13.20 Common knee conditions

The knee is one of the most common joints that paediatric orthopaedic surgeons are asked to evaluate. All children who complain of knee symptoms also need to be assessed for ipsilateral hip and lumbar spine disorders. This chapter will discuss common knee conditions seen in the paediatric population. Knee disorders specific to young athletes will be reviewed in the section on sports medicine (see Chapter 13.23). The adolescent patellofemoral joint has also been covered in Chapter 8.10.

The patellofemoral articulation is a complex joint that relies on bony conformity as well as on static and dynamic soft tissue components for stability. Any disturbance of the normal anatomical relations due to dysplasia, malalignment, or trauma can affect this balance and lateral subluxation and dislocation are common.

The patella forms during the seventh week of embryonic life. The cells develop deep to the patellar tendon as an uncalcified cartilaginous anlage that grows over time, ossifying between 4–6 years. The soft tissues surrounding the patella contribute significantly to patellofemoral joint stability. More specifically, the medial patellofemoral ligament (MPFL) and the vastus medialis obliquus (VMO) provide the greatest restraints to excessive lateral patellar displacement. The MPFL crosses the anteromedial aspect of the knee from the adductor tubercle of the femoral epicondyle to the superomedial aspect of the patella (Figure 13.20.1). It has been estimated to provide 50–80% of the restraining force to lateral translation and isolated release of the MPFL increases lateral displacement of the patella by 50%. The VMO is important as the primary dynamic medial stabilizer and is intimately associated with the MPFL.

With the knee in full extension, the patella naturally rests superolateral to the femoral sulcus. Engagement between the patella and trochlea does not occur until the knee flexes about 10–30 degrees. This can be affected by changes in patellar tendon length. Patients with patella alta, for instance, engage the trochlea at greater flexion angles, leading to less bony constraint at earlier degrees of flexion, theoretically increasing the risk for dislocation (Figure 13.20.2). Trochlear dysplasia has also been identified as a contributing factor to patellar instability. Broadly defined as flattening of the trochlear sulcus, dysplasia has been seen in 29–85% of patients with patellofemoral instability (Figure 13.20.3). Various torsional deformities of both the femur and tibia have also been implicated in this disorder. Historically, increased Q angles have been considered a risk factor for patellar instability: larger Q angles subject the patella to a larger overall lateral force vector (Box 13.20.1). Recent reports, however, question the significance of this finding. Generalized ligamentous laxity has been implicated in as many as two-thirds of patients with patellar instability but again the relevance of this has been queried recently.

Congenital dislocation of the patella is uncommon and two clinical syndromes have been described. One is referred to as a fixed lateral dislocation of the patella and the second described as habitual dislocation of the patella. Others have used the term obligatory dislocation of the patella to describe habitual, acquired, or atraumatic dislocation. Congenital or persistent lateral dislocation of the patella and obligatory dislocation of the patella have two different clinical presentations as shown in Table 13.20.1.

The child with congenital lateral dislocation of the patella presents with a knee flexion contracture and no patella palpable anterior to the femoral condyles. Palpation of the hypoplastic patella in its lateral position is difficult. A magnetic resonance imaging (MRI) scan may be necessary to ascertain the location of the cartilaginous patella. This child may present with a delay in the ability to walk independently or with an abnormal gait related to a knee flexion contracture and the associated external tibial torsion. Affected patients may have a musculoskeletal syndrome of which the patella dislocation is one feature. Congenital dislocation of the patella may occur bilaterally but more commonly it is unilateral (Box 13.20.2).

The pathoanatomy of congenital patellar dislocation always includes a joint contracture, with contracted posterior capsule and hamstring tendons, and may include congenital absence of the cruciate ligaments. In addition, there are varying degrees of contracture of the lateral retinaculum, iliotibial band, vastus lateralis, rectus femoris, vastus intermedius, and also the lateral patellofemoral, patellotibial, and patellomeniscal ligaments. In cases of fixed lateral dislocation of the patella, the extensor mechanism becomes a flexor and external rotator of the knee, leading to progressive genu valgum.

