Cartilage Problems Related to Growth in Youth

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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
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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:
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AMSSM Annual Meeting; New Orleans
Holly J. Benjamin, MD, FACSM, FAAP
[email protected] Phone: 773-702-0003
April 8, 2014
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