Paediatric Leg and Foot (Non-Trauma)

Last updated: November 17, 2025

Definition of terms

TermDefinition
GenuKnee
TalusAnkle
PesFoot
ValgusInward curving of bone relative to each other
VarusOutward carving of bone relative to each other
Cavussteep arch or depression

Genu Valgum

Genu valgum is aka ‘knock knees’. It is normal in children aged 2-6 years and is always abnormal in adolescents. It can be unilateral or bilateral. Diagnosis is clinical, but laboratory tests for rickets can be obtained

  • Causes
    • Vitamin D-resistant rickets
    • Idiopathic
  • Investiagtions
    • Screen for rickets
    • Leg X-ray: to document severity and progression
  • How do you determine the severity of Genu Valgum?
    • Using the Q-angle of the knee (a knocked knee > 20 degrees)
  • Operative treatment
    • Osteotomy is the only effective management

Genu Varum

Genu varum is aka ‘bow leg’. It may be unilateral or bilateral. It is normal for children aged 3 – 4 years.

  • Causes of genu varum
    • Blount’s disease (idiopathic cause)
    • Rickets
    • Hypophosphatemic rickets
  • Investigations
    • Screen for rickets
    • X-ray of the leg: for severity and presence of bone demineralization (rickets)
  • Treatment
    • Treat underlying cause (rickets or hypophosphatemic rickets)
    • Surgery

Blount’s disease (Tibia Varus)

Blunts disease is a developmental disease involving disordered growth of the proximal tibia. It presents as genu varum persisting past the normal physiological period of varum (aged 3 – 4 years). It is common in obese children and is the most common cause of pathological genu varus.

  • Signs and symptoms
    • Obvious genu varus
    • Internal rotation of the foot and leg length discrepancy (shorter on the affected side)
  • Treatment
    • Osteotomy

Congenital Talipes Equinovarus (CTEV/Club Foot)

Congenital talipes equinovarus (CTEV) is a common congenital anomaly foot/ankle in which there is internal rotation, plantarflexion and adduction of the foot. The cause is idiopathic, but a combination of congenital and environmental factors play a role. It is more common in those with a family history of clubfoot. The most important pathology in clubfoot is medial displacement of the navicular bone on the talus. Shortening of tendons and ligaments of the inner foot secondary to the bony malalignment ****creates the classical positioning of the foot and ankle. It has a typical presentation and is easily identifiable at birth. Diagnosis is clinical.

Occurs in 1 per 1000 births (very common. Affects males more than females (2:1). 80-90% of clubfoot occurs in low- and middle-income countrieas (incidence is 2-3 in 1000 births in southern and eastern Africa). 50% of cases are bilateral.

Pathoanatomy of clubfoot (CAVE)

AcronymComponent
CMidfoot Cavus
AForefoot Adductus
VHindfoot Varus
EEquinus
  • Associated conditions
    • Edward syndrome (47, +18)
    • Ehlers-Danlos
    • Arthrogryposis
    • Tibia hemimelia
    • Amniotic band syndrome (Streeter dysplasia, upper extremity and hand anomalies are also common)
    • Pierre Robin syndrome
    • Opitz syndrome
    • Larsen syndrome
    • Myelodysplasia
  • Pathophysiology
    • Bony deformity
      • Medially displaced navicular and cuboid on the talus
      • Medially and plantarly deviated talar neck
      • Calcaneus in varus and rotated medially around talus
    • Muscle contracture
      • Cavus due to tight intrinsics, FHL and FDL
      • Adductus of forefoot due to tight tibialis posterior
      • Varus due to tight tendoachilles, tibialis posterior, and tibialis anterior
      • Equinus due to tight tendoachilles
  • Physical examination
    • Foot is plantarflexed, internally rotated and adducted
    • Medial crease
    • Posterior crease
    • Empty heel
    • Ankle dorsiflexion
    • Always associated with permanent decrease in calf circumference related to fibrosis of cslf musculature
  • Conservative treatment
    • Ponsetti casting: weekly manual manipulation and casting starting at 2 weeks of age to correct the cavus, adduction and varus
      • At 1 week intervals for the first month then 1-2 week intervals thereafter
      • Started early because the younger the child is the more lax their ligaments
      • Corrected in this order : cavus → adduction → varus
      • After correction achilles tenotomy is performed to correct the equinus
    • French method: daily physical therapy, manipulation and splinting
    • Percutaneous tenotomy of the Achilles tendon to correct the equinus after casting
    • Abduction bracing (orthosis) using a Denis Browne bar/splint worn at night until at least 4 years old
  • Operative treatment of recurrent or complex cases (due to teratogenic clubfoot or decreased brace compliance)
    • Posterior-medial release (Turco’s procedure): for 1 – 3 years of age
    • Tibialis anterior tendon transfer
    • Midfoot osteotomies
    • Talectomy: salvage procedure for severe, rigid and recurrent clubfoot
    • Triple arthrodesis: for > 10 years old. Fusion of the talonavecular, subtalar and calcaneo-cuboid joint. Rarely done. Contraindicated in insensate feet
  • Complications of CTEV
    • Deformity relapse
    • Rocker bottom deformity (due to overcorrection)
    • Dynamic supination
    • Pes planus (from overcorrection)
    • Undercorrection
    • Intoeing gait (due to internal tibial torsion and/or internal rotation of the talus within the mortise)
    • Osteonecrosis of talus