Acute atraumatic, habitual, or obligatory dislocation of the patella characteristically presents after the child begins to walk. Patella alta, trochlear dysplasia, and hyperelasticity contribute to the pathoanatomy. These patients do not have a flexion contracture but they do complain of knee instability which may be surprisingly well tolerated. Knee extension may be weak. In childhood, dysfunction and deformity, rather than pain, are the presenting complaints (Figure 13.20.4).

Relocation of the patella can encourage the development of an adequate trochlea and patellofemoral congruence and thus surgical intervention is recommended when the child presents at an early age. For the adolescent, reduction and reconstruction is recommended only if symptoms warrant.

Whether the patella dislocation is fixed or obligatory, the surgical management can be quite complex. Understanding that the pathoanatomy includes significant soft tissue contractures is critical. An extensive release of all abnormally tight lateral structures is necessary: this includes the lateral retinaculum, the lateral capsule with the imbedded patellofemoral ligaments, and the lateral patellomeniscal ligaments found within the fat pad of the knee. The retinaculum is repaired in a lengthened position after the patella has been realigned. The vastus lateralis is also invariably involved and either shortened or abnormally adherent to the iliotibial band or lateral intermuscular septum. To avoid overcorrection, lengthening of the vastus lateralis after release from surrounding adhesions is preferred to release alone.

After an extensive lateral release, the patella should lie well-centered within the trochlea. However, in most cases, there is still a contracture of the central portion of the quadriceps mechanism which must be lengthened if the patella stability is to be maintained as the knee flexes. In the presence of an arthrogrypotic like flexion contracture of the knee, a formal posterior approach may be required for a hamstring lengthening and release of the posterior capsule.

The medial retinaculum with the inclusion of the MPFL is always severely attenuated with congenital patellar dislocations. In the fixed type, the retinaculum may be adherent to the underlying medial femoral condyle and requires a careful dissection to free it from the underlying joint surface. After appropriate lateral releases and lengthenings have allowed the patella to be reduced, the medial retinaculum is repaired and the MPFL is reconstructed. In older patients, additional augmentation of the medial repair vector is required. Transferring the semitendinosus tendon into the patella accomplishes this.

In obligatory atraumatic dislocation, the contractures are generally not severe. Lengthening rather than release of the lateral retinaculum is performed to prevent overcorrection and to maintain the positive effect of the lateral retinaculum on patellar stability. MPFL reconstruction can be included if it is not associated with hyperelasticity and/or significant trochlear dysplasia.

The mean annual incidence of acute traumatic lateral patellar dislocation is 5.8:100 000 increasing to 29:100 000 in the subgroup of 10–17-year-olds. Contrary to previous beliefs, the most commonly affected person is not an obese, sedentary female but rather a young athlete of either gender. Two common mechanisms of traumatic patellar dislocation are sports (61%) and dance (9%) injuries (Box 13.20.3). Dislocation may result from a non-contact injury with a mechanism similar to that responsible for anterior cruciate ligament injuries or it may be a result of blunt trauma producing either a valgus/external rotation moment about the knee or a laterally directed force on the patella that exceeds the tensile strength of the MPFL in patients predisposed to dislocation. Particular care should be taken to determine whether the patient has had a previous patellar dislocation on the index or contralateral knee. A history of contralateral patellar dislocation increases the risk of recurrence sixfold: as much as a previous dislocation event on the index knee. A family history of patellar dislocation can be elicited in 9–15% of patients (Box 13.20.3).

A significant number of patients with acute traumatic patellar instability will experience chronic instability or chronic patellofemoral pain. Reported redislocation rates range from 15–44% but perhaps more troublesome is that at least 30–50% of patients can be expected to have anterior knee pain more than 2 years after injury.

Medial dislocations are uncommon and almost universally iatrogenic: secondary to overzealous release of the lateral patellar retinaculum in the treatment of lateral instability. Intra-articular dislocations are exceedingly rare.

Physical examination for patellar instability should include assessment of resting position of the patella standing and in extension and tracking of the patella from flexion into extension looking for lateral translation (J sign) and from extension into flexion looking for capture into the trochlea. More than 50% passive lateral translation of the patella is abnormal, more so if it is accompanied by apprehension. Knee hyperextension and signs of general laxity should be sought and the strength and tightness of hamstrings and quadriceps should be assessed. A rotational profile often reveals internal femoral torsion and external tibial torsion, ‘squinting knees’, which may predispose to lateral subluxation of the patella.

