Cartilage Problems Related to Growth in Youth
Transcription
Cartilage Problems Related to Growth in Youth
Cartilage Problems Related to Growth in Youth Holly J. Benjamin, MD, FAAP, FACSM Associate Professor of Pediatrics & Orthopedic Surgery University of Chicago Center for Sports Medicine [email protected] Disclosure • Neither I, Holly J. Benjamin, nor any family member(s), have any relevant financial relationships to be discussed directly or indirectly, referred to or illustrated with or without recognition within the presentation. Objectives • Identify and understand the various contributing factors to overuse growth plate injuries in pediatric athletes • Describe various cartilage injuries seen in youth athletes – Osteochondritis Dessicans (OCD) – Little League Shoulder – Gymnast Wrist • Identify common imaging modalities used in the evaluation of cartilaginous injuries in youths • Become familiar with treatment principles Epidemiology • National Council of Youth Sports survey found 60 million children ages 6-18 years old participate in some form of sports – 27 million in organized sport – 7 million kids in school programs – 25 million in unstructured recreational sports • 1,000’s of career ending/career limiting injuries each year – Sprains, strains, fractures, tendonitis, cartilage injuries – Why are overuse injuries on the rise? – Are they preventable? CJSM: 2014,24(1): 3-20. Overuse Injury Types Unique to Children • Physeal stress injury • Apophyseal stress injury • Articular cartilage injury “The Weak Link” • An injury occurring at end of long bone is a growth plate injury until proven otherwise. Osteochondritis Dissecans • Term was coined by Dr. Franz Konig in 1887 • Described it as inflammation of the bone-cartilage interface • Historically terminology has been confusing – – – – – Osteochondral fracture Osteonecrosis Accessory ossification center Osteochondrosis Hereditary epiphyseal dysplasia Definition • A fragment of cartilage and subchondral bone that undergoes necrosis and can separate from the articular surface • 2 distinct populations of patients – Differentiated by the status of their physes • Common locations include femoral condyles, capitellum, talus • Symptoms depend on stage of the lesion • Untreated, may lead to early OA with chronic pain and functional impairment Important Points • Not all cartilage is created equal – Age, gender, location, genetics play a role • Different cartilaginous injuries have different natural histories • Chondrocytes and pressure – “Not too little and not too much” – Beneficial = physiologic & cyclic – Harmful = static, supraphysiologic or none Osteochondritis Dissecans • Incidence – 30-60/100,000 • 10-20 years of age – can occur up through 50 years of age • Male/Female-3:1 • 75% of cases occur in the knee • Bilateral 30% • 2 Types – Juvenile (JOCD) • 5-15 yr olds • before epiphyseal closure – Older teen/Adult (ACOD or OCD) • closed physes Pathophysiology • • • Currently believed to be multifactorial Proposed etiologies & predisposing conditions – Skeletal maturation (accessory centers of ossification) • Rapid growth – Genetic conditions (e.g., multiple epiphyseal dysplasias) – Metabolic (endocrine) factors – Hereditary factors – Anatomic variation Inciting event?? – Trauma as the starting point in predisposed individual • Single traumatic event or repetitive microtrauma may interrupt the vascular supply – Vascular insufficiency ultimately leads to subchondral bone death => AVN => fragmentation +/- fragment separation Knee OCD Clinical Symptoms • Vague and poorly localized knee pain, swelling, +/- stiffness in varying degrees • Occasional clicking or popping • Activity related symptoms exacerbated twisting / cutting movements • “Locking” or “catching” • “Giving way” of the knee • +/- history of trauma Physical Exam • Look for effusion, crepitus +/- joint line tenderness • positive Steinman’s test • Joint line pain when the tibia is rotated internally and externally while the knee is flexed over the examination table • positive Wilson test • Knee flexed 900 IR tibia and extend knee slowly • may have “false positive” McMurray’s test Osteochondral Defect : Imaging • Plain Radiographs: useful 1st line imaging – AP & lateral views: OCD on the condyles – Sunrise or Merchant View: patellar OCD – Notch or Tunnel AP View: medial femoral condyle OCD • MRI with or without gadolinium – staging • Technetium bone scan – Occult bilateral OCD; normal variant • CT scanning: helpful in preop planning when