Blount Disease

Blount disease is a developmental disorder of the medial proximal tibial growth plate that causes progressive varus deformity (tibia vara) with internal tibial torsion. It is divided into infantile (onset before 4 years) and adolescent forms.

It is more frequent in children of African descent, in those who walk early, and in obesity. Infantile disease is often bilateral, and adolescent disease is often unilateral. Obesity is the main modifiable risk factor.

Untreated disease causes progressive deformity, leg length discrepancy, joint pain, early knee arthritis and gait disturbance.

Pathophysiology.

Excess compressive load across the medial proximal tibial physis in a vulnerable growing child suppresses medial growth, while lateral growth continues. This causes a metaphyseal beak and a depressed medial plateau.

Physiological bowing is a different process: a symmetrical bowing of the femur and tibia that resolves spontaneously by 2 to 3 years.

• Progressive bowing of the legs with a lateral thrust during walking, internal tibial rotation, and a sharp angulation just under the knee.
• Typically painless in infants. Adolescents often present with knee pain, leg length difference and a waddling gait.
• Obesity and early walking are common, and the knees do not correct with growth.

Red flags.

• Unilateral or asymmetric deformity, and progression after 2 years of age.
• Short stature, family history of rickets or skeletal dysplasia (suggests rickets or dysplasia).
• Severe pain, fever or a rapidly worsening deformity.

• Clinical examination of the alignment, gait and leg length. Measure thigh foot angle and intercondylar distance.
• Standing anteroposterior radiograph of both legs from hip to ankle, with the patellae facing forward. Diagnostic features are a metaphyseal diaphyseal angle over 11 degrees, a medial metaphyseal beak and irregular physis. Measure the mechanical axis and joint orientation angles.
• MRI or arthrography to assess the physis and joint surface before surgery.
• Calcium, phosphate, alkaline phosphatase and vitamin D to exclude rickets.

Differential diagnosis. Physiological bowing, rickets, skeletal dysplasia (metaphyseal chondrodysplasia, achondroplasia), focal fibrocartilaginous dysplasia, post-traumatic or post-infective physeal arrest and osteogenic lesions.

• Observe a child under 2 years with bowing and no radiographic changes, and repeat review in 3 to 6 months.
• Infantile disease under 3 years with an early radiographic stage: full time knee-ankle-foot orthosis, for about 23 hours daily, with success being likelier before age 3. Progression after bracing or late presentation needs surgery.
• Surgical options:
  • Proximal tibial osteotomy with correction of varus, rotation and length, ideally before 4 years of age because the recurrence rate is higher later.
  • Growth modulation with a lateral hemiepiphysiodesis plate for younger children with mild to moderate disease and for adolescents with growth left.
  • Medial plateau elevation or physeal bar resection for depression or bars, and gradual correction with an external fixator for severe deformity or limb length discrepancy.
• Weight loss and physical activity for obese children, and treatment of any metabolic cause.

Monitoring. Clinical and radiographic review every 3 to 6 months during growth, with surveillance for recurrence until skeletal maturity.

Referral and escalation. Refer to paediatric orthopaedics for any persistent bowing beyond 2 years, a measured angle over 11 degrees, or asymmetry.