Traditionally, plain radiographs have been the standard form of initial radiographic assessment to document patellar location and identify osteochondral fractures (Box 13.20.4). MRI may delineate the pathology further: it is 85% sensitive and 70% accurate in the diagnosis of MPFL ligament injury. The sensitivity for chondral injuries is variable but improves with specific cartilage imaging sequences. In addition, ultrasound has recently been reported to detect MPFL injury reliably in addition to identifying bony avulsions.

For patients with acute traumatic patellar dislocation without osteochondral injury, the knee should be immobilized, following reduction, with a compressive dressing and a knee immobilizer. Weight bearing as tolerated is allowed, with the assistance of crutches. At first review, a failure to improve, as evidenced by persistent pain, swelling, and limited motion, heralds more significant intra-articular pathology which should prompt further radiographic investigation and/or arthroscopy. Early operative intervention should be considered in patients with associated osteochondral injuries, defects of the MPFL–VMO complex, and in children with high-level athletic demands. Damage to critical weight-bearing articular surfaces may require repair, debridement, or one of the many types of cartilage restoration procedures. These can be performed open or arthroscopically, depending on the size and condition of the lesion.

In children with recurrent atraumatic dislocation or persistent patellar instability despite a well-controlled rehabilitation programme, operative management should be considered to prevent progressive articular damage. Invariably the underlying aetiology is due to fixed pathoanatomy, which may be bony (trochlear dysplasia, increased Q angle, increased tibial tuberosity:trochlear groove distance). Many different surgical techniques for the treatment of patellar instability have been described (Box 13.20.5).

These can be grouped broadly into soft tissue balancing and realignment or bony procedures. In children with open growth plates, procedures such as the Elmslie-Trillat technique are contraindicated because damage to the growth plate risks subsequent deformity. Proximal or distal soft tissue realignment procedures, with or without tibial tuberosity transfer have had limited success in patients with trochlear dysplasia. In these knees, ligamentous insufficiency is not a cause, but rather a consequence of recurrent dislocation. Different surgical techniques have been described in an attempt to correct trochlear dysplasia and femoral or tibial osteotomies may be necessary to correct the overall limb alignment.

This is an acquired condition affecting subchondral bone that manifests as a pathological spectrum ranging from softening of the overlying articular cartilage with an intact articular surface, through early articular cartilage separation, with or without partial detachment of an articular lesion, to osteochondral separation with loose body formation. The prevalence of osteochondritis dissecans (OCD) is 15–29:100 000 individuals with males affected in a ratio of 5:3. The increasing participation of young children in competitive sports has led to a decrease in the mean age of presentation and an increased prevalence amongst girls. The site of the lesion in the femoral condyles does not differ between age groups, and more than 70% of lesions are found in the ‘classic’ area of the posterolateral aspect of the medial femoral condyle (Box 13.20.6 and Figure 13.20.5). Patellar involvement is uncommon.

Idiopathic OCD must be differentiated from similar lesions resulting from avascular necrosis associated with chemotherapy, haemoglobinopathy, and steroid use. Several causes of OCD have been postulated, including inflammation, genetic influences, ischaemia, and defects in ossification but there is insufficient evidence to support any single factor. Histologically, the typical OCD lesion of the medial femoral condyle resembles a subchondral stress fracture. Lesions are typically associated with osteoid production and giant cell resorption and generally appear avascular. Fairbanks in 1933 suggested that OCD was the result of violent inwards rotation of the tibia, driving the tibial spine against the inner aspect of the MFC. Repetitive trauma may also induce a stress fracture within the underlying subchondral bone and if repetitive loading persists and prevents the subchondral bone from healing (non-union), necrosis of the fragment may occur and lead to fragment dissection and separation. External tibial torsion is increased in patients with bilateral OCD and even more so in patients with persisting complaints which suggests that tibial torsion has a role in the development of OCD of the knee.

OCD is traditionally divided into juvenile (open physes) and adult (closed physes) based on skeletal maturity. This distinction is useful because higher rates of healing have been seen in juvenile OCD than in the adult form. Juvenile OCD is seen more frequently in athletic children. Symptoms are preceded by a history of trauma to the knee in 40–60% of cases. It typically presents as anterior knee pain: worse with activity and improved by rest. Patients with early, intact OCD lesions, present with vague symptoms of poorly localized knee pain, stiffness with or after activities, and occasional swelling after activity. Mechanical symptoms such as grinding, locking, and catching are more commonly associated with the late stages of OCD where loose or detached OCD lesions are present.

