Osteochondritis dissecans (OCD) of the elbow is localised most commonly at the capitellum. It is a localised condition of the subchondral bone which may result in segmentation and separation. Irreversible changes, pain, restriction of motion and limitation of activities may result because of this. Elbow OCD afflicts athletes in the second decade, especially adolescents engaged in repetitive elbow overuse such as gymnasts, pitchers and swimmers. A high index of suspicion is warranted to prevent delay in the diagnosis. Imaging studies begin with standard elbow radiographs, but in later stages MRI or CT scan are indicated. Lesions are classified as ‘stable’ or ‘unstable’. In general stable lesions are treated conservatively, whereas unstable lesions are indicated for surgical management. Geographical variation exists in techniques for arthroscopic procedures for OCD of the elbow. In Europe and the USA most surgeons use classic arthroscopic debridement and microfracturing for lesions which are not amendable to a solid fixation, whereas in Australia some surgeons use dry arthroscopy for optimal assessment of the articular surface and the presence or absence of subchondral bone. In Japan fixation of the OCD with bone pegs is favoured. Numerous other surgical techniques have been reported, including internal fixation of large fragments and osteochondral autograft transfer. The aim of this article is to explore OCD of the elbow with regard to aetiology, clinical presentation, the diagnostics prior to the intervention, the different surgical techniques, possible complications and pitfalls, clinical outcome and future directions.
- Orthopaedic Sports Medicine
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Elbow Osteochondritis Dissecans (OCD) presents typically in adolescent athletes engaged in repetitive overhead or upper extremity weightbearing activities (eg, baseball, tennis, volleyball, weight lifting and gymnastics).
As advanced OCD can be related to degenerative changes it is of utmost importance to detect and treat OCD at its early stages. The screening of young athletes, participating in high-risk sports as baseball, tennis and gymnastics, has been proposed in some countries.
Prevalence and societal impact of the disease
OCD is a localised condition of the subchondral bone which may result in segmentation and separation. In athletes, OCD lesions are most commonly found in the knee, followed by the ankle and the elbow.1 OCD of the elbow, is most commonly affecting the central and anterolateral part of the capitellum; it has also been reported in the olecranon, radial head and trochlea. This sport-related injury occurs during the growth phase and is seen in ∼2–8% of school-age baseball players. The prevalence of OCD of the humeral capitellum was 3.4% among more than 2000 adolescent baseball players.2
The patients usually are in their second decade of life, with an age ranging from 11 to 23 years. The onset of the disease is typically at 11 years just prior to the closure of the growth plate. Involvement of both elbows is seen in up to 20% of the patients.3
OCD is a typical sports-related problem with high suspicion but, with an early diagnosis, the impact of OCD on daily life is relatively small. Sports activities are restricted to allow regeneration in stable lesions. Unstable OCD may develop symptoms from loose bodies and over time from osteoarthritic changes with restricted motion, ulnar nerve symptoms and pain at night.
Longstanding OCD can be related to osteoarthritic changes. These osteoarthritic changes do not necessarily inhibit patient's sports-related activities. When osteoarthritic changes progress, with restricted range of motion, ulnar nerve symptoms or pain at rest or at night, symptoms can result in difficulties in sports and daily life.
Historic perspective of OCD
Elbow OCD should be distinguished from osteochondrosis of the capitellum or Panner's disease. A Danish orthopaedic surgeon—Dr Dane Panner—first described radiographical changes of the capitellum in a young adult, eponymised as Panner's disease in 1927. The etiopathogenesis of this condition was considered to be similar to osteochondrosis of the hip epiphysis (Legg-Calvé-Perthes).
Panner's disease is encountered in younger children (aged 4–12 years). This condition is characterised by ischaemia and necrosis of the capitellar epiphysis, followed by regeneration and recalcification. In general it is a self-limiting disorder that is probably not sports related and resolves with rest. Surgery for Panner's disease is in most cases not indicated. It is possible that osteochondrosis and OCD of the capitellum are different stages of a single condition affecting the maturation of the capitellar epiphysis.4
Panner's disease probably is underdiagnosed, because the clinical symptoms and findings on radiographs can be subtle. In the literature Panner's disease is often confused with OCD, because of some similarities of both diseases, which makes the conclusion of systematic reviews on this topic sometimes confusing.
