Open Reduction Internal Fixation Metal Compression Techniques for Juvenile Osteochondritis Dissecans
Davietta C. Butty
Adam B. Yanke
Brian J. Cole
INTRODUCTION
The hallmark of osteochondritis dissecans (OCD) is pathologic destruction of the subchondral bone with secondary changes to the overlying articular cartilage. These changes can lead to pain, instability, and early-onset arthritis. The true etiology is not well understood; however, it has been proposed that the following are contributing factors: repetitive microtrauma, vascular insufficiency,1 genetic predisposition, ossification abnormalities, and endocrine dysfunction. OCD lesions are most common in the knee but can also occur in the wrist, elbow, and ankle. In the knee, the lateral aspect of the medial femoral condyle is the most common lesion location, followed by the lateral femoral condyle and patellofemoral joint. The prevalence of OCD lesions is 15 to 29 per 100,000 individuals, with an average age of onset ranging from 11.3 to 13.4 years.2 Males are 2 to 3.8 times as likely to have an OCD compared to females, and bilateral lesions are present in 12% to 30% of cases.3,4,5 Moreover, ethnic and demographic data demonstrates that blacks have the highest odds ratio of OCD in the knee compared to other ethnicities.5 The overall incidence of OCD lesions is increasing in addition to the incidence of OCD in females, a trend which some attribute to earlier participation in more competitive sports.2,6 Adult OCD lesions are mainly juvenile lesions that become symptomatic after the closure of the physis and therefore present in adulthood.7 This delineation is important, as the treatment of OCD lesions depends greatly on the ability of the host to heal the lesion. Therefore, treatment of juvenile lesions with open physes varies greatly from those in patients with closed physes, as 50% of stable juvenile OCD lesions will heal on their own within 10 to 18 months.8 Concerns for the early development of arthritis and its associated morbidity provide the impetus for early operative treatment in symptomatic unstable lesions.9
HISTORY AND PHYSICAL EXAM
Because the incidence of OCD lesions has been reported to be 0.015% to 0.03% in asymptomatic patients, making an accurate diagnosis is critical.10 It is important to elicit from the patient how long the symptoms have been present and determine if prior treatments have been offered, including specific amounts of time spent with protected weight bearing or relative rest from higher impact activities. Longer duration of symptoms may manifest itself in quadriceps atrophy at the time of exam. The signs and symptoms of a patient with a juvenile OCD lesion are often very sensitive but nonspecific. Typical findings include knee pain, swelling after activity, and, occasionally, mechanical symptoms such as catching and locking. However, the presence of mechanical symptoms is suggestive of and potentially pathognomonic for the presence of a loose body or unstable osteochondral fragment.6
On physical exam, the examiner may observe an antalgic gait, and the patient may be tender to palpation over the anteromedial knee if the lesion is in the classic location of the distal medial femoral condyle. Although the “Wilson” test (internal rotation of the tibia while extending the knee against resistance)11 has been described for these lesions, it is not very reliable.6,10,12 The examiner may differentiate an OCD lesion from meniscal pathology by noting more tenderness at the femoral condyle than the joint line itself. Although physical exam is important for confirming objective signs of intra-articular pathology, imaging is the keystone for determining surgical treatment.
IMAGING
Initial evaluation of the patient with a suspected OCD lesion should include standard radiographs of the knee with bilateral anteroposterior (AP) and lateral weight bearing, Merchant (axial), and Rosenberg (posteroanterior at 45-degree flexion) views.10,13 Tunnel and skyline views may also be beneficial.14 These views allow for an assessment of physeal status and lesion size, location, sclerosis, fragmentation, and displacement.10,13 Magnetic resonance imaging (MRI) is also used to evaluate lesions and has recently been referred to as the gold standard15 to further delineate the lesion. The most crucial
portion of the MRI is determining the presence of signal deep to the lesion, indicating instability (Fig. 24.1). The De Smet MRI criteria are the most prevalent classification system used16:
portion of the MRI is determining the presence of signal deep to the lesion, indicating instability (Fig. 24.1). The De Smet MRI criteria are the most prevalent classification system used16:
Figure 24.1. Skeletally immature patient with OCD lesion to the trochlea with high signal intensity deep to the lesion (double arrow) and cystic changes with bone marrow edema as well (single arrow). |
A thin line of high signal intensity measuring 5 mm or more in length at the interface between the OCD lesion and the underlying bone
A discrete, round area of homogeneous high signal intensity 5 mm or more in diameter beneath the lesion
A focal defect with a width of 5 mm or more in the articular surface of the lesion
A high signal intensity line traversing the articular cartilage and subchondral bone plate into the lesion
TREATMENT
The goal of any treatment is to reduce pain and improve function of the knee. Surgical decisions are based on a number of factors including clinical symptoms; patient age; physeal maturity; and lesion stability, location, and size.17
Nonoperative Treatment
Currently, there is no role for treatment of an incidental juvenile OCD lesion. Most juvenile OCD lesions respond well to activity modification and limited weight bearing when stable. Nonoperative management consists of anti-inflammatory medications, relative rest, and protected weight bearing for 6 to 8 weeks. After this time, if the patient is symptom-free, a gradual return to sports and other high-impact activities takes place over another 6 to 8 weeks. Immobilization is controversial, as this can lead to stiffness and contradicts the initial work done by Salter et al.10,18 Immobilization for a period of greater than 16 weeks can lead to stiffness, cartilage degeneration, muscle atrophy, and poor healing10,19 and should be avoided. In a multicenter review by Hefti et al.,4 young patients treated nonoperatively had better results when they had lesions less than 2 cm2, had no signs of infection, and no effusion at the time of diagnosis. Classic location on the medial femoral condyle was also associated with higher healing rates,2 whereas larger lesions and those on the lateral femoral condyle had lower healing rates.20 Healing rates for skeletally immature patients with nonoperative treatment range from 50% to 94% at 10 to 18 months.21