ICL #1 - ISAKOS

Transcription

ICL #1 - ISAKOS

ICL #1
BASIC SCIENCE AND CLINICAL USE OF CELL THERAPY IN ARTICULAR CARTILAGE REPAIR
Tuesday, March 11, 2003 • Location: Carlton Hotel, Room: Carlton I
Chairman: Lars Peterson, MD, PhD, Sweden
Faculty: Scott Gillogly, MD, USA, Bert Mandelbaum, MD, USA, Anders Lindahl, MD, PhD, Sweden, Wayne Gersoff, USA
and Carl Winalski, MD, USA
Introduction. Indications for cell therapy in cartilage repair
Lars Peterson
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Basic Scientific background for cell therapy
Anders Lindahl
Different treatments for cartilage repair and results of autologous chondrocyte transplantation (ACT) and
Report from Cartilage Repair Registry Data
Bert Mandelbaum
ACT, surgical technique and pearls and pitfalls
Scott Gillogly
ACT and meniscus transplantation
Wayne Gersoff
ACT and long-term results
Lars Peterson
Magnetic resonance imaging in diagnosing cartilage lesions and evaluation of cartilage repair
Carl Winalski
Discussion
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ICL #2
COMPUTERS IN CLINICAL PRACTICE
Tuesday, March 11, 2003 • Location: Carlton Hotel, Room: Carlton II
Chairman: Don Johnson, MD, Canada
Faculty: Vladimir Bobic, MD, United Kingdom, Nicola Maffulli, MD, MS, PhD, FRCS, United Kingdom and Ronald Selby,
MD, USA
NOTES:
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3.2
ICL #3
ISSUES IN ACL SURGERY
Tuesday, March 11, 2003 • Aotea Centre, Kupe/Hauraki Room
Chairman: Peter J. Fowler, MD, FRCS, Canada
Faculty: Charles Brown, Jr., MD, USA, Burt Klos, Netherlands and Philippe Neyret, MD, France
INDICATIONS FOR ANCILLARY SURGERY IN ACL DEFICIENT KNEE
Ph. NEYRET, T. LOOTENS, T. AIT SI SELMI, E. SERVIEN
,
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N
J
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A
C
L
“Isolated”
Complete
Partial
Evolved
ACLaxity
with
Pre-OA
OA
due to
Acl Laxity
Posterolateral < 5%
25-35y
1/ Isolated Chronic Anterior Insufficiency
To better understand the place and the indication of this ancillary surgery let introduce this diagram. An ACL
deficient knee can be seen in different circumstances. The so called "complete isolated" anterior chronic laxity is where the end point of the Trillat-Lachman test is soft, the pivot shift is positive and the differential
anterior tibial translation is under 6 mm measured with telos and under 4 mm measured with the differential lateral X-Rays on monopodal stance.
The anterior chronic insufficiency is partial and isolated if the end point is hard and delayed and a slip is
found.
In such an isolated laxity we can propose an ACL graft, but one may add an extraarticular reconstruction particularly if the patient practices strenuous activities. Sometimes intraarticular gestures can be associated, as
osteochondral grafting.
Over time, the anterior chronic laxity become evolved .
2/ Evolved chronic Anterior laxity.
Following ACL rupture, secondary lesions occur as a result of recurrent instability causing medial lesions:
postero-medial capsular detachment, medial meniscus , or menisco-tibial tears. The end point of the TrillatLachman test is obvious as the pivot shift.Often one can find an anterior drawer or a medial meniscus tear.
The differential anterior tibial translation is superior to 6 mm measured with telos and superior to 4 mm
measured with the differential lateral X-Rays on monopodal stance.
In evolved anterior laxity we can discuss ancillary or complementary gestures. Particularly, one may discuss
postero-medial gestures medial meniscus repair or proximal postero-medial reefing.
In 1995, we analyzed a series of 34 proximal posteromedial reefing at 5 years follow-up. We concluded this
gesture permits to better control the recurvatum and the anterior tibial translation on monopodal stance.
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Nevertheless the postero-medial structures are stretched and the quality of the capsule not good.We continue to perform this gesture only in case of severe asymmetrical recurvatum or very large amount of anterior tibial translation.
3/ Chronic Anterior laxity with Preosteoarthritis
In the absence of treatment progressively, due to the repeated episodes of instability, secondary intraarticular lesions happen. The patient complains mainly instability, rarely swelling or pain.
X-Rays permit to detect an incomplete narrowing of the medio femorotibial compartment.
We called this stage chronic Anterior Laxity with Preosteoarthritis.
3a/ Frontal Imbalance
The frontal imbalance can be due to medial femoro-tibial narrowing. This situation is very different of a
frontal imbalance due to lateral opening without medial narrowing.
Anterior chronic laxity with pre-osteoarhritis is frequent when the delay injury-operation is superior to five
years or when an isolated previous medial meniscectomy had been performed in this unstable knee.
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Let me give a short overview of the publication we did in 1994 (Dejour, Neyret, Boileau Corr 1994) :It was a
series of 50 patients with symptoms of ACL insufficiency and varus malalignment. 44 were available at follow-up. At 3.5 years follow-up we noted improved clinical symptoms, particularly objective and subjective
stability. Moreover Osteoarthritis seemed to be stabilized. Nevertheless only one patient was able to return
to competitive sport activities.
We recently evaluate the results of the combined operation at ten years follow-up. The inclusion criteria were
very strict. Only 47 knees with mild or moderate radiological preoperative changes, it means grade B or C in
the IKDC classification, were operated on between 1983 and 1999. At follow-up, 35 knees were avalaible.The
mean delay Injury-Operation was 8 years with a large standard deviation. In 66% of cases a previous medial
meniscectomy had been performed.
A closing wedge Osteotomy was performed at the beginning of our experience and progressively we preferred
to combine an opening wedge Osteotomy.
The IKDC subjective score depends on symptoms, functional evaluation and sport activities. The average
score is 79 at more than 10 years follow-up. Considering the index of satisfaction, 96% considered their knee
as normal or almost normal
At follow up 42% of patients practiced recreational sports and only 6% continue competitive sports. The final
evaluation allows to underline that 60% of patients belong to the grade A or B, 34% to the grade C and only
6% to the grade D.
Radiologically we noticed a tendancy to decrease the tibial slope in case of closing wedge osteotomy and a
tendancy to increase the tibial slope in case of opening wedge osteotomy, but the difference was not statistically significative, in this short series.
Sometimes In ACL Insufficiency with pre-osteoarthritis we do not find frontal imbalance. In fact the imbalance in saggital
3b/ Saggital Imbalance
This imbalance is observed when there is long history of instability, a previous medial meniscetomy or a tibial slope superior to 15 degrees.
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Deflexion High Tibial Osteotomy combined with ACL Reconstruction. This option must be discussed when
there is a grade B or C radiological changes without frontal malalignment.
You see the tibial slope was decreased by the anterior closing wedge osteotomy and the anterior tibial translation was controlled.
Technically a Bone-Patellar tendon Bone graft is harvested, if necessary on the contralateral knee, the tunnels are drilled. Then the deflexion osteotomy is performed, the tibial tunnel is calibrated and the graft fixed.
To control the recurvatum a posterior medial reefing is neccessary, once the ACL graft fixed. Two sagittal pins
allow to fluoroscopically control the direction of the osteotomy.The osteotomy starts above the ATT and go
to the tibial insertion of the PCL. Remember that 1 mm is about 2 degrees of correction of the tibial slope.
The osteotomy is fixed with two staples.
4/ Postero lateral chronic Anterior Insufficiency.
In a very few percentage of cases, less than 5 %, there is postero-lateral lesions.It’s a different entity. Lateral
Collateral Ligament and postero-lateral corner can be torn.
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The Trillat-Lachman test is soft and the pivot shift is present. One must detect a varus laxity, a thrust when
walking, a Hughston’Recurvatum test or a lateral hypermobility as described by Bousquet.
The differential anterior tibial translation is most often from 2 to 6 mm measured with telos and inferior to 4
mm measured on monopodal stance.An asymmetrical lateral opening on weight-bearing X-Rays confirms the
diagnosis.
One needs to obtain a complete preoperative check-up to detect an asymmetrical lateral opening.
These postero-lateral lesions lead to an frontal imbalance. But the problem is very different in case of asymmetrical lateral opening without medial narrowing.
In case of asymmetrical lateral opening due to an intersticial rupture of the lateral collateral ligament we
recommand to perform, during the same surgery, The ACL Reconstruction, The opening wedge HTO and a
Lateral Collateral Ligament graft, using a 6mm Bone-Patellar tendon-Bone graft harvested on the contralateral knee. The role of the Osteotomy is to protect the grafts and a small amount of valgus, 2 or 3 degrees is
enough. In the absence of LCL graft an obvious hypercorrection would be required.
5/ Place of the extra articular tenodesis.
The most controversy ancillary surgery is an additional extra-articular tenodesis or " Lemaire plasty". In the
past we used a 10mm large strip of fascia lata. To reduce the approach and the scar we proposed a new technique using the semi-tendinosus or the gracilis to perform the extra articular tenodesis. We shall give you
some details about the technique before to present our results.
5a/ Technique
We perform a 6 cm long skin incision and then we open the fascia lata, in direction of the Gerdy’ tubercle.
The ACL graft is prepared with the gracilis passed through the bone block. We prepare a tunnel under the
Gerdy’s tubercle with an awl. Once the femoral tunnel drilled just behind the femoral attachment of the LCL,
we insert the ACL graft and impact the bone block with Gracilis tendon in the femoral tunnel. The Gracilis is
passed and crossed under-neath the LCL. The two bundles are passed through the Gerdy’tunnel in an opposite way. During fixation of extraarticular tenodesis (sutures) the knee is in neutral rotation. Excessive bundles are removed and fascia is closed without tension.
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5b/ Results will be presented (1)
5c /Discussion
Even if Draganish (8) demonstrated that isolated extra-articular tenodesis can control some amount of laxity at 30° flexion we know that after isolated extra-articular tenodesis without ACL Reconstruction, clinical
failures are frequent. The anterior tibial translation is not controlled. At long term the arthrosis is frequent.
O’ Brien [14], Holmes [9], Buss [4], in different retrospective studies found no superiority to add an extra
articular tenodesis.
At the contrary Frank Noyes [13] underlined the benefits to add an extraarticular tenodesis when an allograft
is performed. Failure rate decreased from 16% to 3% and the control of anterior laxity is better.
Very recently during the FRENCH SOCIETY, Hulet from Caen in a retrospective study did not find statistical
difference between two groups with and without extraarticular tenodesis but the factor ß was unknown and
the number of patients in the two groups not large enough.
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Recently, F Cladiere ( Lerat-Moyen) [5] compared in a prospective randomised study two groups with and
without extraarticular tenodesis and recommanded a lateral complementary procedure when there is a preoperative differential anterior tibial translation measured on the lateral compartment, called "TACE" of more
than 8 mm.
Conclusions
The place of extraarticular is still discussed. We need prospective study with larger groups and longer Followup. Personally I continue to discuss and perform extraarticular tenodesis combined to ACL reconstruction in
case of sport at risks like soccer, basket, volley..; in case of evolved anterior chronic laxity, and in revision surgery.
The take-home message is to consider that the treatment of all the types of ACL insufficiencies cannot be the
Isolated ACL graft under Arthroscopy. The next step will be considered each element, variable or component
of the ligament evaluation IKDC form pre and post-operatively to try to distinguish the different situations.
This is the key to improve our results and to avoid unnecessary gesture.
Bibliography
1- AIT SI SELMI T, FABIE F, MASSOUH T, POURCHER G, ADELEINE P, NEYRET Ph. Greffe du LCA au tendon
rotulien avec ou sans plastie antero externe : Etude prospective randomisée à propos de 120 cas in « le genou
du sportif » Sauramps Medical, Montpellier 2002 : 221-224.
2- BONIN N, AIT SI SELMI T, DEJOUR H, NEYRET Ph, Association Reconstruction du LCA et ostéotomie tibiale
de valgisation. A 11 ans de Recul in « Le Genou du sportif », Sauramps Medical, Montpellier 2002 : 225-235.
3- BOSS A, STUTZ G, OURSIN C, GACHTER A. Anterior cruciate ligament reconstruction combined with valgus tibial osteotomy (combined procedure). Knee Surg. Sports Traumatol Arthrosc 1995: 3: 187-91.
4- BUSS D, WARREN RF, WICKIWICZ TL & COL. Arthroscopically assisted reconstruction of the anterior cruciate ligament with use of autogenous patellar ligament grafts. J. Bone Joint Surg., 75A : 1346-1355,1993.
5- CLADIERE F, Etude comparative de la reconstruction du ligament croisé antérieur isolée ou associée à une
plastie extra articulaire externe. Thèse Médecine Lyon 2000.
6- DEJOUR H, DEJOUR D, AIT SI SELMI T, Chronic anterior laxity of the knee treated with free patellar graft
and extra-articular lateral plasty : 10 year follow-up of 148 cases, Rev. Chir. Orthop. 1999: 85: 777-89.
7- DEJOUR H, NEYRET P, BOILEAU P, DONELL ST. Anterior cruciate reconstruction combined with valgus tibial osteotomy. Clin Orthop 1994: 220-8.
8- DRAGANISH LF, REIDER B, MILLER PR. An in vitro study of the Muller anterolateral femorotibial ligament
tenodesis in the anterior cruciate ligament deficient knee. Am.J. Sports Med. 17: 357-362, 1989.
9- HOLMES PF, JAMES SL., JAMES SL., LARSON RL & COL. Retrospective direct comparaison of three
intraaticular anterior cruciate ligament reconstructions. Am.J. Sports Med. 19: 596-600, 1991.
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10- LATTERMANN C, JAKOB RP. High Tibial osteotomy alone or combined with ligament reconstruction in
anterior cruciate ligament-deficient knees. Knee Surg. Sports Traumatol Arthrosc 1996: 4: 32-8.
11- LEMAIRE M, COMBELLES F. Technique actuelle de plastie ligamentaire pour rupture ancienne du ligament croisé antérieur. Rev. Chir. Orthop. 1980: 66: 523.
12- NEYRET P., PALOMO JR, DONELL ST, DEJOUR H. Extra articular tenodesis for anterior cruciate ligament
rupture in amateur skiers. Br. J. Sports Med. 28: 31-34, 1994.
13- NOYES FR, BARBER SD. The effect of an extra-articular procedure on allograft reconstructions for chronic ruptures of the anterior cruciate ligament. J. Bone Joint Surg., 73A : 882-892, 1991.
14- O’BRIEN WR, WARREN RF, WICKEWICZ TL & COL. The iliotibial band lateral sling procedure and its effect
on the results of anterior cruciate ligament reconstruction Am.Sports Med. 19:21-25, 1991.
15- SHELBOURNE KD, GRAY T. Results of anterior cruciate ligament reconstruction based on meniscus and
articular cartilage status at the time of surgery : five to Fifteen-year evaluations. Am.J. Sports Med. 2000 vol
28 (4): 446-452.
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16- VAIL TP, MALONE TR, BASSET FH. Long term functional results in patients with anterolateral rotatory
instability treated by iliotibial band transfer. Am.J.Sports Med.20: 274-282, 1992
17- WU WM, HACKETT T, RICHMOND JC. Effects of meniscal and Articular Surface Status on knee Stability,
Function and Symptoms after anterior cruciate ligament reconstruction. A long term Prospective Study.
Am.J.Sports Med. 2002 vol 30(6): 845-850.