Anatomy and etiology
The exact aetiology of OCD is poorly understood. There are many factors associated with the aetiology and development of avascular necrosis. These include genetics, anatomy, trauma, vascular, metabolic, haematogenous, endocrine, nutritional and inflammatory disorders.5–8 Based on twin studies a genetic predisposition has been suggested.9 There is considerable evidence to support the traumatic theory, as it is more common in the dominant arm of those involved in pitching and gymnastics. Most of the work on the vascular concepts of the capitellum is based on the histology, which has demonstrated that there is avascular necrosis and the known arterial supply of the capitellum.
The capitellar ‘condyle’ is the common site of avascular necrosis (AVN). It is to be noted that the subchondral bone plate on the convex capitellar surface is only a single trabecular layer. Being only 0.1 mm thick, makes it susceptible to trauma, and prone to fractures and OCD (figures 1 and 2). The remainder of the distal humerus subchondral bone plate has secondary layers that support the subchondral plate. Avascular necrosis is often considered to be a compartment syndrome of bone8 ,10 (figure 3). The capitellum is the compartment, and the mechanical factors act on this fixed osseous structure. The factors that can change the pressure within the capitellum compartment include the (1) arterial inflow, (2) embolisation, (3) the compartment contents and (4) venous outflow.
There has been much attention to the arterial supply of the distal humerus (figure 4). Arterial obstruction can cause avascular necrosis of the bone; however, it is really very uncommon for AVN to occur, except for complex injuries of the lateral condyle. The humeral canal is supplied by nutrient vessels from the canal, while the capitellum is supplied by vessels from the lateral condyle (figure 5). The nutrient vessels supply the humeral shaft but do not supply the distal humerus. The capitellum is supplied by vessels from the lateral epicondyle that enter the posterior aspect of the capitellum.11 ,12 The capitellum does not receive blood supply from the anterior or medial aspects of the humerus. Prior to age five, the capitellum has a rich vascular supply. After age five, the capitellar nucleus is supplied by only one or two very small vessels end arteries. As the capitellum grows and ossifies, the surrounding areas of the epiphysis become relatively avascular, and if the one or two small vessels supplying the capitellum are disrupted, local ischaemia can be the result. Surgery on the lateral epicondyle and posterior aspect of the capitellum can compromise further the vascularity of the capitellum. Embolisation of the arteries can cause localised necrosis, but it is really uncommon for AVN to be a complication of atrial fibrillation or other embolic diseases.
The main contents of the bony compartment are the bone marrow and its fat. There are conditions that can increase these components, such as Gaucher's disease and alcohol abuse. The intraosseous fat is very sensitive to ischaemia and once necrosis occurs there is significant oedema, and this can have a real impact of local vascularity of the bone. Therefore the contents of the bone are unlikely to initiate the AVN, but are likely to potentiate the condition.