MRI is contraindicated or not available • Sonography: only advantage is cost Imaging • Tunnel view • Allows you to see posterior femur • Similar to skiers view (standing flexed PA) Osteochondral Knee Defect: Common locations • Medial femoral condyle: 75-85% – 70% occur in the posterolateral aspect • Lateral femoral condyle: 10-25% OCD versus Normal Variant** • Clinical – Correlate symptoms with location of lesion – Occasionally NV may be incidental finding • Radiographic – Stage I OCD vs NV – Location of lesion often in nonweight-bearing area of bone (posterior femur) – Absence of signal change on MRI **Keats TE. Atlas of Normal Roentgen Variants That May Simulate Disease; 6th Ed. pp 570-574. Pediatr Radiol 2005 Sept;35(9):880-6. Radiographs: AP, notch/tunnel/skier’s, lateral, sunrise/merchant AP: medial femoral condyle Notch: medial femoral condyle lateral Anderson MRI staging of osteochondritis dissecans Stage Evaluation Findings I Early IIA Stable Subchondral bone flattening in the epiphyseal plate before closure Subchondral cyst present IIB Unstable III Unstable IV Terminal Incomplete separation of the osteochondral fragment Effusions around an nondisplaced osteochondral fragment Loose bodies MRI: Coronal and Axial MRI: Coronal MRI: lateral Osteochondral Defect : Grading Osteochondral Fragment Stability OCD Algorithm Hixon AL. Gibbs LM. Am Fam Physician. 2000;61(1) 151-156. Treatment • Varies depending on age, skeletal maturity, location, size and stability of the lesion • Presence of open physes with adequate remaining skeletal growth is vital • Successful radiographic healing is reported in 50-91% of cases of JOCD’s Osteochondral Defect: Treatment Categories • Based on physeal status and OCD size & stability • Category 1 – females < 11 y/o, males < 13 y/o, no loose body on XRay – Do well with non-operative treatment • Category 2 – females 11-15 y/o, males 13-17 y/o – Near skeletal maturity; treatment depends on location, size, and stability of the lesion • Category 3 – Physeal closure and skeletal maturity have occurred – Treatment based on the location, size, and stability of the lesion Clinical Treatment • Initial – Stop high risk activities (running, jumping, pivoting) – Non-weight-bearing vs partial WB – Initiate therapy (core, closed chain ex, flexibility) • Follow-up – Every 4 weeks – Consider imaging radiographically at 1 month, 3 months, 4-6 months, 1 year – MRI unlikely to change for several weeks Treatment • Knee OCD treatment • • Kocher, et al, reported on a three phase • treatment plan (AJSM, 2006) • • Phase 1: 4-6 weeks in knee immobilizer with • partial weight bearing with crutches OCD Treatment 2 & 3 • Phase 2: 6 weeks of full weight bearing without • immobilizer while avoiding strenuous activities • Phase 3: After radiographic/ clinical signs of • healing can gradually increase activities Return to play • • • • When asymptomatic AND….. Radiographic improvement This does not mean serial MRI’s are the gold standard! • Average time for return to play can range 3 mo-9+months. Surgical Consultation • Skeletally immature – Failed conservative therapy – Stage III-IV lesions (instability/loose body) • Skeletally mature – Physeal closure (adult type lesion) • Surgical Procedures – Micro fracture – OATS/ Mosaicplasty – Autologous Chondrocyte Implantation – Osteochondral allografts Summary: Osteochondral Injuries • Injuries are common in children and require a high index of suspicion • multifactorial • Imaging is helpful but challenging • Lack of blood supply leads to healing difficulties • Individualized treatment • “Regenerated” cartilage has same properties as original – “Repaired” cartilage not quite the same Case 1: Shoulder Pain-Baseball • 12 yr old RHD baseball pitcher with a 1 mo. hx shoulder pain w/ pitching • Recent loss of velocity noted • Grew 4 inches last 6 months • Has new coach • DIAGNOSIS?? Little Leaguer’s Shoulder: Proximal Humeral Epiphysiolysis • SH1 physeal fx • ages 11-13 (often elite) • insidious onset of proximal shoulder pain • TTP proximal humerus • Pain with resisted IR Differential Diagnosis • stress fracture • osteochondrosis of the physis • instability physis • impingement syndrome • SLAP lesion • other labral injury • neoplasm A G H LLS:xray AP int/ext rot & “Y” view R physis L Treatment • weeks to months of rest from throwing • physical therapy – general conditioning & strengthening – sport-specific exercises • return to pitching gradually – biomechanics – limits on #’s of pitches – sport-specific