3.7
ICL #4
CURRENT CONCEPTS IN POSTEROLATERAL INSTABILITY OF THE KNEE
Tuesday, March 11, 2003 • Aotea Centre, ASB Theatre
Chairman: Robert F. LaPrade, MD, USA
Faculty: Fred A. Wentorf, MS, USA, Lars Engebretsen, MD, PhD, Norway and Steinar Johansen, MD, Norway
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I. Introduction/Incidence
A. Mechanism
1. Hyperextension
2. Varus blow
3. Noncontact twisting
B. Incidence
1. 6-11% MRI studies
2. Previous underestimated
C. Importance
1. Do not heal
2. Lead to residual instability/DJD
3. Compromise cruciate ligament reconstructions
II. Applied Anatomy of the Posterolateral Knee (LaPrade)
A. Fibular Collateral Ligament (FCL)
1. Primary stabilizer to varus opening
2. Femoral attachment - proximal/posterior to lateral epicondyle
3. Fibular attachment - midway along lateral fibular head
B. Popliteus Complex (Stäubli, 1990)
1. Important stabilizer to posterolateral rotation of the knee
2. Popliteus attachment on femur
• 2 cm from FCL attachment on femur
• attaches on anterior fifth of popliteal sulcus
• anterior to FCL attachment
3. Popliteofibular Ligament (PFL)
• originates at popliteus musculo-tendinous junction
• attaches to medial aspect of posterior
• fibular styloid (posterior division) and anterior medial downslope of styloid
(anterior division)
• important static stabilizer of external rotation
C. Mid-Third Lateral Capsular Ligament
1. Secondary stabilizer to varus opening
2. Thickening of lateral midline capsule - equivalent to "deep MCL"
3. Meniscotibial portion - frequently injured. Site of Segond fracture and soft-tissue
Segond injuries.
D. Biceps Femoris Complex
1. Two heads - through attachments to capsule, FCL, tibia, and fibula - help to dynamically
stabilize the lateral com-partment of the knee
2. Short Head Biceps Femoris
• 5 components at the knee
• main attachments are to fibular styloid, posterolateral capsule, and an anterior
tibial arm
3. Long Head Biceps Femoris
• 5 components at the knee
• main attachments are to fibular styloid
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Diagnosis of Posterolateral Knee Complex (PLC) Injuries (LaPrade)
A. History
1. Usually due to varus or hyperextension injuries
2. Fifteen percent have a common peroneal nerve injury
3. Majority (but not all) occur as combined ligamentous injuries (ACL/PLC, PCL/PLC most
common)
B. External Rotation Recurvation Test (Hughston, 1980)
1. Lift up the big toe
2. Observe for increased recurvation and relative varus
3. Usually indicative of a combined PLC/cruciate ligament injury
C. Varus Stress Test at 30º
(Hughston, 1966)
1. Fingers over joint line to assess amount of opening
2. Apply varus stress through foot/ankle
3. Compare opening to contralateral (normal) knee
D. Posterolateral Drawer Test (Hughston, 1980)
1. Knee flexed to 90º, foot external rotation to 15º
(I sit on the foot)
2. Apply a gentle posterolateral rotation force and assess amount of posterolateral rotation
(compare to normal contralateral knee)
E. Dial Test (Gollehon, 1987; Grood, 1988)
1. Assesses ER component of posterolateral knee injury (Grood, 1988; Veltri, 1995)
2. Perform with knee flexed over side of examining bed, apply an external rotation force
through the foot and look for external rotation of the tibial tubercle
3. Increased amount of external rotation at 30º indicates a posterolateral knee injury (arc 13º)
4. Dial test at 90º
• isolated posterolateral knee injury – slightly decreased external rotation
compared to 30º (may not be visually detectable difference) (usually 5º ER)
C an increased amount of external rotation is indication of a combined PCL/
posterolateral knee injury (Gollehon, 1987; Grood, 1988) or a combined ACL/
posterolateral knee injury (Wroble, 1993)
F. Reverse Pivot Shift Test (Jakob, 1981)
1. Largest variability among all motion tests - 35% in normal knees (Cooper, 1991)
2. Knee flexed to 45º, foot externally rotated
3. Knee is then extended. If subluxed in flexion, the knee is reduced by the iliotibial band
as it changes function from a flexor to an extender of the knee
G. Varus Thrust Gait
1. Usually (but not always) have underlying varus alignment
2. Patients learn to adapt with flexed knee gait
H. Radiographs
• AP varus thrust or stress x-ray
• AP (Segond, arcuate fractures)
• Long leg alignment x-ray
I. MRI (LaPrade, 2000)
a. Thin slice (2mm), include entire fibular head/styloid, add coronal obliques
b. Iliotibial band
• superficial layer
• deep layer
c. Long head biceps femoris
• direct arm
• anterior arm
d. Short head biceps femoris
• direct arm
• anterior arm
e. Fibular collateral ligament
f. Popliteus complex
• femoral attachment
• popliteomeniscal fascicles
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III.
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• popliteofibular ligament
g. Fabellofibular ligament
J. Arthroscopic Evaluation (LaPrade, 1997)
a. "Drive-through" sign – > 1 cm lateral joint line opening
b. Popliteus attachment
c. Mid-third lateral capsular ligament
• meniscofemoral
• meniscotibial
d. Popliteomeniscal fascicles
e. Coronary ligament
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IV. Biomechanics of the Posterolateral Knee (Wentorf)
A. Varus instability
• FCL is major restraint to varus at all knee flexion angles. The popliteus complex, postero
lateral capsule (including FFL, PFL), and cruciates also play an important role in preventing
varus
1. Grood, et al, 1988
• Additional sectioning of popliteus tendon and other structures (PFL, capsule, etc)
increases varus
2. Gollehon, et al, 1987
• Additional sectioning of popliteus tendon increases varus
3. Cruciate ligaments and varus
• Recruited with deficient posterolateral complex (PLC) to resist varus
a. Markolf, et al, 1993
• section of PLC increases mean force on ACL at all flexion angles
• section of PLC increases force on PCL at >45º
b. Gollehon, et al, 1987
• section of PCL after PLC resulted in large increase in varus rotation
B.
Rotational instabilities
1. External rotation
• Sectioning of PLC structures increases ER (Grood, et al, 1988)
a. 30º of flexion = 13º increase ER
b. 90º of flexion = 5.3º increase ER
• Additional sectioning of PLC/PCL increases ER at 90º Flexion (Gollehon, 1987;
Grood, 1988; Kaneda, 1997)
• Additional sectioning of ACL/PLC also increases ER at 90º (Wroble, 1993)
2. Internal rotation
• Isolated/combined cutting of FCL, popliteus, PLC joint structures increases IR
(Grood, et al, 1988; Noyes, et al, 1993, LaPrade, 1999)
• Variable differences across knees
C. Anterior/posterior translation
1. Sectioning PLC results in no primary increase in anterior translation (Gollehon, et al,
1987; Grood, et al, 1988)
a. PLC is important 2º restraint to ATT with combined ACL/PLC injury (Nielsen, 1986;
Wroble, 1993; Veltri, 1995)
b. Clinically detectable as increased ATT on Lachman test
c. Force on PLC with ACL intact is minimal; significant forces present on PLC with
ACLD (Kanamori, 2000) – suggests need for combined ACLR with PLC repair/
reconstruction
2. Posterior tibial translation
a. Between 0º and 30º of flexion no difference in posterior translation between
isolated PLC versus isolated PCL sectioning (Gollehon, et al, 1987)
b. Combined PCL/PLC cutting significantly increases posterior translation compared
to isolated section of either (Gollehon, et al, 1987; Grood, et al, 1988)
c. Effect of popliteus on posterior translation (Harner, et al., 1998)
d. Simulated popliteus contraction decreases in situ forces on the PCL at 30º and
90º (Harner, et al, 1998)
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D. Does the PLC heal?
1. In vivo model-rabbits
2. FCL/popliteus do not heal
E. Forces in the intact PLC
1. FCL loaded at all flexion angles – varus
2. FCL loaded near extension in ER
3. Popliteus/PFL complementary to FCL – loaded in flexion to ER
F. Effect of PLC injuries on ACL reconstructions
1. Effect of grade III PLC injuries on an ACL reconstruction graft (LaPrade, 1999)
a. Significant increase in graft force seen for varus and combined varus-IR at 0º and 30º
b. Recommend to repair/reconstruct PLC injuries at time of ACLR to reduce risk of
ACLR failure
2. Effects of tensioning on an ACL graft and integrity of the PLC on tibiofemoral orientation
(Wentorf, AJSM, 2002)
a. Significant increase in ER seen with increasing ACL graft tension
b. Recommended to repair/reconstruct PLC injuries first, prior to ACL graft fixation,
to reduce risk of ER deformity
G. Effect of PLC injuries on PCL reconstructions
1. Effect of grade III posterolateral knee injuries on a PCL reconstruction graft (LaPrade, 1999)
a. Significant increase in graft force at 0º, 60º, and 90º with FCL, PFL, and popliteus
tendon cut
b. Significant increase in graft force at 30º, 60º, and 90º with FCL, PFL, and popliteus
tendon cut
2. No significant increase in PCL graft force for an isolated posterior drawer or external
rotation torque when the posterolateral structures were sectioned
a. Recommend to repair/reconstruct posterolateral structures in knees with varus
and/or coupled posterior drawer-external rotation instability at time of PCL
reconstruction to decrease chance of post-reconstruction PCL graft failure
b. Important – assess for posterolateral knee injury prior to PCL graft fixation.
Once the PCL graft is fixed, possible pathologic amounts of posterolateral instability
– which may cause graft failure – will not be detectable on the operating table
3. Effect of tensioning on the PCL graft and the integrity of posterolateral structures on
tibiofemoral orientation (Wentorf, unpublished data, 1999)
• No significant increase in external rotation seen before/after PLC sectioning.
Therefore, if the PCL graft is fixed at 90º, it makes no difference if the PCL graft or
the PLC structures are secured/repaired first
4. Effect of deficient PLS on PCLR (Harner, 2000)
a. Forces on PCL graft significantly increased for PLS deficiency
b. PCL graft is ineffective and overloaded with PLS deficiency if PLC not repaired
H. Summary of key points of PLC biomechanics
1. FCL is key structure for preventing abnormal varus motion
2. FCL and popliteus complex prevent abnormal ER
3. Understanding PLC applied anatomy, abnormal motion with injuries, and biomechanics
assists in treatment of combined ACL and/or PCL injuries
4. It is important to recognize PLC injury prior to cruciate ligament(s) reconstruction;
performance of an isolated cruciate ligament reconstruction with a PLC injury places
the cruciate ligament graft at risk for failure
V. Surgical Treatment Options for Acute Posterolateral Knee Injuries (Engebretsen)
A. Acute grade III PLC injuries
1. Repair/reconstruct < 2 weeks after injury
a. Attempt anatomic repair
b. Prior to scar tissue planes developing
2. Surgical incision
• Lateral hockey stick
• Center over Gerdy’s tubercle
• Align along posterior border iliotibial band
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3. Fascial incisions (Terry and LaPrade, 1997)
a. Split iliotibial band in line with its fibers (Gerdy’s tubercle and proximal)
b. Posterior to LH biceps concurrent with peroneal neurolysis
c. Posterior border of iliotibial band (optional)
d. In acute injuries, may need to follow injury plane
4. Diagnostic arthroscopy after surgical approach completed (LaPrade, 1997)
a. Assist in surgical approach
b. Accurate to diagnose popliteus tendon, popliteomeniscal fascicle, coronary
ligament, and mid-third lateral capsular ligament injuries
5. Avulsions off femur
a. Popliteus avulsion-recess procedure (Stäubli)
b. FCL avulsion – recess procedure
c. Lateral gastrocnemius tendon – direct repair (suture anchor)
6. Avulsions off tibia
a. Lateral capsule – direct repair to bone
b. Anterior arm of short biceps – direct repair to bone
c. Coronary ligament of posterior horn of lateral meniscus - direct repair to bone
d. Popliteomeniscal fascicle tears – direct repair if lateral meniscus unstable
7. Avulsion off fibular head/styloid
a. Popliteofibular ligament – suture anchor
b. Direct arms of long-short heads of biceps femoris – suture anchors
c. FCL – suture anchor
d. Arcuate avulsion fracture – cerclage suture fixation
8. Midsubstance tears
a. Consider augmentation (biceps femoris, ITB, hamstrings)
b. Anatomic reconstruction (Johansen)
B. Rehabilitation for Acute PLC Repairs (Engebretsen)
1. Nonweight bearing – 6 weeks crutches
2. Range of motion
1. "Safe zone" at time of PLC repair
2. Strive for full extension initially
3. Goal of 0-120º by 6 weeks postop
3. Exercises
1. Quads sets/straight leg raises in immobilizer only
2. Exercise bike POW #7 (based on ROM)
3. Rehab like ACLR POW #10-12
VI. Surgical Treatment Options for Chronic Grade III Posterolateral Knee Injuries
1. Assess for varus alignment first
a. Long leg standing x-ray
b. Correct for varus alignment or soft tissue reconstruction will stretch out
c. Proximal tibial opening wedge osteotomy (to tighten up structures)
d. Reassess at 6 months postop osteotomy for need for soft tissue reconstruction
2. Posterolateral corner reconstructions - historical
a. Most previous reconstructions
• Sling procedures
• Nonanatomic
• Few biomechanical studies
b. Biceps tenodesis – Sling procedure
• Redirect LH biceps tendon over a screw and washer
• Requires intact biceps attachments to posterior capsule (capsular arm) and FCL
• If fails, difficult to reconstruct due to loss of biceps dynamic function
c. FCL reconstruction (Tibone)
• Patellar tendon graft
• Reconstructs FCL attachments to femur and fibula
d. Popliteus complex reconstruction
• Muller, popliteus bypass
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• Stabilize against ER
3. Anatomic reconstruction of FCL/popliteofibular ligament/popliteus tendon
• Cooperative biomechanics project between Universities of Minnesota and Oslo
• Two tailed reconstruction of FCL/PFL and popliteus tendon
• Biomechanically restores function of native ligaments
a. Tunnel placement
• Fibular head (7 mm)
• Tibia (9 mm)
• Femur (7 mm x 20 mm x 2)
b. Split achilles graft
• Bone blocks in femur
• Fix in fibular head (FCL) and on tibia (PLT/PFL)
• Bone plugs (7 mm x 20 mm) in femur
• Fix in fibula (bioscrew – FCL)
• Fix PLT/PFL on tibia (staple)
A. Rehabilitation of Chronic PLC Surgery
A. Weight bearing status
1. Nonweight bearing for 6 weeks
2. Crutches/protected weight bearing POW #7-10
3. Wean off crutches
B. Range of motion
1. Full ROM immediately
2. Gentle ROM out of immobilizer Q/D on CPM
C. Exercises
1. Quad sets/straight leg raises in immobilizer only for 6 weeks
2. Exercise bike/leg presses (20 kg to 70º) at POW #7
3. Rehab "slow track" ACLR at POW #12
References:
1. Cooper DE: Tests for posterolateral instability of the knee in normal subjects. J Bone Joint Surg, 73A:30-36, 1991.
2. Gollehon DL, Torzilli PA, Warren RF: The role of the posterolateral and cruciate ligaments in the stability of the human knee: A biomechanical study. J Bone Joint Surg, 69-A:233-242, 1987.
3. Grood ES, Stowers SF, Noyes FR: Limits of movement in the human knee: Effect of sectioning the posterior cruciate ligament and posterolateral structures. J Bone Joint Surg, 70-A:88-97, 1988.
4. Harner CD, H—her J, Vogrin TM, et al: The effects of a popliteus muscle load on in situ forces in the
posterior cruciate ligament and on knee kinematics. Am J Sports Med, 26:669-673, 1998.
5. Harner CD, Vogrin TM, H—her J, et al: Biomechanical analysis of a posterior cruciate ligament reconstruction. Deficiency of the posterolateral structures as a cause of graft failure. Am J Sports Med,
28:32-39, 2000.
