Paediatrics: Knee disorders

Knee disorders

Anterior knee pain

Common in the growing child and is usually due to overuse. Pain is worse with load-bearing, going downstairs, and prolonged sitting with knee flexed.

Common causes include the following:

•   Osteochondroses: Osgood–Schlatter’s disease.

•   Sinding–Larsen–Johansson disease

•   Bipartite patellae: usually bilateral and a normal variant of ossification. There is a risk of developing an avulsion fracture; thus the child should rest, stop sports, and the knee should be splinted. NSAIDs may help. Once resolved, a gradual return to activities is possible.

•   Patella maltracking: several causes including dysplasia of the femoral condyles, malalignment of the quadriceps mechanism with relatively weak vastus medialis, genu valgum, tibial torsion, increased laxity.

Presents with vague anterior knee pain, instability, +/– episodes of patella dislocation. Treatment is physiotherapy, but some may need surgery.

•   Chondromalacia patellae: softening of the articular cartilage, which may progress to osteoarthritis (X-rays may be normal) Treatment physio strengthening and stretches.

Genu recurvatum

Congenital hyperextension

•   Commonest in breech presentations.

•   Associated with arthrogryposis, spina bifida, DDH, talipes equinovarus.

•   Severity varies from mild hyperextension to dislocation. Management: look for other abnormalities (e.g. DDH).

•   Gentle stretching, serial casting, quadriceps lengthening at 1–3mths if necessary.

Acquired recurvatum

•   Physiological ‘curved’ knee occurring in girls due to joint laxity. May be familial and predispose to sprains or patella instability.

•   Consider neurological causes if not bilateral.

•   Clinical features include a hyperextended knee, generalized lax joints.

•   May be caused by trauma to the proximal anterior tibial physis causing a progressive deformity with growth.

Genu valgum (knock knees)

Defined by position of knees such that, when standing with knees to-gether, the medial malleoli are not touching (therefore it is a frontal plane deformity). Commonly observed between ages 2 and 7yrs.

Causes

Bilateral

•   Physiological: most common.

•   Metabolic: renal osteodystrophy, rickets, hypophosphataemia.

Skeletal dysplasia: Kniest’s syndrome, congenital dislocation of patella.

• Haematological: myelodyplasia.

Unilateral

Asymmetric growth—trauma/infection/tumour/epiphyseal dysplasia to tibia or femur.

Presentation 

Child is noticed to walk knock-kneed. Establish rate of pro-gression, diet, and family history.

Examination

• General: height and body proportions. May be overweight or have dysmorphic features. Full lower limb examination (standing and lying); often accompanied by flat feet (pes planus); measure knee angle and intermalleolar distance.

• Specific signs. Tibiofemoral angle assessment. The angle at which the long axis of tibia bisects the long axis of femur can be measured clinically and radiologically. Widened intermalleolar distance (distance between medial malleoli of ankles).

Investigations 

No X-ray required until >18mths age; then AP and lateral standing full leg length views.

Treatment

• Non-operative: mainstay for physiological genu valgum.

• Operative: reversible epiphysiodesis (physeal stapling or eight plate) of medial side tibia. If skeletally mature corrective osteotomy

Prognosis 

95% physiological valgus resolves with growth achieving normal adult alignment by 7–8yrs.

Genu varum (bowed knees)

Bowing of the knees if patient stands with ankles together. Normally genu varum (15°) at birth progresses to physiological genu valgum by 4–5yrs. Genu varum is common in children <3yrs (especially obese children who start walking <1yrs old)

Causes

• Physiological: in utero (curled up) foetal position results in a bowed appearance due to:

o a tight posterior hip capsule which causes external rotation of the hips;

o internal tibial torsion.

• Structural: osteogenesis imperfecta.

• Metabolic: vitamin D deficiency (nutritional rickets)/resistant rickets, hypophosphataemia, calcium deficiency.

• Skeletal dysplasia: metaphyseal dysplasia, achondroplasia, enchondromatosis.

•   Local asymmetric growth: Blount’s disease (abnormal growth of medial  aspect of proximal tibial epiphysis), osteochondromas, physeal injury (e.g. trauma, infection), dysplasia.

History

Parents notice child is walking bowlegged/in toeing of feet. Establish developmental milestones and rate of progression, family history, diet, social history, etc.

Examination

General examination including height and weight; full lower limb examina-tion including rotational profile, widened intercondylar distance (distance between medial femoral condyles).

Investigations

Weight-bearing AP and lateral lower leg views

Symmetrical physiological bowing, flaring of tibia and femur. Can also mea-sure tibiofemoral angle, metataphyseal–diaphyseal angles.

Treatment

Severe physiological genu varum may be treated by guided growth (re-versible epiphysiodesis) using staples or eight plates. Blounts disease may require corrective osteotomes. Refer to orthopaedic paediatric surgeon Prognosis 95% of cases of physiological varus resolve with age.

Osteochondritis dissecans of the knee

Occurs when an area of subchondral bone becomes avascular and frag-ments and separates from the underlying bone. May involve the overlying cartilage, leading to mechanical problems (e.g. loose bodies) and joint in-congruity. Most commonly involves the lateral aspect of the medial femo-ral condyle. It may progress to early degenerative osteoarthritis.

•   Risk factors: adolescents (10–15yrs). Boys > girls. Often secondary to trauma, ischaemia, abnormal epiphyseal ossification.

•   Clinical features: non-specific knee pain, +/– locking and +/– stiffness. Knee swelling after activities, but no history of acute trauma or injury. May be tender over affected articular cartilage of medial femoral condyle if knee is fully flexed.

•   Disease progression: the overlying articular cartilage is usually intact in younger children and the bone heals as revascularization occurs. The risk of articular fracture with separation and loose body formation increases with increasing age, larger lesions, and a weight-bearing location.

Investigations

X-rays of knee in AP, lateral, and notch views to assess femoral condyles. MRI may be useful for determining integrity of articular cartilage and defining whether synovial fluid is behind the lesion.

Treatment

Depends on patient age, size, and stability of fragment. Usually a short treatment with rest, anti-inflammatory drugs, and splintage will suffice. However, it may require surgery:

•   Non-operative: as above, including observation with periodic X-rays and MRIs to assess degree of healing. Bracing and restricted weight-bearing/activities if significant growth remaining.

Operative: adolescent with minimal growth left/loose lesion— arthroscopic assessment with possible debridement and microfracture through subchondral plate to promote revascularization and healing. Fixation of large fragments.

Prognosis 

Worse with large lesions in lateral femoral condyle in older children.