Osgood-Schlatter Disease (Apophysitis of the tibial tubercle)

Osgood-Schlatter disease is apophysitis of the tibial tubercle casued by repetitive microtrauma at the insertion point of the patellar tendon in the tibial tuberosity. It is common in athletically active adolescents. This condition is self-limiting.

  • Signs and symptoms
    • Pain at the patellar ligament insertion on the tubercle apophysis (insertion growth plate
  • Investigations
    • X-ray of the knee joint:
      • Widening of the apophysis
      • Calcified ossicles within the patellar dendon
      • Soft tissue swelling at the insertion
  • Treatment
    • Activity modification until symptoms resolve or the patient reaches skeletal maturity

Sever’s Disease (Calcaneal Apophysitis)

Sever’s disease is apophysitis of the calcaneus. It may be associated with repetitive microtrauma of the heel. It is self-limiting.

  • Signs and symptoms
    • Posterior heel pain
      • Aggravated by running and jumping
  • Investigations
    • X-ray of the foot
  • Treatment
    • Activity modification or rest
Reference Intervals
Biochemistry
ACTHP: <80 ng/L
ALTP: 5–35 U/L
AlbuminP: 35–50 g/L
AldosteroneP: 100–500 pmol/L
Alk. phosphataseP: 30–130 U/L
α-AmylaseP: 0–180 IU/dL
α-FetoproteinS: <10 kU/L
Angiotensin IIP: 5–35 pmol/L
ADHP: 0.9–4.6 pmol/L
ASTP: 5–35 U/L
BicarbonateP: 24–30 mmol/L
BilirubinP: 3–17 μmol/L
BNPP: <50 ng/L
CRPP: <10 mg/L
CalcitoninP: <0.1 mcg/L
Calcium (ionized)P: 1.0–1.25 mmol/L
Calcium (total)P: 2.12–2.60 mmol/L
ChlorideP: 95–105 mmol/L
CholesterolP: <5.0 mmol/L
VLDLP: 0.128–0.645 mmol/L
LDLP: <2.0 mmol/L
HDLP: 0.9–1.93 mmol/L
Cortisol AMP: 450–700 nmol/L
Cortisol MidnightP: 80–280 nmol/L
CK ♂P: 25–195 U/L
CK ♀P: 25–170 U/L
CreatinineP: 70–100 μmol/L
FerritinP: 12–200 mcg/L
FolateS: 2.1 mcg/L
FSHP: 2–8 U/L ♂; >25 menopause
GGT ♂P: 11–51 U/L
GGT ♀P: 7–33 U/L
Glucose (fasting)P: 3.5–5.5 mmol/L
Growth hormoneP: <20 mu/L
HbA1C (DCCT)B: 4–6%
HbA1C (IFCC)B: 20–42 mmol/mol
Iron ♂S: 14–31 μmol/L
Iron ♀S: 11–30 μmol/L
Lactate (venous)P: 0.6–2.4 mmol/L
Lactate (arterial)P: 0.6–1.8 mmol/L
LDHP: 70–250 U/L
LHP: 3–16 U/L
MagnesiumP: 0.75–1.05 mmol/L
OsmolalityP: 278–305 mosmol/kg
PTHP: 0.8–8.5 pmol/L
PotassiumP: 3.5–5.3 mmol/L
Prolactin ♂P: <450 U/L
Prolactin ♀P: <600 U/L
PSAP: 0–4 mcg/mL
Protein (total)P: 60–80 g/L