The venous concepts of AVN have been previously described. Hungerford demonstrated that the intraosseous pressure is significantly raised in the femoral head AVN.13 Jensen demonstrated that the intraosseous pressure in Kienböck's lunate was significantly increased compared with the normal population.14 ,15 The intraosseous pressure rose significantly on wrist extension, especially in the Kienböck's disease of the lunate. In some cases the Kienböck’s lunate's intraosseous pressure exceeds arterial blood pressure. He postulated that the compromised venous outflow, and the increased intraosseous pressure, were factors in the development of Kienböck's disease. Crock11 has published images of the venous drainage of the distal humerus (figure 6A,B). He described the subarticular plexus of veins, which are wavy parallel veins immediately deep into the subchondral bone plate. He also published the amazing images that demonstrate how the veins drain the subchondral bone plate (figure 7A,B). The subarticular venous plexus is directly adjacent to the subchondral bone plate, making it particularly at risk, even with a minor fracture, such as a stress fracture. Venous ischaemia is not a new concept. There are examples of both acute and chronic venous engorgement that can lead to necrosis. Acute venous obstruction will lead to a free flap failure within hours, if the venous drainage is not restored. Chronic venous engorgement due to failure of the valves of the saphenous vein produces venous hypertension, which ultimately leads to perivenous fibrosis, local ischaemia and subsequent ulceration of the cutaneous tissues. Acute or chronic venous obstruction will cause devastating effects. In a predisposed patient, repeated insults lead to hypoperfusion and ischaemia of the lunate. There is support from the literature that impairment of venous drainage plays a critical role in the pathoanatomy of AVN.9
Acute trauma or repetitive micro traumas play an important role especially a valgus load on the throwing elbow (figure 8).5 ,6 OCD in the non-dominant hand of overhead athletes are very rare. Repeated loading, in the predisposed individual, causes a stress fracture and injury to the subarticular venous plexus, which is directly adjacent (figure 9). This leads to localised venous hypertension, ischaemia, oedema of the fat cells, and subsequent fat and osseous necrosis. There are other factors which are all part of the complex picture which defines the at risk individual, and are areas in which there will continue to be further research. Subsequently, this focal avascular necrosis can result in loss of support for the overlying articular cartilage and eventually breakdown and starting the formation of loose fragments once the mechanical support of the articular cartilage is compromised5 ,6 (figure 10).
Repeated valgus force aggravates the defect, as the radial head falls into the defect with repeated stress across the capitellum (figure 11). OCD usually evolves through three stages.3 ,6 In stage 1, hyperaemic bone and oedematous periarticular soft tissues are found. In stage 2, the epiphysis deforms, sometimes with fragmentation. In stage 3, the necrotic bone is replaced by a granulation tissue. The articular surface may separate and form a loose body as the bone heals. Patients with OCD are probably predisposed to early osteoarthritis of the elbow. However, the relation between cartilage defects in general and the development of osteoarthritis in the long term has not been elucidated to date. Most evidence is available for cartilage lesions in the knee and ankle.14 ,17 Large chondral and osteochondral lesions of the knee are presumed to predispose to osteoarthritis, although scientific evidence is limited.14 In the ankle, however, a relation between OCD and osteoarthritis has not been shown.17 Only 4% of ankle OCDs develop a narrowed joint space up to 20 years of follow-up.18 With regard to the OCD of the capitellum of the elbow, little is known about the risk of developing degenerative changes in the long term. Bauer et al19 investigated osteoarthritic signs of the elbow among 31 OCD patients after a mean follow-up of 23 years. One-third had degenerative changes on standard radiographs. Forty-two per cent of those patients reported of pain and/or reduced range of motion at the time of follow-up. Younger patients had better odds of having a pain-free elbow without radiographic signs of degeneration in the long term. Takahara et al20 noted a poorer long-term outcome of patients with relatively large cartilage lesions compared with those with small lesions. The natural course of cartilage defects in general and untreated OCD at the elbow in particular remains incompletely understood to date. Larger lesions and older age seem associated with more symptoms and radiographic changes in the long term. No data are available whether any of the available cartilage defect repair strategies stop or slow down the development or progression of osteoarthritic changes.14
As OCD of the elbow is highly related to specific athletic activities, the incidence and treatment of this pathology varies around the world. In the USA and Japan, most OCD are described in baseball players, whereas in Europe and Australia OCD is also seen in tennis players and gymnasts. Geographical variation exists in techniques for arthroscopic procedures for OCD of the elbow. In Europe and the USA most surgeons use classic arthroscopic debridement and microfracturing for lesions which are not amendable to solid fixation, whereas in Australia some surgeons use dry arthroscopy for optimal assessment of the articular surface. In Japan fixation of the OCD with bone pegs is favoured under some conditions in which European surgeons might advise conservative treatment. The screening of young athletes, participating in high-risk sports as baseball, tennis and gymnastics, has been proposed in some countries. Especially in Japan and the USA national guidelines exist to limit excessive upper extremity activity in the young baseball players. This will probably reduce the number of OCD in the near future in Japan and in the USA.
