidism; treatment needs biochemical and renal monitoring. [15]
- The lecture point remains: do not label every bowlegged child as having rickets. Normal developmental alignment is common, while rickets is progressive and supported by history, examination, radiographs and laboratories.
"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 uses Perthes as a visual example beside abnormal gait; true shortening can contribute but is not the only mechanism [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 supports for her pain-free 3-year-old with flexible flat feet. What do you advise?" → Reassure; they do not create a permanent arch |
| 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 |
| Saying orthotics are always useless in flexible flatfoot | They do not permanently reshape the arch, but a simple insert can relieve symptoms |
| Performing growth modulation after skeletal maturity | Fused physes cannot be modulated; options depend on the problem and may include lift, shortening, lengthening or osteotomy |
| Forgetting to check if flatfoot is rigid vs flexible | Use heel rise and/or Jack test, assess subtalar motion and heel-cord tightness |
| 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 |
High Yield Summary
- Children are not small adults: growth plates, ossification centres, remodelling potential and normal alignment all change with age.
- Start with trajectory and pattern: serial growth, age, symmetry, progression, pain/function, body proportions and trauma/infection history.
- LLD: confirm with a standing block test and long-leg imaging when needed; plan from predicted discrepancy at maturity, not one present-day threshold.
- Alignment: physiological varus becomes valgus and settles by about age 7. Unilateral, progressive, painful or out-of-age-range deformity is concerning.
- Guided growth: tether the convex side while physes are open; monitor closely for correction, overcorrection and rebound.
- Intoeing: localise with the rotational profile (hip rotation, thigh-foot angle, heel bisector). Most idiopathic cases improve; corrective shoes and braces do not accelerate this.
- Flatfoot: distinguish painless flexible feet from painful or rigid feet. Orthoses do not permanently build an arch but may relieve symptoms.
- Operate for an identified structural problem with symptoms or predicted functional consequence, not merely because a child's appearance differs from an adult's.
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) [8] American Academy of Orthopaedic Surgeons. Lower Limb Length Discrepancy. https://www.orthoinfo.org/diseases--conditions/limb-length-discrepancy [9] Pediatric Orthopaedic Society of North America. Epiphysiodesis Prediction and Technique. https://posna.org/physician-education/study-guide/epiphyseodesis-prediction-and-technique [10] Pediatric Endocrine Society. Child with Suspected Short Stature. https://pedsendo.org/clinical-resource/child-with-suspected-short-stature/ [11] Legare JM, Modaff P. Achondroplasia. GeneReviews (updated 2026). https://www.ncbi.nlm.nih.gov/books/NBK1152/ [12] Pediatric Orthopaedic Society of North America. Genu Valgum. https://posna.org/physician-education/study-guide/genu-valgum [13] Pediatric Orthopaedic Society of North America. Torsional Problems. https://posna.org/physician-education/study-guide/torsional-problems [14] Pediatric Orthopaedic Society of North America. Flat Feet (Acquired Flexible Flat Feet). https://posna.org/physician-education/study-guide/flat-feet-%28acquired-flexible-flat-feet%29 [15] X-Linked Hypophosphatemia. GeneReviews. https://www.ncbi.nlm.nih.gov/books/NBK83985/
CFB PAE02 Child Growth And Development
Child growth and development encompasses the progressive physical, cognitive, emotional, and social maturation from infancy through adolescence, assessed through standardized milestones and growth parameters.
CFB PSY02 Classification And Diagnosis Of Psychiatric Illness
Classification and diagnosis of psychiatric illness involves the systematic categorization of mental disorders using standardized criteria such as the ICD and DSM to guide clinical assessment, communication, and treatment planning.