6. Hughston JL, Norwood LA: The posterolateral drawer test and external rotation recurvation test for posterolateral rotatory instability of the knee. Clin Orthop Rel Res, 147:82-87, 1980.
7. Jakob RP, Hassler H, Stäubli H-U: Observations on rotatory instability of the lateral compartment of the
knee: Experimental studies on the functional anatomy and pathomechanism of the true and reverse
pivot shift sign. Acta Orthop Scand, 52(Suppl):1-32, 1981.
8. Kanamori A, Sakane M, Zeminski J, et al: In situ force in the medial and lateral structures of intact and
ACL-deficient knees. J Orthop Sci, 5:567-571, 2000.
9. LaPrade RF, Terry GC: Injuries to the posterolateral aspect of the knee. Association of Injuries with
Clinical Instability. Am J Sports Med, 25(4):433-438, 1997.
10. LaPrade RF: Arthroscopic evaluation of the lateral comparison of knees with grade 3 posterolateral
complex knee injuries. Am J Sports Med, 25(5):596-602, 1997.
11. LaPrade RF, Hamilton CD: The fibular collateral ligament-biceps femoris bursa. Am J Sports Med,
25:439-443, 1997.
12. LaPrade RF, Resig S, Wentorf FA, Lewis JL: The effects of grade 3 posterolateral knee injuries on force
in an ACL reconstruction graft: A biomechanical analysis. Am J Sports Med, 27:469-475, 1999.
13. LaPrade RF, Bollom TS, Gilbert TJ, Wentorf FA, Chaljub G: The MRI appearance of individual structures
of the posterolateral knee: A prospective study of normal and surgically verified grade 3 injuries. Am J
3.13
ICLs
3.14
Sports Med, 28:191-199, 2000.
14. LaPrade RF, Muench CW, Wentorf FA, Lewis JL: The effect of injury to the posterolateral structures of
the knee on force in a posterior cruciate ligament graft. A biomechanical study. Am J Sports Med,
30(2):233-238, 2002.
15. LaPrade RF: The medial collateral ligament complex and the posterolateral aspect of the knee. Sports
Medicine Orthopaedic Knowledge Update - 2nd ed., AAOS, 1999.
16. LaPrade RF, Hamilton CD, Engebretsen L: Treatment of acute and chronic combined anterior cruciate
ligament and posterolateral knee ligament injuries. Sports Med and Arth Rev, 5:91-99, 1997.
17. Markolf KL, Slauterbeck JL, Armstrong KL, et al.: A biomechanical study of replacement of the posterior
cruciate ligament with a graft. Part II: Forces in the graft compared with forces in the intact ligament. J
Bone Joint Surg, 79-A:381-386, 1997.
18. Maynard MJ, Deng X-H, Wickiewicz TL, et al.: The popliteofibular ligament: Rediscovery of a key element
in posterolateral stability. Am J Sports Med, 24:311-316, 1996.
19. Noyes FR, Barber-Westin SD: Surgical reconstruction of severe chronic posterolateral complex injuries
of the knee using allograft tissues. Am J Sports Med, 23(1):2-12, 1995.
20. Noyes FR, Barber-Westin SD, Hewett TE: High tibial osteotomy and ligament reconstruction for varus
angulated anterior cruciate ligament-deficient knees. Am J Sports Med, 28(3):282-296, 2000.
21. Simonian PT, Sussman PS, van Trommel M, Wickiewicz TL, Warren RF: Popliteomeniscal fasciculi and
lateral meniscal stability. Am J Sports Med, 25:849-853, 1997.
22. Stäubli H-U, Birrer S: The popliteus tendon and its fascicles at the popliteus hiatus: gross anatomy and
functional arthroscopic evaluation with and without anterior cruciate ligament deficiency. Arthroscopy,
6:209-220, 1990.
23. Terry GC, LaPrade RF: The biceps femoris complex at the knee: Its anatomy and injury patterns associated with acute anterolateral-anteromedial rotatory instability. Am J Sports Med, 24:2-8, 1996.
24. Terry GC, LaPrade RF: The posterolateral aspect of the knee. Anatomy and surgical approach. Am J
Sports Med, 24(6):732-739, 1996.
25. Veltri DM, Deng X-H, Torzilli PA, et al.: The role of the cruciate and posterolateral ligaments in stability
of the knee: A biomechanical study. Am J Sports Med, 23:436-443, 1995.
26. Wascher DC, Grauer DJ, Markolf KL: Biceps tenodesis for posterolateral instability of the knee: An in
vitro study. Am J Sports Med, 21:400-406, 1993.
27. Wentorf FA, LaPrade RF, Lewis JL, Resig S: The effect of ACL graft force on the tibiofemoral orientation
in knees with posterolateral corner injuries. Am J Sports Med, 2002.
ICL #5
CLAVICLE FRACTURES AND DISLOCATIONS
Tuesday, March 11, 2003 • Aotea Centre, Kaikoura Room
Chairman: Ulrich Bosch MD, Germany
Faculty: Reinhard Fremerey, MD, PhD, Germany, Stephen J. Snyder, MD, USA and Eugene Wolf, MD, USA
Acute and Chronic AC Joint Dislocation
Classification and Diagnosis
R. Fremerey
8’
R. Fremerey
S. Snyder
E. Wolf
10’
15’
15’
Degenerative Disorders of the AC Joint
How to treat?
S. Snyder
10’
SC Joint Dislocation
Diagnosis and Management
R. Fremerey
10’
Clavicular Fractures
Classification and Treatment Options
U. Bosch
12’
Treatment: When and How?
Nonoperative
Mini-Open Technique
Arthroscopic Technique
Discussion
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Outline
10’
Acute and Chronic AC Joint Dislocation
Classification and Diagnosis
Treatment: When and How? – Nonoperative Treatment
R. Fremerey, MD, Phd.
Trauma Department
Krankenhaus Hildesheim GmbH
Weinberg 1
D-31141 Hildesheim
[email protected]
Epidemiology
- about 12% of all dislocations of the shoulder girdle
- caused by direct or indirect trauma
Anatomy and Biomechanics
Anatomy:
- the AC-joint is a diarthrodial joint involving the medial facet of the acromion and the distal clavicle
- the articular surfaces are covered with hyaline cartilage
- a fibrocartilaginous disk of varying size and shape is present in the joint
- along with the SC-joint, it provides a bony link of the shoulder to the axial skeleton
- in children, the clavicle is surrounded by a thick periosteal tube that extends all the way to the acromioclavicular joint, so that children are more prone to fracture and pseudodislocations than true dislocation of
the acromioclavicular joint
3.15
Biomechanics:
- enhances overhead activity
- there is only little motion between the acromion and clavicle in rotating and lifting of the arm, hence,
most scapulothoracic motion occurs at the SC-joint.
- the anteroposterior (horizontal) stability is provided by the acromioclavicular ligament
- the superoinferior stability (vertical) is provided by the coracoclavicular ligaments (conoid and trapezoid)
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Classification
ROCKWOOD:
Type I:
Sprain of the acromioclavicular ligaments only
Type II:
Acromioclavicular ligament and joint capsule disrupted
Coracoclavicular ligaments intact
Up to 50% vertical subluxation of the clavicle
Type III:
Acromioclavicular ligament and capsule disrupted
Coracoclavicular ligaments disrupted
Dislocation of acromioclavicular joint
Type IV:
Acromioclavicular joint dislocation with clavicle displaced posteriorly into or through the
trapezius muscle
Type V:
Complete detachment of deltoid and trapezius fascia from the distal clavicle
Acromioclavicular joint dislocated with extreme superior elevation of the clavicle (100% to
300% of normal)
Type VI:
Acromioclavicular joint disrupted with the clavicle displaced inferior to the acromion or
coracoid process
Diagnosis
- swelling, deformity, distal clavicle superior, dropping of the shoulder girdle
X-ray:
- ap acromioclavicualar joint radiograph, 15-degree-cephalic tilt view (Zanca), stress or weighted radiographs of both AC-joints
Treatment – Acute Injury
Nonoperative:
Type I:
- conservative treatment, analgesic medications, sling, physiotherapy
Type II:
- conservative treatment, analgesic medications, sling, physiotherapy
Type III:
- the trend in the treatment of these injuries is toward a more conservative approach
- a distinct advantage of surgical treatment over conservative care has never been clearly demonstrated
- for the throwing athlete’s dominant extremity, the stabilization remains controversial because the results
of nonoperative treatment are similar as compared to the operative procedure even in those patients
- nonoperative treatment includes analgesia, icing and a sling
- acceppting the deformity and skillfull neglection" is the trend because correction of the deformity by
external stabilizers (e.g. braces, taping) is rarely possible
Operative
Type IV:
- the goal is to reduce the deformity, either by closed reduction or open reduction and stabilization
Type V:
- operative reduction because of the significant stripping of deltotrapezial fascia
- reconstruction of the coracoclavicular and of the acromioclavicular ligaments
3.16
- conservative treatment remains controversial
Type VI:
-open reduction and stabilization
Injuries in Children
Type I, II, III:
- conservative treatment with a sling, ice, and mild analgesics
Type IV,V,VI:
- open reduction and stabilization
Literature
1. Fremerey RW, Lobenhoffer P, Bosch U, Freudenberg E, Tscherne H (1996) Die operative Behandlung der
akuten, kompletten AC-Gelenksprengung. Indikation, Technik und Ergebnisse. Unfallchirurg 99: 341-345
2. Phillips AM, Smart C, Groom AFG (1998) Acromioclavicular dislocation. Conservative or surgical therapy.
Clin Orthop 353: 10-17
3. Rockwood CA Jr. (1985) Disorders of the acromioclavicular joint. In: Rockwood CA Jr, Matson FA III, eds.
The shoulder. Philadelphia: WB Saunders: 413–476.
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Complications
- posttraumatic arthritis of the AC-joint: if symptomatic, resection of the distal end of the clavicle
- very rarely slight loss of power in overhead activities in both conservative and operative treatment
SC-Joint Dislocation
Diagnosis and Management
R. Fremerey, MD, Phd.
Trauma Department
Krankenhaus Hildesheim GmbH
Weinberg 1
D-31141 Hildesheim
[email protected]
Epidemiology
- about 3% of all dislocations of the shoulder girdle
- most commonly caused by indirect trauma
- ratio of anterior:posterior dislocation: 4:1 – 20:1
Anatomy and Biomechanics
- the SC-joint is a diarthrodial joint and is the only true articulation between the clavicle of the upper
extremity and the axial skeleton
- it creates a saddle-type joint with the clavicular notch of the sternum
- the joint has only few bony stabilization so that it is stabilized by the Intraarticular Disk Ligament, the
Costoclavicular Ligament, the Interclavicular Ligament and by the Capsular Ligament
- the joint is freely movable and has motion in almost all planes
- it is most likely the most frequently moved joint of the long bones in the body because almost any
motion of the upper extremity is transferred proximally to the sternoclavicular joint.
Classification
Anatomic Classification:
- Anterior Dislocation: most common.
- Posterior Dislocation: uncommon.
Etiologic Classification:
- Traumatic Injuries: Sprain or Subluxation, Acute Dislocation, Recurrent Dislocation (rare), unreduced Dislocation
3.17
Diagnosis
- swelling, deformity, pain
X-ray:
routine x-ray, CT scan to distinguish between anterior and posterior dislocation
Signs Common to Anterior and Posterior Dislocations:
Anterior Dislocation:
- medial end of the clavicle is visibly prominent anterior to the sternum and can be palpated anterior to
the sternum, either being fixed or mobile
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Posterior Dislocation:
- usually more painful than anterior dislocation
- the usually palpable medial end of the clavicle is displaced posteriorly
- venous congestion may be present in the neck or in the upper extremity
- breathing difficulties, shortness of breath, or a choking sensation, circulation to the ipsilateral arm may
be decreased
- complete shock due to injury of the great vessels or pneumothorax
- CAVE: the distinction between anterior and posterior dislocation may be difficult by clinical findings or
routine x-ray alone!
- CT-Scan should be performed to make a clear diagnosis!
Treatment
Traumatic Injuries
Anterior Dislocation:
- mild sprain: analgesics, ice, sling for 3 to 4 days
- moderate sprain (Subluxation): analgesics, ice, figure-of-eight dressing
- anterior dislocation: nonoperatively, closed reduction, but most acute anterior dislocations are unstable
following reduction: “skillfull neglect”
After reduction:
- joint stable: figure-of-eight dressing for 6 weeks
- joint unstable: figure-of-eight dressing for 4-7 days
- in patients up to 25 years of age, usually there are no dislocations of the sternoclavicular joint but type I
or II physeal injuries, which heal and remodel without operative treatment
Posterior Dislocation:
- rule out damage to the pulmonary and vascular system
- closed reduction under general anaesthesia, the joint is almost always stable
- figure-of-eight dressing for 4 to 6 weeks
Recurrent or unreduced posterior Dislocation:
- open reduction and stabilization, figure-of-eight dressing for 4 to 6 weeks
Atraumatic Problems
Spontaneous Subluxation or Dislocation:
- spontaneous anterior subluxations and dislocations of the SC-joint are seen most often in patients under
20 years of age, and more often in females
- associated with laxity in other joints of the extremities
- self-limiting condition which should not be treated with attempted surgical reconstruction
- spontaneous posterior dislocations are not reported in the literature
Complications
Anterior dislocation
- cosmetic "bump" or late degenerative changes
3.18
Posterior dislocation
- pneumothorax and laceration of the superior vena cava, respiratory distress, venous congestion in the
neck; rupture of the esophagus, pressure on the subclavian artery,,myocardial conduction abnormalities,
compression of the right common carotid artery, brachial plexus compression, hoarseness of the voice
- migration of pins in operative procedures, cardiac tamponade, damage to the vessels
Clavicular Fractures
Ulrich Bosch, MD
Professor of Orthopaedic Traumatology
Hannover Medical School
Center of Orthopaedic Surgery, Sports Traumatology
International Neuroscience Institute
Hannover, Germany
ICLs
Literature
Gangahar DM and Flogaites T. (1978) Retrosternal Dislocation of the Clavicle Producing Thoracic Outlet
Syndrome. J Trauma, 18: 369–372.
Kanoksikarin S and Wearne WM (1978) Fracture and Retrosternal Dislocation of the Clavicle. Aust. NZ J
Surg, 48: 95–96.
Rockwood CA, Jr. Injuries to the Sternoclavicular Joint (1984). In: Rockwood, CA, Jr., and Green, DP (eds.):
Fractures, 2nd ed. vol. 1, pp. 910–948. Philadelphia, J.B. Lippincott
Rockwood CA, Jr and Odor JM (1988). Spontaneous Atraumatic Anterior Subluxation of the Sternoclavicular
Joint in Young Adults: Report of 37 Cases (abstract). Orthop Trans, 12: 557.
Epidemiology
- about 4% of all fractures, 35% of all fractures in the shoulder region
- distribution of clavicular fx:
76% middle third
21% distal clavicle
3% medial clavicle
Anatomy and Function
anatomy:
- first bone to ossify in the embryo
- ossification proceeds from two separate centers
- "s"-shaped curvature with an apex anteromedially and an apex posterolaterally
- made up of very dense trabecular bone, no well defined medullary canal,
- the midportion is the thinnest and narrowest portion of the clavicle, mechanically weak area, most
common site of fracture
- stabilization of clavicular articulation:
medial - costoclavicular and sternoclavicular ligaments
lateral - coracoclavicular and acromiocalvicular ligaments, trapezius
muscle and deltoid origin (deltotrapezoid fascia)
-close relation to the brachial plexus, subclavian vessels, and apex of lung
function:
- enhances overhead activity
- serves as framework for muscular attachment,
- provides protection for underlying neurovascular structures
- transmits forces of accessory muscles of respiration
Classification
Allman:
middle, distal, proximal third
Neer:
fx distal to the trapezoid ligament
type I
lateral to the cc-ligamants, cc-ligaments intact
type II
medial fragment displaced, conoid ligament ruptured
type III
similar to type I, with extension into AC-joint
Craig:
medial fx
type I - minimally displaced
3.19
type II - displaced
type III - intraarticular
type IV - physeal separation
type V – comminuted
- pseudodislocation of AC-joint in children:
distal physeal injuries with displacement of the proximal fragment separated from the surrounding
periosteum, cc-and ac-ligaments remain attached to the periosteal sleeve.