Red cell folateB: 0.36–1.44 μmol/L
Renin (erect)P: 2.8–4.5 pmol/mL/h
Renin (recumbent)P: 1.1–2.7 pmol/mL/h
SodiumP: 135–145 mmol/L
TBGP: 7–17 mg/L
TSHP: 0.5–4.2 mU/L
T4P: 70–140 nmol/L
Free T4P: 9–22 pmol/L
TIBCS: 54–75 μmol/L
TriglyceridesP: 0.50–2.3 mmol/L
T3P: 1.2–3.0 nmol/L
Troponin TP: <0.1 mcg/L
Urate ♂P: 210–480 μmol/L
Urate ♀P: 150–390 μmol/L
UreaP: 2.5–6.7 mmol/L
Vitamin B12S: 0.13–0.68 nmol/L
Vitamin DS: 50 nmol/L
Arterial Blood Gases
pH7.35–7.45
PaCO₂4.7–6.0 kPa
PaO₂>10.6 kPa
Base excess±2 mmol/L
Urine
Cortisol (free)<280 nmol/24h
Hydroxyindole acetic acid16–73 μmol/24h
Hydroxymethylmandelic acid16–48 μmol/24h
Metanephrines0.03–0.69 μmol/mmol cr.
Osmolality350–1000 mosmol/kg
17-Oxogenic steroids ♂28–30 μmol/24h
17-Oxogenic steroids ♀21–66 μmol/24h
17-Oxosteroids ♂17–76 μmol/24h
17-Oxosteroids ♀14–59 μmol/24h
Phosphate (inorganic)15–50 mmol/24h
Potassium14–120 mmol/24h
Protein<150 mg/24h
Protein/creatinine ratio<3 mg/mmol
Sodium100–250 mmol/24h
Haematology
WCC4.0–11.0 ×10⁹/L
RBC ♂4.5–6.5 ×10¹²/L
RBC ♀3.9–5.6 ×10¹²/L
Hb ♂130–180 g/L
Hb ♀115–160 g/L
PCV ♂0.4–0.54 L/L
PCV ♀0.37–0.47 L/L
MCV76–96 fL
MCH27–32 pg
MCHC300–360 g/L
RDW11.6–14.6%
Neutrophils2.0–7.5 ×10⁹/L (40–75%)
Lymphocytes1.0–4.5 ×10⁹/L (20–45%)
Eosinophils0.04–0.44 ×10⁹/L (1–6%)
Basophils0–0.10 ×10⁹/L (0–1%)
Monocytes0.2–0.8 ×10⁹/L (2–10%)
Platelets150–400 ×10⁹/L
Reticulocytes0.8–2.0% / 25–100 ×10⁹/L
Prothrombin time10–14 s
APTT35–45 s
Paediatric
Pulse Rate (bpm)
Neonate140–160
Infant <1yr120–140
1–5 years110–130
5–12 years80–120
>12 years70–100
Respiratory Rate (tachypnoea)
0–2 months≥60/min
2–12 months≥50/min
1–5 years≥40/min
>5 years≥30/min
Blood Pressure (mmHg)
Term65/45
1 year75/50
4 years85/60
8 years95/65
10 years100/70
Weight Formulas
3–12 months(a + 9)/2 kg
1–6 years2a + 8 kg
>6 years(7a − 5)/2 kg
Haemoglobin (g/dL)
Term newborn13–20
1 month11–18
2 months10–15
1–2 years10–13
>2 years11–14
MUAC (6 months–5 years)
Obese>17.5 cm
Normal13.5–17.4 cm
At risk12.5–13.4 cm
Moderate malnutrition11.5–12.4 cm
Severe malnutrition<11.5 cm
Developmental Milestones
Social smile1.5 months
Head control4 months
Sits unsupported7 months
Crawls10 months
Stands unsupported10–12 months
Walks12–13 months
Talks18 months
CSF WBC (/mm³)
Term newborn0–25
>2 weeks0–5
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