Reviews and state-of-the-art or current concept articles
Systematic reviews of the literature on OCD of the elbow are scarce. Most studies present case series with a review of the literature. Two proper systematic reviews were published in the last decade on the treatment of OCD of the elbow. One systematic review by de Graaf et al suggests that surgical treatment must be contemplated after a period of unsuccessful conservative therapy for athletes with OCD. Nevertheless, their conclusion was that larger studies with enhanced methodological quality and longer follow-up should be performed to support this conclusion.21 A second systematic review on the location of OCD lesions of the capitellum suggests that lesions located on the lateral capitellum, particularly those involving the lateral cartilage margin, require more aggressive surgical management than those located medially22 (box 1).
Key articles, according to the authors, on osteochondritis dissecans (OCD) of the elbow
Minami23 described one of the first, relatively large series, with 25 cases of OCD of the elbow.
Bauer et al19 investigated elbow degeneration among 31 OCD patients at a mean follow-up of 23 years. One-third had radiographic degenerative changes and 42% of patients reported of pain.
Byrd and Jones24 described the technique for arthroscopic surgery for isolated capitellar OCD in adolescent baseball players in 2002.
Kijowski and De Smet25 show that the radiographs of patients with a capitellar OCD appear normal in 50% of the cases.
The prevalence of OCD of the humeral capitellum is 3.4% among more than 2000 adolescent baseball players.26
Bain and coauthors describe ‘dry arthroscopy’ for the elbow joint as a very helpful technique in the treatment of OCD.27
Initial symptoms of OCD are often vague. Patients report about subtle discomfort, swelling and limitation of extension after training. In general the pain is initially mild but improves with rest. Consequently athletes can often continue playing until the condition of the OCD progresses, and they finally seek medical help. These vague clinical symptoms of OCD of the elbow result often in a patient's delay and a doctor's delay. Therefore, a high index of suspicion and directed imaging studies are necessary. In fact, any child or young athlete presenting with lateral or diffuse elbow pain should be suspected of having an OCD lesion until proven otherwise. Patients present with an insidious onset of elbow pain, tenderness and swelling over the lateral aspect of the elbow.17 In later stages, particularly with increased activity, loss of motion or mechanical symptoms such as popping, clicking or even giving way during load bearing activities are seen. Findings on physical examination are not very distinct in the early stages of OCD. Swelling of the posterolateral elbow plica, with or without impingement in combination with loss of terminal extension can be seen. Provocative tests for the lateral compartment are painful in more advanced cases. Forearm pronation and supination motion are usually not limited. Provocative tests for the radiocapitellar joint as the ‘grip and grind’ test can be positive with a crepitus and even a clicking sensation. No evidence is available yet on the sensitivity and specificity of these tests.
It is of utmost importance to detect OCD in all cases as early as possible to prevent expansion of the lesion with fragmentation of the OCD and finally degeneration of the joint.
Standard anteroposterior and lateral radiographs are often used as an initial screening method. Radiographic signs of an OCD can be flattening of the capitellum, a focal defect of the articular surface and loose bodies. Routine radiographs of the elbow are not sensitive in identifying OCD of the capitellum.28 Almost half of the radiographs of patients with a capitellar OCD appear normal.28 An anteroposterior view with the elbow in 45° of flexion may better depict the lesion than in an anteroposterior view in extension.29
When an OCD is suspected in a young athlete, additional imaging is indicated as the sensitivity of plain radiography is low. Ultrasound scan of the elbow has been described to detect capitellar OCD and can be useful as screening tool outside the hospital.30–32 However, the quality of the ultrasound scan is, as with all ultrasound examinations, highly dependent of the experience of the observer.32 CT scan and MRI are most useful in the assessment of OCD of the elbow. MRI demonstrates early OCD and is valuable in determining the stability and viability of the OCD fragment.19 ,32 ,33 CT scans are more sensitive and better depict loose bodies in advanced stages of OCD. In a group of 25 patients with OCD proven by arthroscopy, who all had preoperative radiographs, MRI and CT scan the OCD was visible on 25 CT scans (sensitivity, 100%). However, OCD was detected only on 24 MRIs (sensitivity, 96%), and on 19 radiographs (sensitivity, 76%). Loose bodies were identified on arthroscopy in 20 cases. These were visible in 18 CT scans (90%), in 13 MRIs (65%) and 11 radiographs (55%). CT thus seems to be the preferred imaging technique to assess OCD of the elbow and loose bodies in advanced cases of OCD.34 In early stages MRI is probably preferred.