Mechanism of Injury
- birth injury
- indirect: fall on outstretched arm
- direct: fall, direct blow on tip of shoulder
- violent trauma
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Clinical Evaluation
swelling, deformity (apex typically superior, shortening), ecchymosis over fracture site, adduction and
dropping of the shoulder girdle, arm is held against trunk, tenderness at fracture site, assessment of
neurovascular status,
associated injuries: vascular, brachial plexus, pneumothorax
Radiographic Evaluation
- middle third:
AP view, 45°-(20° to 60°)-cephalad tilted view
- distal third:
15° cephalad tilted view, axillary view, stress/wighted views
- medial third:
AP view, 40°-cephalad tilted view, CT scan often necessary
Treatment
- midclavicular fx
nondisplaced, minimally displaced fx - nonoperative
• figure of eight bandage or sling for 4 wks
• good functional results despite residual deformity in most of the fractures
displaced fx – best treatment still disputed
• closed reduction, figure of eight bandage
• plate fixation (ORIF) according to the AO/ASIF technique – more extensive exposure
• Prevot-Nail (intramedullary fixation of the clavicle with elastic pin) – limited exposure
- distal clavicular fx
little or no displacement: sling
displaced fx: Kirschner wires in combination with tension
band wire or small T-plate
- medial clavicular fx
nonoperative for most of the fx, sling until discomfort subsides
operative only in specific situations
resection of the medial clavicle if symptoms persist
Complications
- nonunion (1-4%)
asymptomatic: no treatment
symptomatic: (deformity, dysfunction, neurovascular compromise) restoration of alignment and
continuity of the clavicle is recommended (ORIF, autogenous bone graft in atrophic nonunions),
resection only for distal and medial nonunions with small fragments
- malunion
if associated with ipsilateral shoulder dysfunction osteotomy through the plane of deformity,
realignment of the calvicle, and plate fixation is recommended. Interposition of a tricortical iliac
crest bone graft may be useful to restore length and alignment an to promote healing
3.20
- neurovascular complications
are rare, can occur delayed as result of compression by malunited fracture or hypertrophic callus/
non-union
correction of cause of compression, removal of callus, reshaping of malunion
S & M (Scope and Mini-Open) Technique for Acromioclavicular Joint Reconstruction
Stephen J. Snyder, MD
ICLs
References:
1. Bosch U, Skutek M, Peters G, Tscherne H (1998) Extension osteotomy in malunited clavicular fractures. J
Shoulder Elbow Surg 7: 402-405
2. Brunner U (2002) Claviculafrakturen. In: Habermeyer P (ed) Schulterchirurgie. Urban & Fischer, München,
Jena, p. 437-451
3. Jupiter JB, Ring D (1999) Fracture of the clavicle In: Iannotti IP, Williams GR (eds) Disorders of the shoulder: diagnosis and management. Lipincott Williams & Wilkins, Philadelphia, p.709-736
4. Miller ME, Ada JR (1992) Injuries to the shoulder girdle. In: Browner BD, Jupiter JB, Levine AM, Trafton PG
(eds) Skeletal Trauma Vol II. WB Saunders, Philadelphia, London, Toronto, p.1291-1310
This outline presents a technique for logical repair of a symptomatic dislocated AC joint.
This technique requires special equipment, including the following: (1) arthroscopic electro
TM
TM
surgical “Subacromial Electrode “ from Linvatec, Inc.; (2) plastic CuffLink from
TM
Innovasive, Inc.; (3) SecureStrand 1mm surgical cable from Surgical Dynamics; (4) a
medium sized rotator cuff suture retriever from Linvatec, Inc.; (5) a Nitenol Wire Suture
TM
Passer from Arthrex, Inc.
Technique:
Scope Portion
1.
(A) Release the entire coraco-acromial (CAL)
ligament from the undersurface of the
acromion and dissect it off the deltoid to the
coracoid process using a Linvatec
Subacromial Electrode (Figure 1).
(B)
Tether the end of the CAL using #1 PDS
suture. Insert a spinal needle through the
ligament, pass the PDS, and retrieve it out
the lateral cannula. Insert the needle again
TM
and pass a Shuttle Relay through the
CAL, out the lateral cannula and carry the
PDS back through the CAL. Pass the
Shuttle and retrieve the PDS a third time to
complete the tethering (Figure 2).
Figure
1
(C) Pull the CAL inside the lateral operating
cannula and clamp the sutures to store it
until it is passed to the open surgical site.
Mini Open Portion
2.
(A) Make a 5 cm mini-open incision from
anterior to posterior one cm medial to and
parallel to the distal clavicle and excise 1
cm of clavicle.
(B)
Prepare the distal clavicle (3 steps)
a. burr a 1mm deep trough from anterior
to posterior 3 mm from the end of the
bone (a);
b. drill 2 parallel suture holes from
Figure
2
3.21
anterior to posterior on either side of
the through (b);
c. drill 2 additional holes for the
SecureStrand® holes from superior to
inferior through the center of the
clavicle 2 cm and 5 cm from the
end.(c) (Figure 3-A)
Figure 3-B
a
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(C) Delivery of the CAL to the surgical site,
passing the lateral cannula under the
acromion and retrieving the lead sutures.
(D) Fixate the end of the CAL with a doublewhip stitch of #2 Ethibond. (Figure 3-A) (d)
3. (A)
Figure
3 A&B
c
Figure 3-A
d
Pass suture leaders through all four drill
holes in the clavicle.
(B)
Pass doubled over suture as a leader
around coracoid using medium-sized
Linvatec suture retriever loaded with an
Arthrex nitenol suture passer. (Figure 3-B).
4. (A)
Using the suture passer, carry both
doubled-over SecureStrands (4 strands
total) around the coracoid insuring that the
looped end is on the posterior side of the
coracoid. (Figure 4)
(B)
b
Carry the loop-end of one of the doubled
SecureStrands through the medial and one
through the lateral drill holes in the clavicle
from inferior to superior using the passing
sutures.
Figure 4
a
5.
6.
7.
3.22
Thread the SecureStrand loop through the Cuff
Link device using a lead suture and seat the
Cuff Links in the bone holes on the superior
aspect of the clavicle (Figure 5-a).
(A)
Reduce the AC joint and cinch and lock the
medial SecureStrand using a “racking
hitch” knot (Figure 5-b).
(B)
Cinch and lock the lateral SecureStrand
with a racking hitch knot.
(A) Carry the lead sutures for the CAL graft
b
Figure 5
through the posterior aspect of the clavicle
and out anteriorly to pull the CAL into the
trough on the top of the clavicle. (a)
(B)
(A) Repair the deltoid and trapezius with sideto-side sutures above the clavicle.
(B)
9.
Imbricate the capsular remnant over the AC
joint.
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8.
Tie the two sutures together, locking the
CAL into the trough on top of the clavicle
(Figure 7).
Figure
Meticulously stop all bleeding and close the
skin with subcuticular closure.
10. Protect the arm postop in an UltraSling® from
d.j. Orthopedics for 4-6 weeks, allowing biceps,
elbow, wrist and hand and gentle pendulum
exercises. Active shoulder motion as tolerated
at 6 weeks progressing to full activities at 4
months.
Figure 7
The S&M AC joint reconstruction was developed in response to the myriad of problems
encountered when using the traditional techniques employing screws, wires and circlage cables.
The steps of this operation are exacting but the final result is a stable AC joint with a small incision
and no need for reoperation for hardware removal. Harvesting the CAL using arthroscopy insures
that there is no injury to the deltoid tendon and the length of the CAL is maximized. The clavicle is
protected by making the drill holes in the center of the bone (AP) and by using the Cuff Links to
stress shield the Secure Strand passing through them. The Secure Strand is extremely strong,
flexible and easy to tie using the “racking hitch” knot. The initial security of the clavicle is insured
by using two drill holes for the Secure Strand located in the position of the two torn ligaments.
Finally, the CAL is anchored over the top of the clavicle in a trough giving it a biomechanically
sound easily adjustable fixation. To date there have been no failures.
3.23
A New Technique All
Arthroscopic Treatment of AC
Joint Disruption
Eugene M. Wolf, M. D.
Acromioclavicular Dislocations
(Rockwoood)
•
•
•
•
•
Types I through VI
Types I and II: non-operative
Types IV, V, and VI: operative
Type III: controversial
Fracture dislocations of ACJ
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Operative Vs Non-operative
Studies
Non-operative Treatment
•
•
•
•
Glick: 35 Type III. None disabled
Dias et al: 52 of 53: Good results
Sleeswijk et al: 90 to 100% satisfactory
Schwartz and Leixnering: 90 to 100%
satisfactory
• Indrekvam et al: less pain, greater function when
operated
• Park et al: higher rating when operated
• Larsen et al: high complication rate in operated
• Taft et al: slightly better results in operated
• Bakalim and Wilppula: surgical reconstruction
superior
• Hawkins et al: equal results
Previously Described Surgical
Approaches
• Since Baum 1886 > 60 procedures
described
• Transarticular Acromioclavicular Repairs
– K-wires, screws, plates
• Coracoclavicular Repairs
– Screws, wires, sutures, tapes, allografts
• Dynamic
– Biceps
3.24
Surgical Morbidity
• Transarticular repairs
– ACJ arthritis
– Pin breakage – migration
• Coraco-clavicular Repairs
–
–
–
–
Hardware or tape failure
Deltoid defects
Coracoid dissection
Failure > clavicular ascent
• Trade bump for a scar
Ideal ACJ Procedure
• Anatomic
– Replicate CHL not CAL(Weaver-Dunn)
Restore the Anatomy
• Conoid and trapezoid ligaments
• Base of the coracoid
• No hardware
– Small targets(coracoid), big errors(plexus)
• Minimal morbidity
– No deltoid detachment
– No coracoid dissection
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• Biologic fixation
Solid Fixation
• #5 FiberWire (Arthrex)
– Doubled (210 lbs)
• Biologic fixation
Arthroscopic Clavicular
Stabilization (ACS)
• Arthroscopic visualization of the base of the
coracoid
• Arthroscopic or open distal claviculectomy
• Intra-articular drill guide (Arthrex)
– Guide pin and cannulated drill through clavicle
and coracoid
• FiberWire retrieved arthroscopically
Minimal Morbidity
• Arthroscopic
• Minimal incisions
• Minimal dissection
ACS – Coracoid Visualization
• Permits drilling through base
– Variable anterior capsular anatomy
• Foramen of Weitbrecht
• Foramen of Rouviere
– Posterior, anterior superior, and anterior inferior portals
• Subscapularis bursa
– Between SS and coracoid
– Radiofrenquency wand clears soft tissue from coracoid
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Intra-articular drill guide (ACLArthrex)
Distal Claviculectomy
•
•
•
•
Eliminates risk of ACJ arthritis
Facilitates clavicle reduction
Sub-clavicular freshening
Prevents posterior impingement
•
•
•
•
•
ACJ marking hook
Tibial drill guide
2.4 mm guide pin
5mm cannuated reamer
Nitenol suture/graft passer
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Fixation
• Fiberwire #5:
– 105 lbs per strand
• Semitendinosis or Tibialis Anterior
– Looped and tied
References:
1.
Rockwood Jr., C.A.; Williams, Jr., G.R.;
Young, D.C.: Disorders of the Acromioclavicular
Joint. In Rockwood Jr., C.A. and Matsen III, F.A.
(eds.): The Shoulder. 2nd Edition. W.B. Saunders
Company. Philadelphia, PA. p. 483-553, 1998.
2. Bosworth, B.M.: Acromioclavicular separation:
A new method of repair. Surg. Gyenecol. Obstet.,
73:866- 871, 1941.
3. Kennedy, J.C.; Cameron, H.: Complete
dislocation of the acromioclavicular joint. J Bone
Joint Surg., 36(B): 202-208, 1954.
4. Kennedy, J.C.: Complete dislocation of the
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Post-operative Care
• Rotational exercises (ER and IR)
• Sling for 6 weeks
• Active ROM after 6 weeks
ICL #6
SPORTS SPECIFIC OUTCOMES IN ACL SURGERY
Wednesday, March 12, 2003 • Aotea Centre, ASB Theatre
Chairman: Jose F. Huylebroek, MD, Belgium
Faculty: Suzanne Werner, Sweden, Stephen Howell, MD, USA, Lars Engebretsen, MD, PhD, Norway and Jean-Claude
Imbert, MD, France
Lars Engebretsen, Department of Orthopaedic Surgery, Ullevål University Hospital
I see sports depended gender difference (team handball 80% females) but also sports specific injury patterns (downhill versus soccer knee injuries MRI pattern)
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Professional experience with athletes: 20 years + experience with professional athletes in all Norwegian
Sports. National Football team doctor. Currently chief of medical coverage for Olympic Athletes. Previously
team doctor for University of Minnesota hockey.
Our clinic does approximately 250 ACLs per year, 50% from team handball, 20% from skiing, 20% soccer,
10% different other sports.
We use hamstrings in patients with a history of previous patellar pain as well as in adolescents, and BPTB
in high loading sports.
We do not use braces on a regular base, but do use it in patients with recurvatum knees to prevent ligament stretching during the early healing phase.
We allow full weightbearing as tolerated and full ROM early. Usually jogging at 8 weeks and return to practice at 4-6 months. No twisting sport participation until 6 months.
Criteria for allowing running: close to normal ROM, at least 70% strength compared to normal side, walk on
threadmill without a limp.
Criteria for allowing jumping: full participation in proprioception rehab protocol, good hip and knee stability control.
Criteria for allowing training participation: full ROM, 70% strength, no episodes of instability, normal running and faking patterns
Criteria for allowing full competition: full ROM, 80% strength, no instability episodes during training, full
running and cutting abilities. (Fitzgerald criteria)
Value of isokinetic testing: doubtful since it has little to do with real sports participation
Value of prevention: I believe ACL injuries can be prevented and we have done exstensive research in this
field see www.ostrc.no
Sport-Specific Factors in ACL Surgery and Rehabilitation
Stephen M Howell, MD
Sacramento, CA USA
Evolution of ACL Reconstruction and Aggressive Rehabilitation
My experience in ACL reconstruction began 17 years ago in August 1986. For six months I performed
extraarticular reconstruction and because of stiffness and poor stability I then switched to an intraarticular
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autogenous DLSTG (double-looped semitendinosus and gracilis graft) combined with an extraarticular tenodesis and a long –leg brace for 4-6 weeks, and sports brace until mid 1987.
Many of these earlier DLSTG grafts failed due to unrecognized roof impingement 4. I erroneously
thought that the hamstring graft was inferior so I switched to autogenous patellar tendon with an extraarticular tenodesis and a long –leg brace for 4-6 weeks, and sports brace until mid 1988. The morbidity of the
patellar tendon graft was high with stiffness, loss of quadriceps strength, and poor stability due to roof
impingement 6.
I learned from 1986 to 1988 that a poor result can be obtained with both a DLSTG and BTB graft when
the surgery is poorly performed (i.e. roof impingement), and that an extraarticular reconstruction does not
protect an impinged graft. Therefore, the return of motion and maintenance of stability was not a rehabilitation issue but a surgical technique issue. In other words the best rehabilitation did not correct poor surgical technique.
