Focus On Paediatric lower limb coronal alignment: assessment and diagnosis

Focus On Paediatric lower limb coronal alignment: assessment and diagnosis

Focus On
Paediatric lower limb coronal alignment:
assessment and diagnosis
A large proportion of referrals from primary care to paediatric
orthopaedic clinics involve ‘bowed legs’ and ‘knocked knees’. It
is important for the treating surgeon to understand the normal
development of a child’s lower limbs in order to ascertain what
is ‘normal’ and what is abnormal.
Assessment
Clinical assessment is aimed at distinguishing physiological
from pathological deformities. The following factors must alert
the clinician to possible pathology if elicited in the history and/
or examination:
•Pain
•Asymmetrical deformity
•Severe deformity
•Deformity not in keeping with normal development
•Suspected syndrome (e.g. short stature) or associated
musculoskeletal abnormalities
Clinical examination should also focus on excluding any rotational
abnormalities and ligamentous laxity as these can exaggerate
the appearance of coronal plane deformities. The intercondylar
distance should be measured with the medial malleoli in contact
and should be less than 6 cm in genu varum. The intermalleolar
distance is measured with the knees in contact and should be
less than 8 cm in those with genu valgum.1
A long leg alignment radiograph (teleoroentgenogram) is a
full-length standing anteroposterior (AP) of the lower limbs with
the x-ray beam centred at the anteriorly facing patella (Fig. 1).
This is only required in cases where pathology is suspected or
for pre-operative planning. The mechanical axis refers to a line
drawn from the centre of the femoral head to the centre of the
ankle joint. This line should pass through the centre of the knee
joint and if it does not, there is Mechanical Axis Deviation (MAD).
Genu varum occurs when the MAD is medial to the centre of the
knee joint and genu valgum occurs when the MAD is lateral.
Normal Development
In 1975, Salenius and Vankka2 described the development of
the tibiofemoral angle during growth (Figure 2). At birth, genu
varum is common and is believed to be secondary to intrauterine
positioning which leads to contracture of the medial aspect of
the knee joint capsule.3 Mild internal tibial torsion is common
and the result of these two normal positions is most noticeable
when the child starts to weight-bear.4 The child externally rotates
the tibia to allow the foot to point forwards and this in turn
places the anteriorly bowed femur into a lateral profile, resulting
in symmetrical bowed legs. Referral for ‘bowed legs’ is very
©2013 The British Editorial Society of Bone and Joint Surgery
common between 10 and 14 months, a period when the average
child starts to stand and ambulate but early walking has been
documented in children of Afro-Caribbean descent and therefore
referrals for this subset of children may occur earlier.
This ‘physiological’ genu varum corrects itself over time as
the contracture stretches and from the age of two onwards, a
genu valgum deformity is encountered. Genu valgum (10° to
15°) occurs between the ages of three and four and it is in this
age group when referral for ‘knock knees’ is most common. This
‘physiological’ genu valgum corrects itself to the normal adult
valgum of 7° to 8° by the age of between six and seven. Genu
valgum may be accentuated by fat thighs, ligamentous laxity
and pes planus. In addition, torsional abnormalities such as
persistent femoral neck anteversion with compensatory external
tibial torsion will make a ‘physiological’ genu valgum look more
severe. Education and reassurance is the mainstay of treatment
for the parents if the deformity is deemed to be physiological.
Pathological Genu Varum
Pathological causes of genu varum should be considered if the
deformity is unilateral, asymmetrical or in the child over the age
of three (Table 1).
Blount’s Disease In this condition, growth disturbance in
the proximal medial tibial physis leads to proximal tibial vara
(Fig. 3). Blount’s disease has preponderance for early walking
obese children of Afro-Caribbean and Scandinavian descent.
The pathophysiology is thought to be based on the HeuterVolksmann principle of growth inhibition caused by excessive
compressive forces and is often bilateral. It may be classified
into infantile (age less than four), juvenile (age between four to
ten) and adolescent (age greater than ten) types based on age
of onset. Lagenskiold’s classification depicts the radiographic
changes seen and grades the severity of the proximal tibial
changes.5 Drennan’s angle (metaphyseal-diaphyseal angle) of
greater than 11° is suggestive of Blount’s disease but use of 16°
as the cut-off may lead to a lower incidence of false positives,
especially in the younger child.6,7 Management options include
hemiephysiodesis, guided growth, osteotomies with fixation and
osteotomies with circular frame correction. Recurrence is more
commonly seen in those who are older at the time of osteotomy,
in Blount’s Disease of higher Lagenskiöld stages and in those
who undergo surgery and have a lack of post-operative valgus
overcorrection.8 Corrective osteotomy before the age of four is
associated with lower recurrence rates.6,9
Rickets Nutritional and vitamin-D-resistant (hypophosphataemic)
rickets are metabolic causes of genu varum. Risk factors
for nutritional rickets include dietary factors, darker skin
pigmentation, the practice of covering up or use of sun screens
1
2
D. KOSUGE, M. BARRY
with SPF > 8.10 Therefore, ethnic minorities are more at risk
of developing rickets and given affected children are often in
the lower tenth percentile with regard to height, biochemical
screening should be performed in these subsets of patients.