Classification of the lesion is critical because current management guidelines are dependent on the type of lesion present and on its stability.
Several classifications have been described for OCD of the elbow; the value of grading of capitellar OCD seems limited.35 Most classifications are based on standard radiographs, as the Minami Classification, CT, MRI, or arthroscopy.23
In the Minami Classification grade 1 describes a stable lesion with a translucent cystic shadow in the capitellum; grade 2, a clear zone between the OCD and adjacent subchondral bone; and grade 3, loose bodies.
The classification, based on MRI, according to Itsubo et al16 distinguishes five stages. In stage 1, a normally shaped capitellum is seen with several spotted areas of high signal intensity. In stage 2, is as in stage 1 the capitellum is seen with several spotted areas of higher intensity than that of cartilage. In stage 3, it is seen as in stage 2 but with both discontinuity and non-circularity of the chondral surface signal of the capitellum and no high signal interface apparent between the lesion and the bottom of the lesion. In stage 4, the lesion is separated by a high-intensity line in comparison with the cartilage. In stage 5, the capitellar lesion is displaced from the floor or a defect of the capitellar lesion is noted.
In a recent study the Minami Classification was the most reliable for classifying different stages of OCD of the capitellum. However, it was unclear whether radiographic evidence of OCD of the humeral capitellum, as categorised by the Minami Classification, guides treatment in clinical practice as a result of this fair agreement.
OCD lesions can be classified during the arthroscopic procedure as well see box 2.
Classification of osteochondritis dissecans (OCD) of the elbow
The Minami Classification is the most reliable for classifying different stages of OCD capitellum.
▸ Grade 1: Localised flattening or radiolucency.
▸ Grade 2: Non-displaced fragment.
▸ Grade 3: Displaced or detached fragment.
The International Cartilage Repair Society has an arthroscopic classification system for OCD lesions.36
▸ Grade 1: A stable lesion with a continuous but softened area covered by intact cartilage.
▸ Grade 2: A lesion with partial discontinuity that is stable when probed.
▸ Grade 3: A lesion with a complete discontinuity that is not yet dislocated.
▸ Grade 4: An empty defect as well as a defect with a dislocated fragment or a loose fragment lying within the bed.
Surgical intervention should be reserved for patients with pain or functional impairment. Progression of the lesion on radiographs, CT scans or MRI, and symptomatic loose bodies or disruption of the cartilage are relative indications for surgery.
In stable lesions conservative treatment is advocated, especially in patients with open growth plates.37–39
For unstable lesions, with a defect of the cartilage or a high signal intensity line through the lesion on MRI, surgery can be indicated if the patient is symptomatic or has the wish to participate in overhead sports or heavy labour (box 3).
Possible outcome measures
Osteochondritis dissecans (OCD) elbow
▸ Timmerman Score
▸ MAESS (derived from Timmerman score)
▸ SANE score
▸ Oxford Elbow Score
▸ Mayo Elbow Performance Index (MEPI)
▸ American Shoulder and Elbow Surgeons (ASES)
▸ Disabilities of Arm Shoulder and Hand (DASH)*
▸ 36-Item Short Form Health Survey (SF-36)*
*Approved by the International Society of Arthroscopy, Knee Surgery and Orthopaedic Sports Medicine (ISAKOS) Scientific Committee.