training program Case 2: Wrist Pain in a Gymnast • 12 yr old RHD level 6 gymnast with 3 month hx of wrist pain • Pain worse with weightbearing and wrist extension • No swelling, clicking, trauma, etc. • Diagnosis? Gymnast’s Wrist: Distal Radial Physeal Injury • weightlifters & gymnasts • repetitive stresses => sclerosis • exam => TTP distal radius or pain w/ axial loading • Complications – premature growth plate closure – ulnar overgrowth & impingement Gymnast’s wrist S L U Rad Rad U Treatment • Primary – Prevention • Secondary – symptomatic to pain – Brace or cast – avoid weight-bearing 46 weeks minimum Teaching Points • “Pain at the end of a long bone in a skeletally immature patient is a growth plate injury until proven otherwise!” • “The growth plate is the weakest link!” • Osteochondral/cartilaginous injuries are common in kids • Imaging important • Healing process slow, varied and lots of individual variation • Know surgical indications References • • • • • • • • • • Difiori, et al. Overuse Injuries and Burnout in Youth Sports. A Position Statement from the American Medical Society for Sports Medicine. CJSM: 2014,24(1): 3-20. Hixon AL. Gibbs LM. Osteochondritis Dissecans: A diagnosis not to miss. Am Fam Physician. 2000;61(1) 151-156. Keats TE. Atlas of Normal Roentgen Variants That May Simulate Disease; 6th Ed. pp 570-574. Pediatr Radiol 2005 Sept;35(9):880-6. Schenck,RC Jr, Goodnight JM, Current Concept Review – Osteochondritis Dissecans, JBJS. 1996;78:439-56. Caffey J, Madell SH, Royer C, Morales P, Ossification of the Distal Femoral Epiphysis, JBJS. 1958; 40:647-714. Mubarak SJ, Carroll NC, Familial Osteochondritis Dissecans of the Knee, CORR. 1979; 140: 131136. Kocher MS, Tucker R, Ganley TJ, Flynn JM, Management of Osteochondritis Dissecans of the Knee, AJSM. 2006; Vol 34 No 7:1181-1191. Kocher MS, Micheli LJ, Yaniv M, Zurakowski D, Ames A, Adrignolo AA, Juvenile Osteochondritis Dissecans of the Knee Treated with Transarticular Arthroscopic Drilling, AJSM. 2001; Vol 29 No 5:562-566. Uozumi H, Sugita T, Aizawa T, Takahasi A, Ohnuma M, Itoi E, Histologic Findings and Possible Causes of Osteochondritis Dissecans of the Knee, AJSM PreView Sept 8, 2009. AMSSM Annual Meeting; New Orleans Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 April 8, 2014 OSTEOCHONDRITIS DISSECANS LEARNING OBJECTIVES 1. To become familiar with common clinical presentations of OCD’s occurring in different areas of the body. 2. To differentiate Juvenile and Adult forms of osteochondritis dissecans in terms of understanding differences in treatment and prognosis. 3. To understand the role of imaging in the diagnosis and treatment of OCD’s HISTORY 1 Osteochondritis dissecans is attributed to Konig in 1888 based on his hypothesis that loose bodies “corpora mobile” were caused by “dissecting inflammation” or an inflammatory reaction in the joint followed by spontaneous subchondral necrosis of bone and cartilage. OCD is a focal injury to subchondral bone that results in results in loss of structural support for the overlying articular cartilage. Degeneration and fragmentation can occur, often with the formation of loose bodies. OCD lesions are seen in the capitellum, trochlea, wrist, femoral head, femoral condyles, patella, distal tibia and talus. Of note, current thinking is that inflammation is NOT present in cases of OCD’s; in fact, loose bodies are commonly composed of dead subchondral bone of varying degrees of thickness with variable vascularization and may or may not be covered with viable articular cartilage. The histopathology of OCD’s reflects the stages of the disease. Not all loose bodies have attached bone. (Chiroff) ETIOLOGY Trauma, ischemia, ossification defects and genetic abnormalities likely all contribute to the pathophysiology. OCD is divided into the juvenile form (JOCD) and the adult form delineated by the closure of the physes. In the adult form it is sometimes difficult to distinguish a traumatic osteochondral fracture from the adult OCD. Green suggested that the major difference is the presence of non-ischemic “normal” bone in the plane of subchondral separation in a fracture. Other authors have suggested that sequential acute trauma might cause the lesion, initially producing necrosis with a subsequent injury causing a vascular injury that leads to cartilage damage and/or separation. Articular cartilage has a limited ability to remodel and rebuild. The role of subchondral bone in providing the cellular and humeral factors for healing contributes to the multilayered organization of articular cartilage and consideration of its ability to heal with conservative management. 