In 1989 I switched back to the DLSTG graft after recognizing that roof impingement was the cause of the
earlier failures as it had been for the BTB graft 5. I thought that the DLSTG graft deserved another evaluation, but this time I placed the tibial tunnel without roof impingement, and eliminated the extraarticular
reconstruction. These patients had better extension and stability than the patients with the previous surgical technique so I thought we were on the right track 11.
In 1990 I was strongly influenced by Dr. Don Shelbourne’s pioneering work in aggressive rehabilitation.
We evaluated open-chain exercises and concluded they did not harm the ACL graft any more than a manual Lachman test 3, which was consistent with Dr. Shelbourne’s teachings.
We published our results of aggressive rehabilitation in patients with a DLSTG graft, without a brace,
without an extraarticular reconstruction, and a return to sport at four months using a two-incision technique. These knees showed no change in stability or motion between 4 months and two years confirming
that the early return to sport with a DSLG graft was safe 10.
In 1993 we continued with the DLSTG graft but switched to a transtibial technique to eliminate the
morbidity from the lateral femoral incision. We confirmed that this newer technique also worked well with
aggressive rehabilitation 7. Even though we eliminated roof impingement and used more secure fixation on
the femur (Bone Mulch Screw) 18 and tibia (WasherLoc) 13, we observed that some patients either lost 510 degrees of flexion or had an increase in laxity 8,12. The cause of the loss of flexion and increase in laxity
was impingement of the ACL graft against the PCL from a vertical tibial and femoral tunnel 16. We now
center the tibial tunnel between the medial and lateral tibial spines and angle the tibial tunnel at 65
degrees from the medial joint line of the tibia, which avoids PCL impingement 16.
The biology of the DLSTG graft, tendon-tunnel healing, and limiting tunnel expansion has been a
research focus since 1995. Studies suggest the DLSTG graft survives intraarticular transplantation 1, and
that the graft relies on synovial diffusion since it does not acquire a blood supply in the first two years of
implantation 9. Therefore, the DLSTG graft may not die or lose strength after implantation, which is consistent with the clinical observations that patients can safely return to unrestricted sports at 3-4 months
7,8,10.
A tendon heals slower to a tunnel than a bone plug during the first six weeks of implantation, which
means that the fixation of a DLSTG graft must be BETTER than BTB 19. Because of this finding there is an
interest in techniques that improve tendon-tunnel healing in order to increase the safety of aggressive
rehabilitation 14,15.
The strength of tendon-tunnel healing is better in long and snug tunnels 2, which indicates that placing
the fixation devices not inside the tunnel (i.e. interference screw) but away from the joint line and compacting bone into the tunnels may promote tendon-tunnel healing 17. Our current practice is to place the
fixation devices 25 mm away from the joint line and insert bone reamings into the femoral tunnel and a
bone cylinder harvested from the tibial tunnel along side the DLSTG graft in the tibial tunnel to fill voids,
increase stiffness, promote biologic fixation at the joint line, and prevent tunnel widening 18.
Male and female athletes with ACL injuries in the NBA (ex. Spurs, Nuggets), NFL (ex. Panthers), and
NHL (ex. Red Wings) and Division 1 college level (ex. Ohio State, Notre Dame, Georgetown, Penn State,
Nebraska) are currently being treated using these surgical and rehabilitation principles, which include:
• Tibial tunnel placement that prevents roof impingement
• Tibial tunnel placement that prevents PCL impingement
• High strength and stiff DLSTG graft
• No extraarticular reconstruction
• Points of fixation 25 mm from joint line
• Bone grafting of femoral and tibial tunnel
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The full rehabilitation program can be downloaded in English or Spanish from
http://www.drstevehowell.com/forms.cfm
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• No brace
• Return to sport at 4 months
Rehabilitation Program
I prefer my patients to self-administer their rehabilitation. I encourage them to get off the crutches as
tolerated, and to walk independently by 2 weeks. At two weeks they are encouraged to go to a health club
and use any machine that they feel comfortable on. I suggest they combine low weight and low resistance
with high repetitions (3 sets of 25). They can begin running at 8 weeks and return to sport between 3 and 4
months.
The criterion for return to sport is:
• Full extension
• Full flexion
• No effusion
• Stable Lachman
• KT-1000 MMT within 3-4 mm of the opposite knee
• Ability to hop 85% of the distance of the normal knee with the reconstructed knee
References
1. Goradia, V. K.; Rochat, M. C.; Kida, M.; and Grana, W. A.: Natural history of a hamstring tendon autograft
used for anterior cruciate ligament reconstruction in a sheep model. Am J Sports Med, 28(1): 40-6, 2000.
2. Greis, P. E.; Burks, R. T.; Bachus, K.; and Luker, M. G.: The influence of tendon length and fit on the
strength of a tendon-bone tunnel complex. A biomechanical and histologic study in the dog. Am J
Sports Med, 29(4): 493-7, 2001.
3. Howell, S. M.: Anterior tibial translation during a maximum quadriceps contraction: is it clinically significant? Am J Sports Med, 18(6): 573-8, 1990.
4. Howell, S. M.; Clark, J. A.; and Blasier, R. D.: Serial magnetic resonance imaging of hamstring anterior
cruciate ligament autografts during the first year of implantation. A preliminary study. Am J Sports Med,
19(1): 42-7, 1991.
5. Howell, S. M.; Clark, J. A.; and Farley, T. E.: A rationale for predicting anterior cruciate graft impingement
by the intercondylar roof. A magnetic resonance imaging study. Am J Sports Med, 19(3): 276-82, 1991.
6. Howell, S. M.; Clark, J. A.; and Farley, T. E.: Serial magnetic resonance study assessing the effects of
impingement on the MR image of the patellar tendon graft. Arthroscopy, 8(3): 350-8, 1992.
7. Howell, S. M., and Deutsch, M. L.: Comparison of endoscopic and two-incision technique for reconstructing a torn anterior cruciate ligament using hamstring tendons. Journal of Arthroscopy, 15(6): 594606, 1999.
8. Howell, S. M.; Gittins, M. E.; Gottlieb, J. E.; Traina, S. M.; and Zoellner, T. M.: The relationship between
the angle of the tibial tunnel in the coronal plane and loss of flexion and anterior laxity after anterior
cruciate ligament reconstruction. Am J Sports Med, 29(5): 567-74., 2001.
9. Howell, S. M.; Knox, K. E.; Farley, T. E.; and Taylor, M. A.: Revascularization of a human anterior cruciate
ligament graft during the first two years of implantation. Am J Sports Med, 23(1): 42-9, 1995.
10. Howell, S. M., and Taylor, M. A.: Brace-free rehabilitation, with early return to activity, for knees reconstructed with a double-looped semitendinosus and gracilis graft. J Bone Joint Surg Am, 78(6): 814-25, 1996.
11. Howell, S. M., and Taylor, M. A.: Failure of reconstruction of the anterior cruciate ligament due to
impingement by the intercondylar roof. J Bone Joint Surg Am, 75(7): 1044-55, 1993.
12. Howell, S. M.; Wallace, M. P.; Hull, M. L.; and Deutsch, M. L.: Evaluation of the single-incision arthroscopic technique for anterior cruciate ligament replacement. A study of tibial tunnel placement, intraoperative graft tension, and stability. Am J Sports Med, 27(3): 284-93, 1999.
13. Magen, H. E.; Howell, S. M.; and Hull, M. L.: Structural properties of six tibial fixation methods for anterior cruciate ligament soft tissue grafts. Am J Sports Med, 27(1): 35-43, 1999.
14. Rodeo, S. A.; Arnoczky, S. P.; Torzilli, P. A.; Hidaka, C.; and Warren, R. F.: Tendon-healing in a bone tunnel. A biomechanical and histological study in the dog. J Bone Joint Surg Am, 75(12): 1795-803, 1993.
15. Rodeo, S. A.; Suzuki, K.; Deng, X. H.; Wozney, J.; and Warren, R. F.: Use of recombinant human bone morphogenetic protein-2 to enhance tendon healing in a bone tunnel. Am J Sports Med, 27(4): 476-88, 1999.
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16. Simmons, R.; Howell, S. M.; and Hull, M. L.: Effect of the angle of the femoral and tibial tunnel in the
coronal plane and incremental excision of the posterior cruciate ligament on anterior cruciate ligament
graft tension: An in vitro study. Journal of Bone and Joint Surgery, In Press.
17. Singhatat, W.; Lawhorn, K. W.; Howell, S. M.; and Hull, M. L.: How four weeks of implantation affect the
strength and stiffness of a tendon graft in a bone tunnel: a study of two fixation devices in an extraarticular model in ovine. Am J Sports Med, 30(4): 506-13, 2002.
18. To, J. T.; Howell, S. M.; and Hull, M. L.: Contributions of femoral fixation methods to the stiffness of
anterior cruciate ligament replacements at implantation. Arthroscopy, 15(4): 379-87, 1999.
19. Tomita, F.; Yasuda, K.; Mikami, S.; Sakai, T.; Yamazaki, S.; and Tohyama, H.: Comparisons of
intraosseous graft healing between the doubled flexor tendon graft and the bone-patellar tendon-bone
graft in anterior cruciate ligament reconstruction. Arthroscopy, 17(5): 461-76, 2001.
Jean-Claude Imbert
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1. What is your professionel experience with athletes, can you give us an idea (%) what athletes (sort of
sport) you're usually dealing with. What is their level: pro? College etc.
Level of sport :
Foot professional : 20 % (DI – DII – DIII)
Amateurs : 70 %
College : 10 %
2. For how long have you been in practice ?
30 years
3. Do you see some differences in pathomechanics per sport? male or female?
INTERNAL ROTATION
NON CONTACT
CONTACT INJURIES
VALGUS EXTERNAL ROTATION
SKI
10 %
50 %
50 %
FOOTBALL
70 %
80 %
20 %
OTHERS
20 %
4. Of all the ACL reconstructions you are doing per year, what is the (approx.) percentage of what type of
athletes.
Same percentage than for the consultants
5. Do you change your technique, relating to the type of sport your pt is competing in? What do you use as
a graft? per sport? gender? PEARLS?
HTG for all patients (sport-gender…) Unless in case of specific contre indication or resurgery or hyperlaxity)
6. Some type of athletes receive a brace? which type: sleeve, derotation-brace?
I’m never bracing
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7. REHAB: all the same? when do you allow what? what are your criteria for allowing your athlete to run, to
jump, to participate in training for contact sports, and to participate full competition?
Home exercising for the first three months, then balanced on light sports progressive recovering under the
medical control (sport medecine practicien). After 6 months patient is allowed to come again for jumping,
contacts, and full competition)
8. What do you think of the value of isocinetic testing at certain times during the postop period? MRI?
Isocinetic testing should be usual after 6 months to estimate the fonctional value of quad ad harmstring
groups, and further if necessary
MRI: no MRI except in case of unusual complication, butCT scan with three dimensional reconstruction
after 2 years.
Prevention should be applied not only to the highest level, but also in small teams.
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9. Any remarks on prevention, related to the sports you are usually dealing with? role of the referees?
changes in rules?
10. Please work out the topics you are « best » in, or where you have done some research or publications:
Topics: ACL reconstruction in female athletes.
Prospective randomized comparative studies.
1) comparing PT and HTG
2) comparing HTG with 2 different femoral suspension system
3) comparing HTG with or without interference screw in the femoral tunnel
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ICL #7
EMERGING TECHNOLOGIES IN KNEE SURGERY
Wednesday, March 12, 2003 • Carlton Hotel, Carlton I
Chairman: Masahiro Kurosaka, MD, Japan
Faculty: Chyun-Yu Yang, MD, Taiwan, Hans-Ulrich Staeubli, MD, Switzerland , Mitsuo Ochi, MD, PhD, Japan, and
Freddie Fu, MD, USA
1. Introduction
Masahiro Kurosaka (2 minutes)
2. Computer Assisted Orthopaedic Surgery; TKA
Chyun-Yu Yang (20 min)
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3. Computer Assisted Orthopaedic Surgery; Ligament reconstruction
Hans-Ulrich Staeubli (20 min)
4. Gene Therapy in Knee Surgery
(20 min)
5. Articular Cartilage Regeneration with Tissue Engineering Technique
Mitsuo Ochi (20 min)
6. Questions and Answers
All (8 min)
Computer assisted surgery and biological technologies such as gene therapy and tissue engineering technique are the forefront of emergent technologies in knee surgery. In this instructional course, experts of
each technique and research will introduce and discuss updated advancement of these challenging knee
surgeries.
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ICL #8
ARTHROSCOPIC EVALUATION AND TREATMENT OF ROTATOR CUFF INJURIES
Wednesday, March 12, 2003 • Aotea Centre, Kupe/Hauraki Room
Chairman: Stephen J. Snyder, MD, USA
Faculty: Stephen Burkhart, MD, USA, James Esch, MD, USA and Alessandro Castagna, MD, Italy
1. Snyder- Introduction of speakers and topics
2
Castagna- Arthroscopic evaluation and treatment of partial rotator cuff tears (PASTA lesions, Bursal tears)
4. Snyder- My technique for Full-thickness Cuff Repair
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3. Esch- Arthroscopic treatment of Full thickness Rotator Cuff tears, (including side-to-side lesions,
retracted tears).
5. Burkhart- Arthroscopic treatment of the Subscapularis tendon.
6. Esch- My technique or Subscapularis Repair using two anterior portals
7. Snyder- Learning Shoulder Arthroscopy (ALEX model, CLASroom etc.).
Arthroscopic evaluation and treatment of partial rotator cuff tears (PASTA lesions, Bursal tears)
A. Castagna
Istituto Clinico HUMANITAS
Milan, Italy
Introduction
The understanding and treatment of the pathology of the rotator cuff muscle-tendon complex is probably
still the most stimulating challenge for the shoulder surgeon. Anatomy, biomechanics, presence of multiple
layers of tissues, limited subacromial space make often difficult a precise assessment of the cuff disorders
and therefore a proper repair. History, clinical examination and imaging will help the surgeon for an exact
diagnosis. Imaging of the rotator cuff tears improved a lot in the last years. MRI, especially with gadolinium
enhancement, allows a rather precise pre-op assessment. But other basic tests like X-Rays (AP, Axillary
and Arch-View) should never skipped.
Finally the radiologist report should be always compared by the surgeon with the history and clinical exam.
This procedure allows to avoid over- or under- diagnosis of rotator cuff disorders. Arthroscopy demonstrated a great role in the assessment of rotator cuff disorders and the operative decision-making.
General Technique of arthroscopic RC assessment
Anatomically four tendons belonging to muscles originating from the scapula form the RC.
Viewing from anterior to posterior they are:
- Subscapularis
- Supraspinatus
- Intrarticular long head of the biceps
- Infraspinatus
- Teres minor
Many authors consider the intra-articular part of the long head of the biceps functionally a part of the RC.
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The arthroscopic evaluation of RC must be done both from the articular side and the bursal side of the tendons, viewing through the standard posterior and anterior portals. It may help also the use of the lateral
portal. The assessment procedure should be performed following a systematic and complete protocol of
review of the shoulder anatomy (1). Use of a pump for distension and a controlled hypotension are very
helpful (almost necessary) for a better view in the subacromial space.