None of the outcome measures is validated for OCD of the elbow.
MAESS, modified Andrews Elbow Scoring System; SANE, Single Assessment Numeric Evaluation.
In stable lesions (International Cartilage Repair Society (ICRS) type I), the majority of OCD lesions should be managed non-operatively.40 This implies that all provoking activities are not allowed.
For baseball players this means that throwing and batting are prohibited, for tennis players any use of the racket is forbidden and gymnasts are not allowed to apply any axial weight on the upper limb. Once signs and clinical symptoms have settled strengthening exercises can be started. In general return to sports-related activities takes at least 6 months. Management in general follows clinical signs and symptoms rather than radiological progress or healing. It is unclear what the optimal frequency is of a MRI to evaluate the healing process. Evidence suggests that return to high-level gymnastics or baseball is unlikely after conservative treatment. Takahara et al40 in 1999 reported a success rate of only 50% after an average follow-up of 12.6 years.
It is unclear what the role of low-intensity pulsed ultrasound is in healing of the OCD.
For the surgical treatment of advanced, unstable OCD or failure of conservative treatment various techniques have been described. Arthroscopic procedures range from simple removal of loose bodies on to more advanced procedures with debridement and drilling or microfracturing of the lesion or fragment fixation. ICRS type II lesions seem to be the optimal lesion for in situ fixation; however, selection of the appropriate surgical procedure is still controversial. ICRS type III lesions are also suitable for fixation with additional filling of the defect with autologous bone, for example from the proximal ulna, before fixation. As an alternative for arthroscopic surgery and in case of a failed arthroscopic procedure several open surgical approaches have been reported, as internal fixation of large fragments, bone peg fixation, osteochondral autograft transfer, autologous chondrocyte transplantation or even a wedge osteotomy of the lateral condyle.29 ,41–44
In comparison to open surgery, arthroscopic surgery offers the advantage of direct visualisation of the pathology and the ability to treat the lesion through limited incisions. Moreover arthroscopy reduces the risk of complications and facilitates rapid rehabilitation.45 Arthroscopic treatment includes debridement or curettage of the lesion to achieve a stable rim, followed by bone marrow stimulation by drilling or microfracture, in combination with removal of loose fragments and, in advanced stages, osteophytes.24 ,46 See box 2 for tips on successful arthroscopy of the elbow.
Promising results are reported after various arthroscopic procedures of OCD of the elbow with improvement in clinical outcome at an intermediate follow-up.24 ,46–49 Despite minimal invasive techniques used in most studies, the average time to return to the preinjury level of sports varies from 1 to 5 months.13 ,26 ,50 ,51
In selected cases, classified as ICRS type II or III, an arthroscopic refixation of the lesion can be indicated for large (sub)acute osteochondral fragments.15 ,43 ,44 Different fixation techniques are available, including metal and bioresorbable screws and pull-out wiring.43 Currently there is no evidence available on which technique is preferred over the other.
The complication rate after arthroscopy of the elbow is low, and depends on the experience of the surgeon and type of pathology. Major complications as permanent nerve injury or deep infection occur in 0.5–5% of cases (box 4).
Tips to prevent complications in arthroscopy of the elbow
Lateral decubitus or prone with a solid support of the arm; check carefully to confirm that support is not squeezing the neurovascular structures towards the joint,
Mark the bony landmarks, portals and ulnar nerve,
Insufflate the joint before the arthroscopic procedure; to move away the neurovascular structures from the instruments use a pump for continues inflow; keep the pressures as low as possible to maintain visualisation and prevent swelling of the extremity,
Use at least five portals to visualise all three compartments,
Most osteochondritis dissecans (OCD) lesions cannot be visualised anteriorly, two portals in the soft spot are necessary (1 viewing portal and 1 working portal) to perform OCD surgery,
Always remove all soft tissues from the coronoid fossa as loose bodies tend to hide therein.