An initial physical finding is tenderness over the involved condyle with the knee flexed. Later, patients develop a joint effusion and a decreased range of motion. The child may limp and the involved leg may be externally rotated to prevent impingement of the tibial spine on the MFC. Pain may be elicited with internal rotation of the tibia (Wilson’s sign) but this sign lacks sensitivity. In stable lesions, there is usually no effusion, crepitus or pain through a range of normal motion. Quadriceps atrophy may be noted in long standing cases.

Mechanical symptoms are pronounced with unstable lesions. An antalgic gait is common and there is usually a knee effusion, possibly associated with crepitus with motion. Both knees should be examined since the condition is bilateral in 20–25% of cases. If bilateral disease is present, lesions are typically asymmetrical in terms of size and symptoms.

Initial investigations include standing AP and lateral radiographs. If OCD is suspected ‘notch’ or ‘tunnel’ views should be requested to localize and characterize the lesion, rule out additional bony pathology, and evaluate skeletal maturity. In children less than 7 years of age, irregularities of the distal femoral epiphyseal ossification centre may simulate OCD but these asymptomatic sites are anatomic variants of normal ossification. The location of the lesion can be described and an estimate of size obtained from the radiographs (Figure 13.20.5). Characteristic findings include a well-circumscribed area of subchondral bone separated by a crescent-shaped sclerotic radiolucent outline of the fragment.

OCD of the knee can be diagnosed using plain radiographs alone but they are poor at establishing the stability of the lesion or the state of the overlying cartilage. MRI is considered the gold standard for evaluation of OCD. MRI can give an accurate estimate of the size of the lesion and status of cartilage and subchondral bone (Figure 13.20.6). The extent of bony oedema, the appearance of a high signal zone beneath the fragment, and presence of loose bodies are additional important MRI findings (Table 13.20.2). The most useful diagnostic feature of MRI is its ability to distinguish between stage II and III lesions. The presence of synovial fluid or granulation tissue at the interface between the fragment and the parent bone, manifested as increased signal intensity on T₂-weighted spin echo MRIs, generally indicates an unstable lesion. Conversely, the absence of a zone of high signal at this interface is a reliable sign of lesion stability. In stage II OCD lesions, the low signal in the interface indicates fibrous attachment stabilizing the lesion. In contrast, stage III lesions will show high signal intensity at the interface, indicating synovial fluid between the fragment and underlying parent bone.

As the natural history of stable OCD lesions is generally favourable in a child with open physes, there is widespread agreement that initial non-operative treatment is indicated.

Kocher advocates a three-phase non-operative management protocol (Box 13.20.7). At the end of phase 1, the child should be pain-free, and repeat radiographs should be obtained. In phase 2, weight bearing as tolerated is permitted without immobilization. A rehabilitation programme is initiated emphasizing knee range of motion and low-impact quadriceps and hamstring strengthening exercises. Sports and repetitive impact activities are restricted. If there are radiographic and clinical signs of healing at 3–4 months after the diagnosis, phase 3 can begin. This phase includes supervised initiation of running, jumping, and cutting sports readiness activities. A gradual return to sports with increasing intensity is allowed in the absence of knee symptoms. An MRI may be repeated in phase 3 to assess healing. If symptoms return or follow-up radiographs show recurrence, repeat non-operative treatment can be considered.

Operative treatment should be considered in patients with detached or unstable lesions (stage III and IV) regardless of the age of the child and in those patients approaching physeal closure whose lesions have been unresponsive to non-operative management (Box 13.20.8). In general, unstable lesions require partial takedown with debridement to remove fibrous tissue and restore vascularity. These techniques are based on the premise that the lesion is essentially a fracture non-union and rely on the penetration of subchondral bone to promote vascular ingrowth into the non-union site. Guhl described the system for arthroscopic staging of the lesions (Table 13.20.3).