Intra-articular rotator cuff evaluation
Posterior portal view (moving the scope from anterior to posterior):
- superior margin of the subscapularis lying anterior between the glenoid and the humeral head
- supraspinatus lying over the bicep tendon
- intraartcular part of the long head of the biceps and its anchor on the glenoid
- anterior aspect of the infraspinatus at his insertion near the bare area of the humeral head
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Anterior portal view (moving the scope from posterior to anterior):
- infraspinatus and teres minor tendons
- supraspinatus tendon
- long head of the biceps
- subscapularis tendon up to its insertion on the lesser tuberosity (sliding up to this point is very critical since the scope can easily be pulled out of the joint. This manoeuvre must be performed smoothly
but is very important to check the subscapularis tendon insertion to the humeral head and have a look
of its relationship with the biceps entering into the groove)
Bursal side rotator cuff evaluation
Bursal tissue covering the cuff tendon may confuse the view. For this reason bursectomy and removal of
frayed tissues is requested to clear the view when a rotator cuff lesion must be clearly identified.
The subacromial space assessment must be performed viewing from anterior, posterior and lateral portals.
Posterior portal view (moving the scope from anterior to posterior and then lateral to medial):
(Note: the scope must be introduced forward since the bursa is an anterior structure and the posterior
bursa may hide the view)
- infraspinatus tendon
- subdeltoid shelf
- greater tuberosity
- musculo-tendinous junction of the cuff
Anterior portal view (moving the scope from posterior to anterior and then from lateral to medial):
- posterior bursa ( it is very important to remove it for a clear view in case of a repair)
- subdeltoid shelf
Lateral portal view (moving the scope from anterior to posterior) :
- subdeltoid shelf
Classifications of RC tears
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Lesions of the rotator cuff may present with different aspects, grades, morphology and severity. A lot of
attempts were made to classify omogenously the rotator cuff tears but so far no one seems to be perfect
(2). When looking at the cuff tendons it is important to understand:
- full thickness or partial thickness
- size of tear
- number of tendons involved
- side (articular and/or bursal) and depth of partial thickness
- retraction of the tendons
- quality of the tendon
- shape of the full thickness tear
CLASSIFICATION OF ROTATOR CUFF TEARS
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The use of a common standard evaluation system is important for exchanging information with other surgeons, follow-up and proper decision-making. For the experienced arthroscopist it is possible to perform a
precise evaluation of the rotator cuff tears. A good system of classification is the one proposed by Snyder
that allows a systematic classification of the intraoperative findings (1) (Tab 1). Unfortunately the intratendinous lesions are not visible for the arthroscopist and they represent an important topic for the treatment of the rotator cuff decease as Fukuda demonstrated (3).
Tendon (s) involved in tear
SS > Supraspinatus tendon
IS > Infraspinatus tendon
SbS > Subscapularis tendon
RI > Rotator interval
Location of tear
A > Articular surface
B > Bursal surface
C > Complete tear, connecting A to B
Severity of tear
0 >
Normal cuff, with smooth coverings of symposium and bursa
I >
Minimal superficial bursal or synovial irritation or slight capsular fraying in a small localized area;
usually < 1cm
II >
Actual fraying or failure of some rotator cuff fibers in addition to synovial, bursal or capsular injury;
usually < 2 cm
III >
More severe rotator cuff injury, including fraying and fragmentation of tendon fibers, often involving
the whole surface of a cuff tendon (most often the supraspinatus); usually < 3 cm
IV >
Very severe partial rotator cuff tear that usually contains, in addition to fraying and fragmentation of
tendon tissue, a sizable flap tear; usually larger in size than grade I-III and often encompass more
than a single tendon
Tab. I Classification of RCT as proposed by Snyder. It makes possible a standard evaluation for the arthroscopist
Partial thickness RC tears
Partial thickness RC tears may involve the articular side and the bursal side. Also intratendinous lesions
may affect the cuff tendons but they are hard to be detected and treated, so far. Most of the partial tears of
the bursal side are related to impingement with the anterior acromion. The clinical diagnosis is generally
supported by the presence of a hooked acromion observing an outlet-view x-ray. Arthroscopically the cuff
appears frayed like the under surface of the coraco-acromial ligament and the anterior acromion. Bursal
inflammatory tissue is frequently observed. Some bursal side partial tears may appear like a flap floating in
the subacromial space. The tendon avulsion from the tuberosity in these cases is frequently a consequence
of a trauma. Preoperative diagnosis is confusing but it can be oriented by an adequate MRI study.
Intrarticular view of the cuff doesn’t show any pathology and the final confirmation is arthroscopic.
Intrarticular partial tears can be graded for severity of the lesion. Some present minimal fraying, some are
deeper erosions, some may involve a relevant amount of the tendon (Tab. I). Snyder described the latter
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case with the acronym P.A.S.T.A. (Partial Articular Supraspinatus Tear Avulsion) lesion. In any case it is
important to observe the cuff from different portals to evaluate and understand the shape and severity of
the tear. After the tear has been assessed and understood, treatment choices are different and related to
their severity. In the bursal side the primary treatment option is to debride the cuff and to perform an
acromioplasty for minimal fraying of the tendon (grade AI and AII). If a significant partial bursal tear is
observed with free-edge tendon avulsed from the tuberosity, a tendon-to-bone repair with suture anchor is
recommended in association with an acromioplasty. In the articular aspect of the cuff, debridement of minimal partial tear is the adequate treatment. If after debriding the amount of left good tendon is significantly
reduced an evaluation of the other side is necessary using the marker suture technique. If the bursal side
tendon is frayed a full thickness tear should be induced and then a RC repair performed. If the bursal side
tendon is healthy and strong the PASTA repair technique is an adequate treatment option.
Arthroscopic subacromial decompression
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Arthroscopic subacromial decompression (SAD) is probably the first surgical procedure that contributed to
make shoulder arthroscopy a popular and accepted procedure. In spite of this it may be not easy and quick
if the surgeon doesn’t follow a logical and well know protocol. It starts with the preoperative planning with
X-ray assessment of the acromion shape and thickness in order to be aware of the amount of bone to
resect without under- or over treat the pathology. Intraoperative steps should always include a careful
debridement of the subacromial space, cleaning of inflamed bursal tissue and removal of the fibrous tissue
on the undersurface of the anterior acromion. These procedures usually induce local bleeding so it is
important to obtain controlled low BP, perform accurate haemostasis and take advantage by the use of an
infusion pump and bipolar electrocautery. After all the soft tissues are removed and bleeding is under control the bone resection procedure can be started. Several techniques have been described to perform SAD
and can be easily found in the large amount of literature available about this topic. Our technique requires
to prepare a lateral portal through which a motorized bone resector is introduced to prepare an "L" shaped
through: the short limb of the "L" is represented by the anterior lateral edge of the acromion and the long
limb of the "L" is aligned with the posterior edge of the AC joint. This will help to delineate the anterior
part of the acromion, responsible of the impingement. The scope is then moved laterally and the motor
posterior. The bone through will help the orientation and the lateral view will allow evaluating the amount
of bone resection while moving from posterior to anterior and from medial to lateral. The diameter of the
motor blade (usually 4,5 mm) will be our gauge. Final haemostasis is usually requested after the final
smoothening of the undersurface of the acromion.
Arthroscopic Treatment of PASTA Lesions of the Rotator Cuff
Alex Castagna / Stephen J. Snyder, MD
PASTA lesion is an acronym for a Partial Articular Supraspinatus Tendon Avulsion. This is a fairly common
finding in shoulder arthroscopy that requires decision making based on the degree of tendon damage and
the tools and skills of the surgeon. Tendon damage is seldom caused by classic impingement but more
often by, a traction-type trauma that pulls a portion of the "footprint" attachment of the rotator cuff away
from the humeral head. The bursal side of the tendon is usually normal. The evaluation and treatment of
PASTA lesions is best suited to advanced arthroscopic techniques.
1. History
a) Patients are generally healthy and athletic.
b) Injury is caused by either an acute event such as a fall or chronic irritation such as prolonged throwing.
c) Symptoms include pain with activities – generally minimal pain at rest or at night.
2. Physical Exam
a) Tender cuff insertion
b) Full range of motion
c) Positive cuff stress signs
d) +/- Weakness with cuff strength testing
e) Impingement test unreliable
3. Imaging
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Figure 1
Figure 2
Figure 3
Figure 4
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a) X-rays are usually normal.
b) MRI (with gadolinium) shows a defect on the articular side of the cuff attachment. The muscles
show minimal atrophy. The bursal side of the tendon is normal.
4. Treatment – Decision Making
a) Diagnostic arthroscopy & bursoscopy always insert suture marker for correlation of articular and bursal sides.
b) Debride frayed tissues especially on the articular side of the footprint of the cuff.
c) Palpate cuff to assess thickness and integrity of remaining tissue. Correlate with MRI. If > 30% cuff
tendon remains, consider transtendon repair, if < 30% good cuff remains, complete the tear and perform a standard tendon to bone repair.
5. Treatment—Transtendon (PASTA) Repair
a) Position the arm in 60 to 70 degrees of abduction.
b) Start with the scope posterior & a Crystal® cannula anterior.
c) Insert a spinal needle as a guide near the lateral acromial edge to determine the proper insertion
point and angle for the anchors. (Fig 1)
d) Drill a pilot hole with a 5/64 inch smooth pin into the prepared bone adjacent to the cartilage.
e) Insert a Revo® 4-mm anchor loaded with one or two sutures into the pilot hole. Use single sutures if
you are not familiar and proficient with the steps of multiple suture management. (Fig 2)
f) Remove one strand of suture out the Crystal® cannula using a crochet hook. (Fig3)
g) Insert a spinal needle through a healthy portion of the cuff medial to the torn surface, pass a Shuttle
Relay® into the joint and retrieve it out the Crystal® cannula with a grasping clamp. (Fig 4)
h) Load the suture located in the Crystal® cannula into the eyelet of the Shuttle® and carry it back
through the tendon. (Fig 5)
i) If a mattress stitch is desired, insert the needle through the cuff the first time 6-mm anterior to the
anchor and a second time 6-mm posterior to the anchor and carry both limbs of the single suture back
through. This will create a 1.2-cm mattress bridge on the bursal side of the cuff.
j) If double sutures are used in the Revo® anchor, repeat the steps for the second suture of the first
anchor passing the needle 1cm posterior to the first suture. Insert all additional anchors and sutures as
needed to complete the PASTA cuff repair. Change the scope to the anterior portal and the Crystal®
cannula posterior to insert the posterior anchors and sutures.
k) Move the arm to the 30 degree abduction position and tie the sutures using sliding-locking knots
progressing from anterior to posterior. (fig 6)
l) Figure 7 is the final bursal side view after the PASTA repair has been completed using one double
suture, one single mattress and one single simple suture.
6. Postop Care
a) Protect the extremity in an Ultra Sling® for four weeks. Encourage elbow, wrist and hand exercises
from the first postop day.
b) Allow pendulum motions and passive elevation to 90 degrees after one week.
c) Begin gentle active elevation at 5 weeks and progress as tolerated to full activities by 4 months.
Figure 5
Figure 7
Figure 6
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Making Arthroscopic Rotator Cuff Repairs Easier • My Experience and Technical Pearls
James C. Esch, M.D.
Tri-City Orthopaedics
Oceanside, CA
[email protected]
www.shoulder.com
Surgeon
Must balance skill versus ego
Practice on a model
Know tools
Know suture management
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OR team
Taught by the surgeon
Know location of your favorite tools and anchors
Can load suture, find correct tool
Knows location of Plan B and Plan C tools
Tie sliding and _ hitch knots
Bleeding control awareness
Inflow pressure and bag awareness
Outflow control
Pump nuisances
Anesthesia BP awareness
Is patient taking a NSAID ?
Plan for today’s patient with a cuff tear
Size of tear
Pain versus weakness
Risk of massive and superior migration
What is your "mini-open" threshold? And experience?
Tear Fix Size
MRI
Supraspinatus
Infraspinatus
Subscapularis
Biceps
Draw the size and shape on paper
Draw Tear
Tear Estimate
Size
Shape
Does it look repairable? (Full? Partial?)
Repair Technique
Margin convergence
Fixation Estimate
Anchors
Suture technique
See the technique steps in your head
See the anchor, suture through tendon, suture management, and tie knot.
You may need to move the scope and suture for these steps.
Exposure
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Portals and Cannulas
Bursectomy to see
Subacromial smoothening (decompression)
Intra-operative Evaluation
Probe tear after bursectomy and cleaning bony bed
Is your Plan now the same as preoperative plan?
Start to run the play. (You are running an option formation.)
Anchor first
Use 18G needle to get the angle
I prefer anchors down a cannula
Consider double row @ tear mobility
Put in all at once if able
Know suture management
Tag ends of each suture
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Margin convergence
Handoff Techniques
A: Direct Permanent Suture
1. Cuff sew #2 Ethibond to ArthoPierce
2. Other permanent handoff devices
B: Shuttle with Crescent hooks to Blitz/Lasso
Tie a good knot
Suture through tendon
Direct trans-tendon grab of suture
ArthroPierce and other penetrating tools
From posterior for Infraspinatus
From anterior for some supraspinatus
From superior behind AC joint for U shaped SS tears
Pass suture through tendon (if angle is good)
Direct with Cuff Sew, Penetrators, Arthrosew
Shuttle suture
Use Caspari punch, crescent hooks, etc
Postoperative care
Immobilize long enough to heal
Some passive motion is good
Rehabilitation phases
Immobilization
Early active motion
Late strengthening
Conclusions:
This is hard
This requires thinking out the steps
This is frustrating
This is rewarding
This balances your skill versus your ego
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1. Three Portals, scope posterior
4. The scope is now in the lateral
portal providing the “50-yard line”
view. Note the anchor insertion portal
adjacent to the acromion.
2. Inside view. Scope and tools are
moved as needed to repair the cuff
tear.
5. Margin convergence with a single
pass cuff sew tool.
6. Retrieve the suture.
3. Estimate the steps necessary for
repair.
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10. Retrieving the suture off of the
anchor with the ArthroPierce.
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7. Tie the knot
11. Final repair with two margin
convergence sutures and two anchors.
8. A sliding knot.
9. A suture “handoff” from the
ArthroPierce to the straight Cuff Sew.
Illustration from Esch: Arthroscopic
Rotator Cuff Repair for Smith+Nephew
Endosocpy.
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Technique of Arthroscopic Rotator Cuff Repair
Stephen J. Snyder, MD
SCOI - Van Nuys, California
Introduction
The field of shoulder arthroscopy has progressed to the point where routine arthroscopic rotator cuff repair
is now possible in many situations. The tools now available, including 5 mm SuperRevo anchors, excellent
quality arthroscopic cannulas and pumps, coupled with the new surgical techniques for passing sutures
and tying knots, have all made this advancement possible. The surgeon must develop the necessary skills
and be supported by a well-trained team, including a skilled arthroscopic assistant, an anesthesiologist
who is comfortable with hypotensive blood pressure regulation, and an operating room technician who
understands and can prepare and assist with the instruments as needed. The recent availability of "Alex",
the shoulder arthroscopic surgery simulator from Sawbones, Inc., has also accelerated the learning curve
for those surgeons who avail themselves of it.
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The outline that follows will highlight the important steps in the repair as it is done at this time at SCOI:
Figure 1:
The rotator cuff tear is carefully evaluated
with an arthroscope on both the articular and
bursal sides, and the frayed edges of the cuff
are debrided. The best view of the rotator
cuff is usually "the 50 yard line" view with
the arthroscope in a lateral subacromial
portal which is located at the center point
of the rotator cuff tear.
Figure 2:
A Spectrum‚ Crescent Suture Hook with a
Shuttle Relay‚ suture passer is
used to perform a side-to-side repair of
longitudinal tears in the rotator cuff tendon.
Figure 3:
After passing the curved suture hook
across the tear, a strong, long lasting
suture is carried with the Shuttle Relay®
back across the tear and the suture
limbs tied together.