Radiographic abnormalities include widening of the physes as
a result of lack of calcification in the provisional calcific zone,
cupping of the physes and bowing of the long bones (Fig. 4).
Treatment involves vitamin-D supplementation as well as
phosphate supplementation in cases of vitamin-D-resistant
rickets. Medical therapy can lead to resolving of the radiographic
changes mentioned.
Pathological Genu Valgum
Pathological causes of genu valgus should be considered if the
deformity is unilateral, asymmetrical, progressive or in the child
under the age of two years (Table 2).
Idiopathic When physiologic variants fail to resolve and the
genu valgum persists or worsens, idiopathic genu valgum is the
diagnosis. It is believed to be as a result of prolonged excessive
forces through the lateral aspect of the knee joint. Associated
factors include obesity, ligamentous laxity, pes planus and lateral
femoral condyle hypoplasia (Fig. 5).11
Post-traumatic Fracture of the proximal tibial metaphysis
(‘Cozen’s fracture’) can be complicated by the development of
a genu valgum deformity.12 Theories postulated to explain this
complication include asymmetric stimulation of the proximal
tibial physis, overgrowth of the tibia relative to the fibula, medial
fracture site soft-tissue interposition and malunion.12,13 The
suggestion that fracture hyperaemia leads to stimulation of
the medial proximal tibial physis is the most accepted theory.14
Fractures of the distal femoral or proximal tibia physis may be
complicated by partial growth arrests (Fig. 6). The susceptibility
of these physes to a growth arrest is thought to be due to the
large and convoluted anatomy of the physis.15
Renal Osteodystrophy Like rickets, renal osteodystrophy can
lead to both varus and valgus deformities. However, unlike rickets,
renal osteodystrophy more commonly leads to genu valgum. This
is believed to be due to the pattern of mechanical loading of the
physes as determined by the alignment of the knee at the time
the disease manifests itself. Renal osteodystrophy manifests
itself in older children with genu valgus whereas rickets is
often present at an early age when the child is in genu varum.
Treatment of deformities in this scenario is best performed once
the renal disease has been stabilised by medical treatment or
transplantation.
Conclusion
The treating clinician must be familiar with normal development
of the lower limb in children and be familiar with factors in the
history and examination that should raise the possibility of the
deformity being pathological.
Fig. 1. A normal
teleoroentgenogram of a 13-yearold male with the mechanical axis
passing through the centre of the
knee joint
Fig. 2. Normal development of the tibio-femoral
angle in children
Genu Varum (Bow Legs)
Physiological – Normal until age of 18 to 24 months
Pathological
• Blount’s disease
• Metabolic e.g. rickets, renal osteodystrophy
• Post-traumatic
• Post-infection
• Congenital e.g. achondroplasia, osteogenesis imperfecta
• Skeletal dysplasias e.g. metaphyseal chondrodysplasia
Table I. Causes of genu varum
Genu Valgum (Knock-Knees)
Physiological – Normal from two years onwards
Pathological
• Idiopathic
• Post-traumatic
• Metabolic e.g. rickets, renal osteodystrophy
• neuromuscular
• Post-infection
• Congenital e.g pseudoachondroplasia
• Skeletal dysplasias e.g. multiple epiphyseal dysplasia
Table II. Causes of genu varum
PAEDIATRIC LOWER LIMB CORONAL ALIGNMENT: ASSESSMENT AND DIAGNOSIS
3
D. Kosuge BMedSci FRCSEd (Trauma & Orthopaedics)
M. Barry MS FRCS (Orth)
The Royal London Hospital
Whitechapel Road
London
E1 1BB
UK
E-mail: dennis_kosuge@hotmail.com
References
Fig. 3. Lower limb alignment in
Blount’s disease. Note the bilateral
varus alignment with evidence of a
previous tibial osteotomy on the left
Fig. 5. Idiopathic genu valgum in a
12-year-old girl
Fig. 4. Lower limb alignment in Rickets in
a three-year-old male who in the middle
of medical treatment. Note the widened
distal femoral physes and the varus
alignment bilaterally
Fig. 6. Post-traumatic valgus after
a Salter-Harris III injury of the distal
femur despite anatomical reducation
and fixation
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