1 AMSSM Annual Meeting; New Orleans Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 April 8, 2014 KNEE CLINICAL PRESENTATION 40-60% of OCD’s in adolescents have a preceding history of trauma. JOCD is more common in young athletes than sedentary juveniles. In a skeletally immature patient with an acute knee injury, chondral injuries occur most frequently at 34% with 23% mensical injury and 24% ACL tears. (Deppen) The early stages of JOCD’s can present with vague symptoms of recurrent pain or “ache”, crepitus, decreased range of motion, muscle atrophy, synovitis, joint line tenderness, and recurrent knee effusions in the absence of mechanical symptoms. Pain is often more severe with weight bearing or high-impact activities. An antalgic or asymmetric gait may be noted. More severe or advances stages of OCD can present with mechanical symptoms or symptoms of a loose body with intermittent pain, swelling, locking or catching. Gait abnormalities are common such as the child who walks with the tibia externally rotated to decrease pressure on the weightbearing surface of the medial femoral condyle. JOCD’s occur most commonly in the lateral nonweight-bearing aspect of the medial femoral condyle (57-83%) [ref Carroll and Mubarak, Linden and Green and Banks]; however they are also seen in the patella and the lateral femoral trochlea. This clinical presentation may mimic patellofemoral pain with symptoms worse with prolonged sitting, stair climbing or kneeling. Wilson’s sign can be positive but the sensitivity is unknown. Wilson’s test is performed by passive extension of the knee from 900 to 300 of flexion with the tibia first held in internal rotation (painful) then performed again with the tibia held in external rotation (less painful). Axhausen is known for describing tenderness to palpation over the affected femoral condyle as the knee is brought progressively into flexion. IMAGING RADIOGRAPHS Diagnosis often made with plain radiographs including standard AP, lateral and axial patellofemoral views of the knee. A notch or tunnel view has been proposed as the preferred technique to view the lateral aspect of the medial femoral condyle. Weight bearing films (example: knee) are likely to demonstrate joint space narrowing reflective of global cartilage loss but are not as useful for focal or asymmetric cartilage damage. BONE SCANS Cahill and Berg performed static bone scans every 6 weeks on 18 adolescents until there was evidence of healing. They reported that the degree of osseous uptake on bone scan was related to regional blood flow and therefore predictive of healing potential. They divided bone scans into five stages: Stage 0 was normal xray and normal bone scan. Stage 1 was abnormal xrays and no activity on bone scan. Stage II and III show progressive increases in uptake reflective of increased vascularization in the area. Stage IV showed increased activity at the defect and associated tibia changes. These authors suggested that increased stages demonstrated increased vascularization and therefore increased potential to heal (i.e. Stage 1 was least likely to heal). Paletta et al found that bone scan was 100% predictive for prognosis of non-surgical treatment of OCD in six patients with open physes but only had 33% predictive value in 6 pts with closed physes. 2 AMSSM Annual Meeting; New Orleans Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 April 8, 2014 MRI (Magnetic Resonance Imaging) MR imaging is valuable in the diagnosis of associated ligament and mensical injuries and to determine the size of the chondral lesion and the degree of displacement. MR imaging is also useful to detect loose bodies and to assess the integrity of the articular cartilage surface. MR imaging must delineate lesion size, depth, and location accurately in order to be helpful. Successful MR imaging of cartilage depends on three major parameters: high image contrast between the tissues of interest, high signal to noise ratio of the structures, and the spatial resolution of the technique. Therefore, not all techniques or scanners yield equally accurate diagnostic information regarding cartilage damage. T1 imaging is not routinely used to evaluate articular cartilage as it is gray on T1 that contrasts with the adjacent low-signal cortex but has suboptimal contrast with gray joint fluid. T1 imaging tends to overestimate