The role of dry arthroscopy
One of the authors has been using dry elbow arthroscopy for diagnostic and therapeutic elbow arthroscopy.27 The key benefits of dry arthroscopy are the quality of tissue definition, (eg, articular surface) and the lack of tissue swelling (figure 12A,B).
With wet arthroscopy fluid is used to distend the joint. During dry elbow arthroscopy, it is necessary to keep the anterior soft tissues away from the articular surfaces to maintain a working space. It may be possible to use an air pump to distend the joint space, but until this has been scientifically verified as safe, we would advise against air insufflation, due to the risk of potentially fatal air embolus. Handheld retractors are used such as a standard right-angled retractors or flat retractors (eg, Mini-Hohmann) to maintain the working space. The retractors are inserted either through the viewing portal alongside the arthroscope or through an accessory portal.
Visualisation can be affected by condensation (fogging), blood and debris on the arthroscopic lens. Tricks include warming the arthroscope in saline before the procedure, wiping the lens with alcohol or glycerine and cleaning the lens on the intra-articular soft tissues. Short bursts of irrigation and low-pressure suction on the shaver will clear the debris and maintain a visual field and dry environment. With radiofrequency devices we use low settings accompanied by frequent irrigation and suction to prevent overheating and aid in removal of debris. Of course we can revert to saline if required. This author now routinely performs all of diagnostic elbow arthroscopies dry, and will continue with any therapeutic procedures dry depending on the technical demands of the procedure. With arthroscopy for capitellar AVN, there is usually extensive synovitis that may obscure visualisation (figure 13A,B). The synovitis floats in the fluid, but in air the synovitis flattens and therefore does not obstructs the view.
Currently this technique is still evolving, and its exact role is still to be defined. However, it certainly provides a fantastic view; at this stage there is no scientific evidence to support its use over conventional insufflation with fluid (table 1).
Open surgical treatment
As an alternative to arthroscopy, open surgery with a lateral approach can be used for the surgical treatment of OCD and can be indicated in lesions not amendable to arthroscopic techniques. In comparison to arthroscopic surgery, open lateral-based surgical procedures may further compromise the vascularity of the capitellum.
Several open surgical procedures as refixation, bone peg grafts osteochondral autograft transfer, autologous chondrocyte transplantation and wedge osteotomy have been described. As in arthroscopic procedures, ICRS type II and III lesions are suitable for fixation with or without additional filling of the defect with autologous bone, using an open surgical procedure. The clinical success rate of refixation is, at medium-term clinical follow-up ∼80%. Reossification on standard radiographs is observed in 44–100%.43 ,44 ,52 An intact lateral wall of the capitellum appears to be important for fixation to be successful.53
That is the reason why some authors promote combined treatment of bone peg fixation and osteochondral autograft transfer in case of extension of the OCD lesion to the lateral part of the capitellum.54 Complications after open fixation of the OCD lesion have been observed in terms of intra-articular protrusion and loosening of screws and non-union of the fragment and injury to the lateral collateral ligament complex.41
Autologous osteochondral transplantation (mosaicplasty), as described in knee and ankle,55 can be indicated in cases with large defects, or cases with involvement of the lateral aspect of the capitellum or in revision cases. After mosaicplasty, which in theory replaces the damaged articular surface with cartilage, the results are encouraging.
This more invasive technique, however, can result in donor-site morbidity in a healthy knee joint.56 More research is needed to assess the possibility of donor sites in the elbow joint, for example, the tip of the olecranon. Rib costochondral autografting has been described for cases with extensive lesions ≥15 mm and those affecting the lateral wall, with satisfactory results after 1–6 years. Closed-wedge osteotomy of the capitellum has been described to widen the radiohumeral joint space, reduce compression and stimulate revascularisation and remodelling of the area of the lesion in the capitellum.13 Although almost all patients returned to full athletic activity, postoperative osteoarthritic changes and enlargement of the radial head occurred in all patients. The role of this invasive treatment method is unclear until more evidence is available.