Figure 4:
The bone is lightly decorticated at the
anatomical neck of the humerus, adjacent
to the articular cartilage, using a high speed
burr and/or shaver. The rotator cuff is
mobilized to minimize tension on the
repair.
A small puncture wound is created adjacent
to the lateral border of the acromion. The
5 mm Super Revo anchor, preloaded with two
strands of #2 braided polyester suture, is
inserted directly through the percutaneous
puncture wound (no cannula is needed to
insert the anchor). The posterior anchor is
usually inserted first. The anchor is directed
to enter the bone in a medial direction below
the subchondral bone at approximately a 45o angle.
Figure 6:
The Super Revo anchor is inserted into the
bone until the seating ring on the driver is just
below the surface. The vertical orientation
mark (solid or dashed line which indicates the
direction the anchor eyelet is facing) is
aligned toward the cuff edge. This ensures
that the suture passes in a direct line from the
eyelet to the cuff without forming a twist.
Figure 7:
The anchor security is tested by
pulling on the suture strands.
Figure 8:
The arthroscope can be positioned in the
anterior or posterior portal but most often
the overall visualization is best from the
lateral acromial portal.
Figure 9:
A crochet hook or suture retrieval forceps i
inserted through the anterior portal and
retrieves the strand of the green suture that
exits closest to the cuff. The retriever
must pass behind (medial to) the suture limbs.
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Figure 5:
Figure 10: A Spectrum Crescent Suture Hook is
inserted into the posterior cannula and
through the bursal side of the posterior edge
of the torn rotator cuff 5 mm posterior to the
anchor. The Shuttle Relay suture passer is
sent through the hook and retrieved with a
grasping forceps out the anterior cannula.
Care must be taken to insure that the
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grasping forceps follows the same path as the
green suture when retrieving the Shuttle
Relay to avoid causing twists in the strands.
Figure 11: The green suture strand is loaded into
the eyelet of the Shuttle Relay suture
passer outside the anterior cannula.
The suture is then carried through the
cuff from the articular side to the
bursal side by withdrawing the
opposite end of the suture passer out
the posterior cannula.
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Figure 12: A crochet hook is used to retrieve the
other limb of green suture into the posterior
cannula. A switching stick is then inserted
through the posterior cannula and the
cannula is removed from the joint.
Figure 13: The cannula is reinserted over the
switching stick, leaving the sutures outside
the cannula where they will be less likely to
be tangled during stitching with the white
sutures.
Figure 14: A crochet hook or suture retrieval forceps is
used to retrieve the limb of white suture that
exits the anchor eyelet closest to the rotator
cuff. The suture is pulled through the
anterior cannula.
Figure 15: The Spectrum Suture Hook is passed
through the torn rotator cuff from top to
bottom approximately 5 mm anterior to the
anchor site. If a crescent suture hook is used
again, it may be inserted through the
posterior cannula. If a more angled suture
hook is used, the posterior cannula can be
removed and the hook passed directly
through the portal without a cannula. The
Shuttle Relay suture passer is passed
through the hook and retrieved with a
grasping forceps through the anterior cannula.
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Figure 16: The white suture strand is loaded into the
eyelet of the Shuttle Relay suture passer
outside the anterior cannula. The suture is
carried through the cuff from the articular
side to the bursal side by withdrawing the
opposite end of the suture passer out
the posterior portal.
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Figure 14a: Alternative method (Modified Caspari
Suture Punch): A crochet hook is used
to retrieve the limb of white suture that is
closest to the cuff. The suture is pulled out
through the lateral cannula.
Figure 15a: Modified Caspari Suture Punch (cont):
With the scope viewing from the anterior
portal, a modified Caspari Suture Punch can
be inserted through a 6 mm ClearFlex
Cannula in the lateral portal to pass a
Shuttle Relay suture passer from the bottom
to top through the cuff. The suture passer is
carried out the posterior cannula with a
grasping forceps.
Figure 16a: Modified Caspari Suture Punch (cont):
The eyelet of the Shuttle Relay suture passer
is loaded with the suture outside the
lateral cannula and carried through the
cuff from bottom to top by pulling on the
opposite end.
Figure 17: The posterior cannula is reinserted and the
remaining white suture limb is retrieved using
a crochet hook or suture retrieval forceps
Figure 18: The ring handled knot pusher is threaded on
to the green suture exiting the top of the cuff.
It is passed into the joint to ensure there are
no twists or obstructing soft tissue. The
green and white suture limbs associated with
the posterior anchor are first tied using a
knot of choice. The second anchor is placed
in a similar fashion, suture limbs passed,
and tied down.
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Figure 19: The arthroscope may be moved to the
posterior cannula for visualization. The third
(anterior) anchor is placed in the same
fashion and suture limbs passed through
the cuff, usually suturing from the anterior
portal.
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Figure 20: The illustration of the final repair shows
three Super Revo anchors in place. Each
anchor has two fixation points through the
rotator cuff oriented 45o from the anchor.
Notice the final side-to-side repair. At the
completion of the repair, the torn end of the
rotator cuff is tightly opposed to the bone to
promote strong rotator cuff tendon healing.
Arthroscopic Knot Tying Technique - Revo Knot
Figure 1:
Both suture tails are the same length
and the loop-handled knot pusher is
threaded onto the suture which has
been passed through the soft tissue.
This original "post" is positioned on
the left side, shown as the darker tail
for illustration purposes. The knot
pusher is passed down the original
post suture to ensure that there are no
twists or soft tissue obstructions.
Figure 2:
An underhand half-hitch is placed
around the original post and advanced into
position on the edge of the soft tissue.
Figure 3:
Tension is held on the post suture while a second underhand half-hitch is worked down the
post suture to reinforce the first hitch.
Figure 1
Figure 2
Figure 3
Figure 4 Figure 5 Figure 6 Figure 7 Figure 8
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Figure 4:
An overhand half-hitch is next placed on the same initial post and worked down into position on the other two throws.
Figure 5:
The knot pusher and clamp are changed to the opposite suture and after checking for twists
and soft tissue, an underhanded throw is advanced down on to the knot stack.
Figure 6:
The knot pusher is advanced to "past point" to lock the half-hitch securely.
Figure 7:
A fifth overhand half-hitch is placed over the second post and worked down into position on
the knot stack.
Figure 8:
Sometimes a sixth half-hitch can be used as the surgeon prefers, and the suture tails are cut
with microscissors.
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Arthroscopic Knot Tying Technique - SMC Knot
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 1:
Thread the knot pusher on the post strand (held in the left hand) and place a clamp on the
post. Pass the knot pusher into the joint to ensure that there are no twists or obstructing
soft tissue. Arrange the suture so that the original post suture is short, with only 10 cm of
the suture outside of the cannula.
Figure 2:
Pinch the two strands together between the thumb and index finger, crossing the loop
strand over the post.
Figure 3:
Pass the loop suture under and then over both strands.
Figure 4:
Pass the loop strand under the post strand between the two sutures and over the top of the
post strand in a direction away from the pinching fingers. There will be a triangular interval
formed between the two previous looks over the post strand (red arrow).
Figure 5:
Feed the free end of the loop strand from bottom to top through this interval under the
post strand. As the suture is pulled through, a "locking loop" is created (blue arrow).
Figure 6:
Release the thumb and index finger and place the left index finger into the "locking loop"
from bottom to top to keep it open. Remove all slack (dress the knot) from the sutures with
the index finger in place to avoid tightening the "locking loop" prematurely.
Figure 7
Figure 8
Figure 9
Figure 10
Figure 11
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Figure 7:
Pull on the post strand and use the knot pusher to guide the knot down to the tissue. Do
not pull on the loop strand until the knot is seated. Maintain tension on the post strand
and back off the knot pusher to assess the knot.
Figure 8:
Once satisfied that the knot is well seated, tighten the "locking loop" by pulling on the loop
strand while maintaining pressure on the knot with the knot pusher.
Figure 9:
The "locking loop" will slide over the knot pusher and secure the knot. For further security,
an underhand half-hitch is worked down the post suture.
Figure 10: An overhand half-hitch is next placed on the post and worked down into position onto the
knot stack.
Figure 11: Suture tails are cut with microscissors.
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Subscapularis Tears:Arthroscopic
Management/Results
Arthroscopic Evaluation
Normal subscap footprint
Normal subscap/biceps relationship
Intact medial sling for biceps (SGHL, CHL)
The Orthopaedic Institute
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Stephen S. Burkhart, M.D.
San Antonio, Texas
Medial Subluxation of Biceps and
Upper Subscap Tear
Biceps located posterior to upper subscap
Subscap Footprint
2.5 cm superior-to-inferior
Types of Subscap Tears
1.5 cm medial-to-lateral
Widest superiorly
Full-thickness partial tear
(upper subscap)
Partial-thickness tears (PASTA-type)
Complete tears
Retracted adhesed tears
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Arthroscopic Subscapularis Repair
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3.50
Full-Thickness Partial Tear
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Subcoracoid Impingement
Repair of Full-Thickness
Partial Tear
Partial -Thickness Tear
(PASTA Type)
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Repair of Partial-Thickness Tear
(PASTA-Type)
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Complete Tear
Comma Sign
Repair of Complete Tear
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Repair of Retracted
Adhesed Tear
Retracted Tears
Arthroscopic
mobilization is
satisfactory
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Retracted Tears
Slight
medialization of
repair (5 mm)
satisfactory
Dissect Subscap from
Coracoid Arch
Do not go
medial to
coracoid
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Methods
Coracoplasty
Do coracoplasty if repair jeopardized
by coracoid impingement
Must have 7mm clearance between
coracoid and subscap
Retrospective review
24 Consecutive patients
25 Arthroscopic Repairs
Indications :
Clinical evidence of Subscapularis tear
(isolated or associated with larger tear)
Results
Results
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24 Consecutive Patients
25 All Arthroscopic Subscapularis Repair
M:F ratio: 17 : 7
Mean Age: 60.7 yrs ( 41 - 78 )
Preop Symptoms: 18.9 months ( 1-72)
6 Heavy Labor
Average duration of Follow-up : 10.7 months
Follow-up Duration > 3 months : 25 patients
Arthroscopic Findings
Arthroscopic Findings
25 Shoulders
25 Shoulders
Combined
with
Posterior Cuff Tear: 17
Average Size : 5 X 8 cm
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Isolated Subscapularis
Tear : 8
Clinical Outcome UCLA Score
Pre-op Average UCLA Score : 10.7
Post-op Average UCLA Score : 30.5
(p < 0.0001)
Humeral Head
Proximal Migration
Clinical Outcome
Forward Flexion Range
Pre-op Average FF: 96°
Post-op Average FF : 146°
(p < 0.01)
Conclusion
10/25 cases ( 40%)
Before Repair
After Repair
Subscapularis repair can reverse proximal
humeral migration and restore overhead
function
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Conclusion
Clinical Outcome
92% good/excellent
Arthroscopic subscapularis
repair must be tailored to the tear
pattern
results by UCLA criteria
Results of arthroscopic repair are
equal to or better than those of
open repair
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Thank you!
Stephen S. Burkhart, M.D.
San Antonio, Texas
Arthroscopic Repair of Subscapularis Tendon Tears
A Simple Technique
James C. Esch, M.D.
C. Kelly Bynum, M.D.
Tri-City Orthopaedics
Oceanside, CA
[email protected]
www.shoulder.com
The authors present a simplified arthroscopic direct technique for diagnosis and repair of partial subscapularis tendon tears. They used the anterosuperior arthroscopic portal to see the subscapularis tendon insertion while probing and repairing from the adjacent anterior portal. Three anatomical dissections were
done to define the tendon insertion of the subscapularis tendon at the lesser tuberosity of the humerus.
The subscapularis tendon was repaired with one or two suture anchors inserted into the lesser tuberosity
from the anterior portal while viewing from the anterosuperior portal. Suture management was via the
standard posterior shoulder portal. A tendon penetrating-grasping device, from the anterior portal, passed
the sutures through the displaced subscapularis tendon. The arthroscopic knots were tied from anterior
portal.
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Video of Anatomical Dissection
Video of Subscapularis Repair
Subscapularis tears are frequently associated with supraspinatus and infraspinatus tendon tears. The surgeon may not appreciate the significance of the subscapularis tendon tear when viewing from the posterior
arthroscopic portal. Direct anterosuperior viewing and anterior probing enables the surgeon to see and
repair these "hidden" subscapularis partial tendon tears.
Associated with the first ten subscapularis repairs were six complete and four partial thickness supraspinatus-infraspinatus rotator cuff tears. There were no isolated subscapularis tears. Three patients had associated biceps lesions.
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The Center for Learning Arthroscopic Skills (CLASroom)
at the Southern California Orthopedic Institute
The Center for Learning Arthroscopic Skills
(CLASroom)
at the
Southern California Orthopedic Institute
An educational center for orthopedists and other medical professionals
to develop and perfect their skills using technologically advanced
arthroscopy “Dry Cadaver” ALEX models and computer simulators
The CLAS Room is the first center of its kind – a state-of-the-art training facility
for physicians, nurses, OR techs and
company reps. Using lifelike
arthroscopy models and high-tech
computer simulators, the CLAS Room
teaches the complex manual surgical
skills needed to perform arthroscopy,
through observation and repetitive
bimanual practice.
Stephen Snyder, MD, and his partners at
the Southern California Orthopedic
Institute have always been strongly
committed to the education of other medical professionals. The CLAS Room is the latest
step in their pursuit of educational excellence. Each year, hundreds of visitors come to
SCOI observe and learn the latest procedures in sports medicine and arthroscopy. With the CLAS
Room, they can now have hands-on training with the masters of arthroscopy.
We would like to thank the following corporate sponsors for their invaluable assistance with the CLAS Room:
Mentice Inc; Linvatec Inc.; Smith & Nephew Endoscopy; Pacific Research; Mitek Inc. and Lippincott WW Inc.
The CLAS Room is located in SCOI’s main office in Van Nuys, California, at 6815 Noble Avenue.
For more information on SCOI, please visit our website at http://www.scoi.com/.
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The CLAS Room includes:
◊ Two computers – a dedicated Macintosh supercomputer, equipped with software and
peripherals for developing and editing digital presentations, both video and PowerPoint; and
a P.C. with a high-speed Internet connection to allow access to online data and interaction
with other centers.
◊ “ALEX” the Shoulder Professor – this is a lifelike arthroscopy model or “Dry
Cadavers”(made by Sawbones, Inc.) is now able to be used with or without an arthroscopic,
to provide a more complete hands-on training experience. “ALEX” will soon be joined by
the new wrist, knee, ankle, elbow and spine models which provide the same experience for
these anatomical locations as “ALEX”
does for the shoulder.
Three complete stations are available
with video equipment to learn and
practice the steps in arthroscopic
surgery of the chosen joint. All
necessary hand tools, suture
anchors and disposable materials
will be available at these stations.
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◊ “Sammy” – The virtual reality arthroscopic simulator produced by the
Mentice Company of Sweden. This extraordinary computerized simulator
Each ALEX station is equipped with
is the most realistic tool currently available for learning shoulder
a scope, video player and monitor
arthroscopy. It is a complete 3-D
so the student can watch and then
simulation of the entire shoulder
practice the operation.
environment, and is a valuable aid for
teaching eye-hand coordination, triangulation, surgical anatomy and surgical repair
techniques. Through a force-feedback system, the surgeon experiences the same
tactile sensations as when actually operating in the shoulder. The simulation is
complete with “fluid” and even “blood” when a vessel is accidentally cut. The
number of procedures that can be performed on Sammy is rapidly increasing.
A 15-point anatomy exam, subacromial decompression, and removal of loose bodies are all
currently available, and soon cuff and labral reconstruction, as well as capsular
plication, will be added.