the cartilage thickness and to obscure focal defects in the presence of a joint effusion. T2 SE (spin echo) sequences, cartilage is not well visualized because of short sequences but joint effusions are seen well. There is a lack of contrast between cortex and cartilage and the images can take time there there is a tendency towards motion artifact. FSE (fast spin echo) and T2 sequences demonstrate high magnetization transfer contrast so articular contrast shows lower signal intensity gray and is easily distinguished. Fat suppression may demonstrate bone marrow edema better therefore indicating an overlying cartilage defect. Clear visualization of the overlying articular cartilage is far more difficult in the elbow than in the knee. Normal anatomic variants such as a pseudo defect of the capitellum can be confused as it simulates the appearance of OCD’s in the elbow. TABLE 1 MRI Staging of Joints with Osteochondritis Dissecans Stage I--Thickening of articular cartilage and low signal changes (stable) Stage II--Articular cartilage breached, low-signal rim behind fragment indicating fibrous attachment (stable) Stage III--Articular cartilage breached, high-signal changes behind fragment and underlying subchondral bone (unstable) Stage IV--Loose body (unstable) MRI = magnetic resonance imaging. Information from Obedian RS, Grelsamer RP. Osteochondritis dissecans of the distal femur and patella. Clin Sports Med 1997;16:157-74. 3 AMSSM Annual Meeting; New Orleans Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 Ref: Hixon, et al. April 8, 2014 Management of Osteochondritis Dissecans of the Knee TREATMENT Varies, depending on patient age, skeletal maturity, location and size of the lesion. OCD in the skeletally immature patient must be differentiated from variations of ossification 4 AMSSM Annual Meeting; New Orleans April 8, 2014 Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 and/or hereditary epiphyseal abnormalities. It is vital to determine that adequate cortical bone is attached to the chondral surface. The presence of adequate remaining skeletal growth as determined by the presence of open physes is the most important determinant of treatment. Successful radiographic healing of JOCD’s has been reported to vary between 50-91%. Initial treatment includes activity modification and protected weightbearing in an immobilizer or brace with intermittent knee motion is favored over casting primarily due to the harmful effects of immobilization on cartilage nutrition. Partial weight bearing with crutches is reasonable in the initial treatment, particularly if the lesion is large or on the weight-bearing surface of the femoral condyle (typical). The most important prognostic factor in the skeletally immature population is the status of the articular cartilage surface. Once the underlying bone has been exposed to synovial fluid the lesion is likely to progress to an unstable loose body requiring surgical excision or stabilization. Indications for surgical referral include persistent symptoms such as recurrent effusions, instability, chronic pain and/or ongoing mechanical symptoms, concomitant injury. JOCD’s that are asymptomatic, and are found as “incidental findings” on xray may be watched with no other treatment intervention required. Linden, et al in 1977 published the only significant long-term follow-up study on 23 patients from Sweden with JOCD’s. The average age was 45.5 years and the average follow-up time was 33 years. Only 2 patients had minimal xray changes and none had pain, or other functional deficits. Adult forms of OCD’s are associated with early DJD. 5 AMSSM Annual Meeting; New Orleans Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 April 8, 2014 ELBOW The evaluation and treatment of the increasing number of overuse injuries to the skeletally immature elbow requires an understanding of the complex developmental and radiographic anatomy, an understanding of pathophysiology and natural history following an injury as well as an awareness of the outcomes and indications for operative versus conservative management. PHYSEAL ANATOMY Childhood includes the appearance of all secondary ossification centers. Adolescent development includes the fusion of the secondary ossification centers to their respective long bones. Young adulthood includes new bone growth and the appearance of the final adult skeletal form. The distal humerus contributes to 20% of the adult limb length. The anatomical weakest link noted at each stage of development