The use of autologous chondrocyte transplantation, a technique with transplantation of cultured autologous cartilage cells on a collagen gel, to the cartilaginous defect, has been described mainly for comparable pathology in the knee. With the current experience this technique is not yet suitable for OCD of the elbow (box 5).
Common pitfalls in treatment
Delay in diagnosis—often up to 2 years; any sporting child with elbow pain has an osteochondritis dissecans (OCD) of the capitellum until proven otherwise!
Fixation of necrotic, loose bodies is not useful; fixation is reserved for large, traumatic and osteochondral lesions.
Standard MRI will often underestimate the number of loose bodies.
The arthroscopic procedure must include all compartments.
Rehabilitation depends on the size and the stage of the lesion and can take weeks to months.
Rehabilitation principles are more or less the same for the surgical procedures mentioned above. An experienced upper limb physical therapist, with special expertise in elbow pathology, supervises the rehabilitation after OCD surgery.
In selected cases after refixation or osteochondral autograft transfer immobilisation in a plaster is applied for 2 weeks. In all sports-related injuries general injury prevention is part of the postoperative rehabilitation. This general injury prevention programme consists of maintaining of range of motion of the kinetic chain, maintenance of the shoulder muscle strength and endurance. This programme is combined with strengthening of the neuromuscular control and core stability training. Rehabilitation is during the first 2–4 weeks aimed at reducing pain and swelling and maintaining range of motion. The recovery after arthroscopic treatment is in general faster than after open surgical procedures.3 Active-assisted motion exercises are started within a couple of days after surgery. After arthroscopic procedures, the range of motion is unrestricted as pain is tolerated. For patients who were treated with mosaicplasty or fixation of the OCD flexion is restricted for the first 6 weeks. Resistive exercises are started at 8 weeks after arthroscopic treatment and at 12 weeks after open treatment, depending on the type of surgery. Axial loading is forbidden up to 4 months after surgery. If the patient has no pain and has normal range of motion, an interval throwing programme is initiated before the patient returns to sports.3 In general this is between 4 and 8 months after surgery, depending on the extent of the lesions, surgery technique used and type of sports.
The opportunity for improvement of patients appears to be at the two ends of the spectrum. First is the prevention by limiting excessive upper extremity activity in the young athlete. In baseball limiting the number of pitches and taking a 3-month break is recommended. Each high-risk sport needs to identify the appropriate limits.
For Europe it means that a guideline for young athletes, especially for tennis players and gymnasts, have to be applied, which limits the excessive sports-related upper extremity activities. In addition staying vigilant with an early diagnosis if it does occur is critical as patients with open growth plates and treated with rest that achieve healing have the best outcomes. Patients who have closed growth plates as well as an unstable lesion that are currently being treated with a variety of arthroscopic procedures with good short-term results may have the opportunity for advanced treatments in the future. We are entering into the era of biological solutions to medical problems. There is no reason to doubt that the right combination of growth factors and stem cells will 1 day be able to completely restore the normal anatomy of this joint.
So hopefully within 5 years the incidence of OCD of the elbow is reduced by national guidelines with limitation of excessive overhead sports in children with open growth plates. Early diagnosis of OCD in combination with an increase in understanding of the biology, including growth factors and stem cells regeneration, will prevent the need for surgical. Over the next 10 years there is likely to be further refinements in the reconstructive surgery, with autologous osteochondral transplantation becoming more reliable.
The authors acknowledge the significant contribution of the images provided by Henry V Crock AO. They are reproduced from ‘An Atlas of vascular anatomy of the skeleton and spinal cord’ published in 1996 by Martin Dunitz. Henry V Crock AO maintains copyright of these images. Adelaide Microscopy, University of Adelaide and Dr Egon Perilli, from the Mechanical Engineering, Flinders University are acknowledged for providing the micro-CT scan images of the distal humerus. They also acknowledge Professor Carlos Zaidenberg, Buenos Aires, Argentina, for the arterial studies of the elbow.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.
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