Arthroscopic drilling of juvenile OCD to create channels for potential revascularization and healing may be transepiphyseal or transarticular. Antegrade drilling through the epiphysis avoids damage to the articular surface but is associated with technical challenges of maintaining accurate drill placement and depth. On the other hand, retrograde transarticular drilling is relatively straightforward, although the channels it creates through the articular cartilage heal with fibrocartilage. If partially unstable lesions have subchondral bone loss, autogenous bone graft is packed into the crater before fragment reduction and fixation.

Mechanical stabilization of unstable OCD lesions increases the likelihood of maintaining joint congruity postoperatively, and allows for the potential of early joint motion. Stabilization can be performed using a variety of implants including Kirschner wires, low-profile compression screws, cannulated screws, bone pegs, bioabsorbable fixation, or fibrin glue. A variety of treatments have evolved over the past few years aimed at addressing irreparable chondral defects and OCD lesions. Interventions include perichondral/periosteal autografts, autologous chondrocyte implantation (ACI) and matrix-induced ACI techniques, abrasion chondroplasty, microfracture, osteochondral autograft transplantation (OAT—mosaicplasty), and osteochondral allografts. Most of these treatment options result in the formation of fibrocartilage covering the exposed defect rather than true hyaline cartilage. The long-term results from these procedures have yet to be clearly determined. A completely separated OCD fragment in a skeletally immature person may be treated by arthroscopic or open excision, or by reduction and fixation. Recent separation and a larger bony fragment favour an attempt at reduction and fixation into the debrided defect. Failure to of the fragment to heal, or a chronic separation, favour excision with debridement of the defect: this itself will result in substantial fibrocartilage healing.

Discoid menisci invariably affect the lateral meniscus and the overall incidence is 3–5% with up to one-fifth of cases being bilateral. Although the condition is a congenital anomaly, or perhaps simply an anatomical variant, no explanation for its occurrence has been found. Discoid menisci are more likely to tear due to the increased stresses on their larger surface area. The meniscus is also often hypermobile. The Watanabe classification (Table 13.20.4) is used most frequently. Type III lesions often present at a young age with symptoms of a ‘snapping knee’ and unexplained falls due to giving way. Pain is not a feature. Physical examination may elicit a reproducible ‘clunk’ on the lateral side of the knee as the flexed and externally rotated knee is brought into extension and internal rotation. Type I and II lesions present in later childhood, following a meniscal tear, with symptoms and signs similar to other types of meniscal injury. A widened lateral joint space may be seen on plain radiography and the diagnosis is often made on MRI.

The asymptomatic discoid meniscus requires no treatment. A torn meniscus may have a stable rim in which case the central portion is simply ‘saucerized’. If there is instability or peripheral detachment of the remaining meniscus, meniscal suturing should be performed (see Chapter 13.23).

As in adults, torn menisci can lead to the formation of meniscal cysts (Figure 13.20.7). Treatment is directed at the meniscal tear and the cyst will usually drain and close spontaneously.

Osgood–Schlatter disease and Sinding–Larsen–Johansson syndrome are typically overuse injuries causing apophysitis of the anterior tibial tubercle and inferior pole of the patella respectively. They are common in active adolescents and associated with local tenderness and palpable swelling. Symptoms are often bilateral but both symptoms and signs may be markedly asymmetrical. Often a history of increased use, rapid growth, or jumping/landing sports accompanies the onset of pain. Repetitive small injuries to the tendon insertion are believed to be important in the aetiology of this condition. Growing children are particularly vulnerable because growth leads to tight muscles especially those, such as rectus femoris, which cross two joints. A tight rectus femoris (positive Ely–Duncan test) can often be elicited among adolescents with Osgood–Schlatter disease or jumper’s knee. Radiographs confirm fragmentation of the apophysis and in such cases other differential diagnoses for unilateral bony pain and swelling in this age group such as a malignancy become much less likely.

Management is conservative with physiotherapy indicated to address tight hamstrings or quadriceps and general advice on the use of cushioned insoles and restriction of sporting activity but only if symptoms warrant this. Attention to jumping and landing technique, or play on soft surfaces, may be useful adjuncts. Most cases of Osgood–Schlatter disease have resolved by skeletal maturity when the apophysis fuses with the rest of the tibial tubercle. For the small minority of cases that continue with symptoms, surgical excision of a painful residual ossicle(s) with decompression of the patella tendon may give dramatic symptom relief.