helps define the specific injury patterns seen during each stage of development. Sport-specific characteristics and biomechanics further affect injury occurrences. Skeletal growth at the elbow starts with the humerus as a single cartilaginous epiphysis encompassing both condyles and epicondyles with one physis. It differentiates into the 2 epiphyses (capitellum and trochlea) and the 2 apophyses (medial and lateral epicondyles) by age 10-12 years. CRITOE is the mnemonic that refers to the appearance of the six secondary ossification centers of the elbow. CRITOE OSSIFICATION CENTERS Capitellum Radius Internal (Medial) epicondyle Trochlea Olecranon External (lateral) epicondyle Age at Appearance 1-2 years 3 years 5 years 7 years 9 years 11 years Age at Closure 14 years 16 years 15 years 14 years 14 years 16 years In throwers the radiocapitellar joint has compressive forces following repetitive valgus loading and the gymnast’s elbow is subjective to repetitive compressive and shear forces during weight bearing. It receives up to 60% of the force from compressive axial loads. This area is particularly susceptible to compressive, rotary, axial and angular forces. Progressive pronation, compression and rotation occur on the anteromedial radial head and inferior and medial capitellar surfaces as the elbow is extended. These stresses are thought to affect the tenuous blood supply to the developing elbow, specifically the capitellum. Haraldsson provided support for the ischemic theory of OCD in demonstrating that the capitellar epiphysis receives its blood supply from one or two isolated transchondroepiphyseal vessels that supply the epiphysis posteriorly and function like end-arteries. The metaphyseal vascular anastomoses do not make significant contributions to the capitellum until 19 years of age. Histopathologically, subchondral osteonecrosis supports the ischemic theory. The traumatic theory weakens subchondral 6 AMSSM Annual Meeting; New Orleans Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 April 8, 2014 bone, results in fatigue fracture, and if osseous repair mechanisms fail then an avascular portion of bone may undergo resorption. The subchondral architecture can no longer support the overlying articular cartilage and leads to fragmentation. EPIDEMIOLOGY Humeral OCD’s account for 6% of all OCD lesions 85% are seen in males 4.1/1000 males 14.6% incidence exists among male relatives of affected males CLINICAL PRESENTATION The history should include age, handedness, position or sport, activity level, mechanism of injury, location, duration and radiation of pain, nature of onset, inciting factors, prior history of injury. The most typical presentation is insidious onset of poorly localized activity-related lateral elbow pain. In the presence of a loose body or an unstable fragment, mechanical symptoms may occur such as locking, catching or clicking. If motion loss is present it will present as loss of extension. The active radiocapitellar compression test, which consists of forearm pronation and supination with the elbow in extension, may reproduce symptoms. The natural history of capitellar OCD is difficult to predict and it is difficult to predict which lesions will collapse and which will heal. Chronic, repetitive stress injuries tend to occur on convex surfaces, and because the injury occurs while the elbow is in flexion and in valgus, the chondral and osseous injuries tend to occur most frequently at the anterior capitellum. DIAGNOSTIC EVALUATION Radiographs may show radiolucency or irregularity or flattening of the articular surface. The lesion may appear as a focal rim of sclerotic bone surrounding a radiolucent crater with rarefaction in the anterolateral aspect of the capitellum. Studies have shown that up to 50% of the time xrays may be nondiagnostic and may not evaluate the chondral component of the OCD lesions adequately. A grading system based on the AP view is as follows: Grade I is a translucent shadow in the central or lateral capitellum; Grade II is a clear zone or split line between the subchondral bone and the lesion; and Grade III is a loose body. MRI is valuable in evaluating the early stages of OCD lesions and is helpful in assessing the articular cartilage overlying the defect. Early OCD lesions may show low signal change on T1 images with normal T2 images. Intervening fluid between a fragment and the capitellum on T2 images is indicative of detachment. Limitations of MRI show a decreased ability to assess radial head involvement. Overall, MR has been shown to be 92% sensitive and 90% specific at differentiating stable from unstable lesions. 7 AMSSM Annual Meeting; New Orleans Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 April 8, 2014 Table: Arthroscopic Classification and Treatment Recommendations for Capitellar OCD Data from 17 elbows from Baumgarten TE, Andrews JR, Satterwhite YE. The arthoscopic classification and treatment of OCD of the capitellum. Am J Sports Med 1998; 26 (4): 520-3. Type Articular Cartilage Status I II Smooth, soft, ballotable Fissuring or fibrillation III Exposed bone with fixed osteochondral fragment Loose, nondisplaced fragment with radial head involvement Displaced fragment with loose body formation IV V Treatment Recommendations Observation or drilling Resection of degenerative cartilage Fragment excision Fragment excision Loose body removal, debridement Reports in the literature that compare conservative versus surgical management are difficult to compare and interpret due to lack of uniformity in methodology. The biggest post-operative problems seen in the series published with outcome results reveal that chronic pain and decreased range of motion (flexion contractures most common) and degenerative changes in the elbow joint (capitellum and/or radius) were common. Treatment for Type 1 lesions (some Type 2) includes benign neglect with a hinged elbow brace, RICE, etc for approximately 6 weeks. Full activity is often reached 3-6 months post-injury. TALUS OCD’s of the talus occur in approximately 6.5% of all ankle sprains. These are usually seen in the 15-35 yr old age group and follow inversion or eversion trauma. 55% occur in the anterolateral aspect of the talus, 45% on the posteromedial talus. Typical size varies from 0.5-1.5 cm. Up to 43% of talar OCD’s have been reported as “missed” on plain radiographs and diagnosis is often delayed until 2 years s/p injury. References: 1. Barrie, HJ. Osteochondritis dissecans 1887-1987. A centennial look at Koenig’s memorable phrase. J Bone Joint Surg 69B:693, 1987. Bruce, EJ., Hamby, T., Jones, DG. Sports-Related Osteochondral Injuries: Clinical Presentation, Diagnosis, and Treatment. Primary Care: Clinics in Office Practice. Vol. 20, 2005. pp. 253-276. Cain EL and Clancy WG. Treatment Algorithm for Osteochondral Injuries of the Knee. Clinics in Sports Medicine. Vol. 20, #2, April, 2001. pp 321-342. Cahill, B and Berg, B. 99m technetium phosphate compound joint scintigraphy in the management of juvenile osteochondritis dissecans of the femoral condyles. Am J of Sports Med 11:329-335, 1983. 8 AMSSM Annual Meeting; New Orleans Holly J. Benjamin, MD, FACSM, FAAP [email protected] Phone: 773-702-0003 April 8, 2014 Carroll, NC and Mubarak, SJ. Juvenile Osteochondritis dissecans of the knee. J Bone Joint Surg 59B: 506, 1977. Green, W and Banks, H. Osteochondritis dissecans in children. J Bone Joint Surg 14A: 26, 1958. Linden, B. Osteochondritis dissecans of the femoral condyles: A long-term follow-up study. J Bone Joint Surg 59A: 769, 1977 Chiroff, RT and Cooke, PC. Osteochondritis dissecans: A histologic and microradiographic analysis of surgically excised lesions. J Trauma 15:689-696, 1975. Loredo R and Sanders TG. Imaging of Osteochondral injuries. Clinics in Sports Medicine. Vol 20, # 2, April, 2001. pp 249-278. Stubbs, Malcolm J., Field, Larry D., Savoie, Felix H. Osteochondritis Dissecans of the Elbow. Clinics in Sports Medicine. Vol. 20, #1, January 2001. pp. 1-9. Stanitski, Carl L. Osteochondritis Dissecans of the Knee. Pediatric and Adolescent Sports Medicine. Vol. 3, 1994. pp.387-405. Manaster, B.J., Johnson, T., Narahari, U. Imaging of Cartilage in the Athlete. Clinics in Sports Medicine. Vol. 24, 2005. pp. 13-37. Rudzki, JR., Paletta, G. Juvenile and Adolescent Elbow Injuries in Sports. Clinics in Sports Medicine. Vol. 23, 2004. pp. 581-608. Wilson, JN. A diagnostic sign in osteochondritis dissecans in the knee joint. J Bone Joint Surg 49A: 467, 1977. Fairbanks, HAT. Osteochondritis dissecans. Br J Surg 21:67, 1933. Hixon, AL and Gibbs, LM. Osteochondritis Dissecans: A diagnosis not to miss. American Family Physician. Vol 61, #1. Jan, 2000. Deppen, RS, et al. Acute injury to the articular cartilage and subchondral bone: a common but unrecognized lesion in the immature knee. AJR 2004; 182: 111-7. Scopp, JM., Mandelbaum, BR., A Treatment Algorithm for the Management of Articular Cartilage Defect. Orthopedic Clinics of North America. Vol. 36, 2005. pp. 419-426. 9