“Sammy” the VR force feedback
simulator allows the surgeon to
practice arthroscopic techniques
with the same feeling as live surgery
◊ “Misty” – A virtual reality task simulator designed to teach bimanual
manipulations using a series of hand tools connected to a computer.
This simulator is remarkably useful for training all levels of surgeons to
Be efficient and precise when operating while viewing on a video screen.
◊ Audio and video cable links – Visitors can observer two ongoing
arthroscopic surgeries being performed in the Center for Orthopedic
Surgery, Inc., while simultaneously practicing on ALEX or Sammy in the
CLASroom, and discussing ongoing cases with the surgeon.
◊ Video teleconferencing - is also available from the CLASroom, SCOI boardroom
and COSI surgery center to permit face-to-face interaction with other centers
throughout the world.
“Misty” is a bimanual task VR
task simulator that scores the
performance of the student and
compares his progress to others.
These exceptional learning tools are available to visitors at the Southern California
Orthopedic Institute. Call Rene, Ed or Jo Ann at (818) 901-6600, ext. 3032 for information and to schedule a
visit or log on to our web site at http://www.scoiclasroom.com./
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ICL #9
Introduction: Arthroscopic Management of Intra Articular Fractures of the Knee
Mahmut Nedim Doral,
O. Ahmet Atay, Onur Tetik, Gürsel Leblebicio_lu
Hacettepe University Faculty of Medicine
Department of Orthopaedics and Traumatology & Department of Sports Medicine
e-mail: [email protected]
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ARTHROSCOPIC MANAGEMENT OF INTRA-ARTICULAR FRACTURES OF THE KNEE
Wednesday, March 12, 2003 o Carlton Hotel, Carlton II
Chairman: M. Nedim Doral, MD, Turkey
Faculty: W. Jaap Willems, MD, Netherlands, Phillip Lobenhoffer, MD, Germany, Freddie Fu, MD, USA and David
McAllister, MD, USA
Arthroscopic management of intraarticular fractures of the knee is a minimal invasive, more accurate, and
outpatient procedure parallel to the technological advances. Fractures are not only important for the adolescence and pediatric group, but also important for the adult population.
The main purpose of arthroscopic fixation of the intraarticular fractures is to give stability to the
fragments and to treat the associated lesions for the restoration of the knee joint. The high degree of success achieved in almost all cases illustrates the amazing recuperative powers of human joints once articular cartilage congruence and stability is re-established together with correction of axial deformities and the
mobilization of joints.
EI (EI) and distal femur are the frequent zones prior to injury for the pediatric group. Also these
problems became very frequent in the adolescence group with the increase in the level of the sportive activity.
Avulsion fractures from EI is mostly treated with the
arthroscopy assisted methods. Detailed evaluation of EI fracture
and the classification according to the Meyers-McKeever system
must be done to plan the arthroscopy-assisted treatment.
In our practice we use transquadricipital portal for the fixation of EI fractures (1). But do not forget the conservative
approaches to the EI fixation (2)
At the same time the natural history of the elongation of
the ACL is not clear in the literature.
Physeal fractures that involve the distal femur must also be considered in the patient presented with hemarthrosis in pediatric
and adolesence age. Magnetic resonance imaging (MRI) permits
noninvasive evaluation of the cartilage of the growth plate and epiphysis so that diagnosis and the treatment of the fracture becomes more precise with the MRI.
The most frequent intaarticular pathology for the adult group is plateau fractures of the tibia. Either
Schatzker or Hohl classification system may be used for systematic evaluation of the fracture. Arthroscopy
assisted treatment is mostly preferred, especially for the lower grades.
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One must keep in mind that periarticular soft tissue is a very important parameter for the planning
of the intraarticular pathologies. Tscherne and Lobenhoffer classification system may be helpful for planning of the pathologies (3).
Patellar fracture is another intraarticular fracture that may interfere with the knee unction. Arthroscopic
assistance is helpful in the internal fixation techniques of the patellar fracture to provide and protect the
cartilage integrity.
Segond fracture and the chondral avulsions are the rare type of the injury but more and more participants in the sports bring these kinds of injuries more frequent in our daily practice.
We can conclude that arthroscopic treatment of the intraarticular fractures of the knee joint is a
more effective and adequate procedure with early active motion and controlled rehabilitation program.
Under the scope of that brief knowledge it’s easy to understand arthroscopic management of major
intraarticular fractures of the knee joint.
An overview of the major intraarticular fractures of the knee, the classification and the mechanics of
tibial plateau fractures. Secondly, the arthroscopic treatment of IA fractures including the arthroscopic
techniques for the treatment of the fracture of EI. Finally, the natural history of ACL after EI fractures, the
potential biological approach and rehabilitation will be discussed in this ICL#09.
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1-Doral MN, Atay OA, Leblebicioglu G, Tetik O. Arthroscopic fixation of the fractures of the intercondylar
eminence via transquadricipital tendinous portal.Knee Surg Sports Traumatol Arthrosc. Nov;9(6):346-9, 2001
2-Atay OA, Doral MN, Tetik O, Leblebicioglu G. Conservative treatment of eminentia intercondylaris fractures of the tibia in children. Turk J Pediatr. Apr-Jun;44(2):142-5, 2002
3-Tscherne H, Lobenhoffer P.: Tibial plateau fractures. Management and expected results. Clin Orthop 1993
Jul;(292):87-100
Tibial Plateau Fractures; classification and biomechanics
W. Jaap Willems
Amsterdam, The Netherlands
Several classifications for these fractures have been described. Hohl (1956) defined 6 types (undisplaced,
Local compression,Split compression,Total,Split and Communited). Based on this system Schatzker (1979)
described 6 types: 1)Split condylar, 2)Split and depression, 3)Joint depression, 4)Medial condylar,
5)Bicondylar, 6)Bicondylar with diaphyseal extension. The AOgroup developed their classification, based on
the ABC categories : A: extra-articular, B: partial intra-artcular, C: total intra-articular.In this classification
for the tibial plateau fractures 9 subgroups are defined. The fractures of the intercondylar eminence are
generally classified according to Meyer: undisplaced, minimally displaced ,displaced.
The tibia plateau fracture is mostly caused by a fall; depending on the valgus or varus moments a lateral
or medial condylar fracture exists.With rotational forces an eminence fracture can arise, comparable to an
ACL injury, with bony detachment of the ACL on the tibial side.
The first results on the arthroscopically assisted treatment of tibial plateau fractures is reported by Reiner
in 1982. From the beginnings of the nineties several studies have been published. In the first decade the
technique was used in the more simple fractures (Schatzker types 1,2 and 3 or AO type B1,B2,and B3).Later
the more complex bicondylar fractures were treated as well with arthroscopic assistance. Nowadays the better visualisation, especially of the fractures in the postero-lateral part of the tibial surface as well as better
interpretation of the concomitant pathology (cruciate ligaments, meniscus) leading to a better reduction as
well as treatment of this concomittant pathology are seen as the great advantages of the arthropscopically
assisted treatment of the tibialplateau fractures. The less invasive approach of the intra-articular fracture
does not preclude a sufficient osteosynthesis, with sometimes the need of plates and screws.
Literature:
Schatzker J et al .(1979) : The tibia plateau fracture: the Toronto experience. Clin Orthop 138:94-104
Reiner MJ(1982): The arthroscope in the tibial plateau fractures : its use in evaluation of soft tissue and
bony injury. J Am Osteopath Ass.
Fowble CD et al (1993): The role of arthroscopy in the assessment and treatment of tibial plateau frac3.60
tures.Arthroscopy 9:584-590.
Berfeld B et al (1996): Arthroscopic assistance for uncollected tibial plateau fractures.
Arthroscopy 12:598-602.
The Evaluation and Natural History of Tibial Spine/ACL Avulsion Fractures
David R. McAllister, M.D.
University of California, Los Angeles
Department of Orthopaedic Surgery
Mechanism of Injury
•
Avulsions fractures in children are the result of stress on the ACL
•
Usually caused by internal rotation of the tibia, hyperflexion or hyperextension
•
Can be the result of falls from bicycles or motorbikes, sports injuries, or MVA
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Introduction
Anatomy:
•
ACL attached to fossa anterior to the medial intercondylar eminence
•
Some ACL fibers pass beneath the transverse meniscal ligament blending with the anterior horn of
the lateral meniscus
Classification
•
Type 1: Minimally displaced
•
Type 2: Fragment elevated but still attached
•
Type 3: Complete displacement of the fragment
Myers and McKeever, JBJS-A, 1970
Associated Injuries
•
Common in Adults (especially MCL injuries)
•
Uncommon in children
Non-Operative Treatment
•
Type I & II usually non-operative treatment with immobilization in a cast for 6-8 weeks
•
15-30 degrees of flexion to relax the posterolateral bundle of the ACL
•
Full extension to allow the femoral condyle to compress the fragment toward its fracture bed
•
Important to verify adequacy of reduction
Operative Treatment
•
Type III fracture usually require ORIF
•
Arthrotomy
•
Arthroscopy
Results (Baxter and Wiley, JBJS-B, 1988)
•
•
•
•
42 children with anterior tibial spine fractures
Type 1: 8 (19%)
Type 2: 13 (31%)
Type 3: 21 (50%)
Treatment:
•
13: Plaster immobilization (all type I; 5 type II)
•
15: Closed reduction (8 type 2; 7 type 3)
•
14: Open reduction (13 type 3; 1 type 2)
Baxter and Wiley, JBJS-B, 1988
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Laxity:
•
Type 1: None
•
Type 2 & 3: 3-4 mm
Loss of extension:
•
All patients lost extension (range 4-15 degrees)
Conclusions:
•
Fractures of the tibial spine may lead to disturbance of the ACL; although asymptomatic in this study
•
Anatomic reduction does not eliminate laxity or the loss of full extension
Results (Myers and McKeever, JBJS-A, 1970)
•
Follow up of 1959 JBJS publication
•
70 patients with intercondylar eminence fracture
•
Types 1 and 2 treated with aspiration and casting (knee flexed 20 degrees) (80%)
•
None treated with closed reduction
•
Type 3 treated with ORIF (20%)
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•
•
•
10/22 adults had poor results
46/47 children had good/excellent results
All type III injuries treated operatively had a good/excellent result
Conclusions:
•
Most fractures in children have good results
•
ORIF is indicated for Type III injuries
•
Closed reduction is not indicated
•
Prognosis not so good in adults
Summary
•
The overall prognosis is good if satisfactory reduction can be maintained
•
Can be some residual anterior laxity although when present this is usually asymptomatic
•
Can be overgrowth of medial tibial eminence
Extension block is common and can occur with or without surgery
The Biological Approach
Freddie H. Fu, M.D., D.Sc. (Hon) and Volker Musahl, M.D.
Freddie H. Fu, M.D., D.Sc. (Hon), David Silver Professor and Chairman of the Department of Orthopaedic Surgery,
Kaufmann Building Suite 1011, 3471 Fifth Avenue, Pittsburgh, PA, 15213
www.orthonet.upmc.edu, email: [email protected]
INTRODUCTION
Limited healing capacity of ACL, PCL, central meniscus, cartilage, muscle injuries, and delayed fracture
healing. Therapeutical approaches addressing the biological base of these injuries are mostly pre-clinical
applications. Improving the biological healing process by means of stem cells, gene therapy, and tissue
engineering may stimulate the healing process
EVALUATION
Conventional Imaging
Limited by inability to directly visualize articular cartilage and menisci
MRI provides non-invasive and direct visualization of bone and soft tissue structures
MRI provides diagnostic advantage over clinical examination only in selected cases [6]
Gadolinium enhanced MRI
More sensitive and specific MRI technique for evaluating articular cartilage abnormalities.
Gadolinium enhanced MRI on the composition of cartilage post ACI. At > 1 year, the grafts have GAG levels
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comparable to normal articular cartilage [4]
Biomechanical Probes
Measures indentation stiffness of articular cartilage
Decrease in indentation stiffness for proteoglycan-depleted specimens compared to normal articular cartilage [10]
Functional tissue engineering
Approach to enhance tissue regeneration and provides the possibility of producing tissue that is biomechanically, biochemically, and histomorphologically similar to the normal
Basic concept is based on the manipulation of cellular and biochemical mediators to affect protein synthesis and to improve tissue formation and remodeling
Ultimately, the process is expected to lead to a restoration of mechanical properties [9]
The available approaches are e.g., the use of growth factors, gene transfer technology to deliver genetic
material, stem cell therapy, and the use of scaffolding as well as external mechanical factors
Each of these approaches, or their combinations, offers the opportunity to enhance the healing process
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Optical Coherence Tomography (OCT)
Ultrasound is an echograph of ultrasonic waves; OCT is an echograph of infrared light
Provide real-time cross-sectional imaging of articular cartilage [2]
Detects gaps that are invisible to the arthroscope, good correlation with histomorphometric analysis
Matrices
Protein-based polymers (e.g. fibrin, collagen)
Carbohydrate-based polymers (e.g. PLA, PGA, hyaluronan)
Artificial polymers (e.g. Dacron, hydroxyapatite)
Combination polymers (e.g. crosslinging, matrix combinations)
Matrix requirements
Porosity (cell migration)
Adhesion (cell attachment)
Biodegradability
Biocompatibility
Bonding (tissue integration)
Elasticity (biomechanical stability)
Stem cells
Cells that can turn into different tissue types, such as bone, cartilage, muscle, or tendon.
A special stem cell population derived from muscle tissue was identified and tissue engineering approaches are currently under development [5]
Biological substitutes for repair, reconstruction, regeneration, or replacement of musculoskeletal tissues
can be engineered with muscle-derived stem cells
For this purpose, growth factors are used, which have been shown to promote the healing of tissues of the
musculoskeletal system.
Growth factors
Growth factors can be liberated by cells at the injury site (e. g. fibroblasts, endothelial cells, muscle cells,
mesenchymal stem cells)
Growth factors are capable of stimulating cells towards proliferation, migration, matrix synthesis and differentiation
Growth factor application is limited by the their short biological half life, and the need for repeated and
high dosages
Growth factors are limited by their need for delivery to the injured site
Among the different methods developed for local administration of growth factors, gene transfer techniques have proven the most promising
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(+ positive effect; - no or
negative effect; blank not
tested IGF-1=insulin like
growth factor 1; bFGF=basic
fibroblast growth factor;
NGF=nerve growth factor;
PDGF= platelet-derived
growth factor; EGF= epidermal growth factor; TGF=
transforming growth factor;
BMP-2=bone morphogenic
protein-2)
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Gene therapy
Gene therapy transfers specific genes into the target tissue
Successful application of gene therapy can promote production of therapeutic levels of desired proteins by
transformed cells at the site of injury or inflammation.
The cDNA must be packaged into a vector to enter the cell, here it is integrated into the host chromosomal
DNA
For expression, the desired gene has to be transcribed, translated, and secreted
Viral and non-viral vectors are available to deliver genetic material
Non-viral vectors, e.g. liposomes, are easy to produce and have a relatively low toxicity and immunogenicity, low efficiency in delivering the gene to the targeted cells
Viral vectors present the most efficient method for gene transfer. Commonly used viruses include adenovirus, retrovirus, adeno-associated virus, and herpes simplex virus
Strategies
Strategies for local gene therapy have been extensively investigated
Vectors can be directly injected in the host tissue, or cells in culture can be genetically altered with a vector
(ex vivo) and transplanted [3]
While the direct method is technically easier to achieve, the cell based ex vivo approach bares less risk,
because gene manipulation occurs outside the body of the host
The genetically engineered and transplanted cells supply the host not only with the desired gene expression but also with cells responding and participating in the healing process
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At the experimental level, the feasibility of gene therapy was shown to the ligament insertion, meniscus,
articular cartilage, and synovial tissue of the knee joint [1, 7, 8]
Future directions
Gene therapy is not yet established as a clinical therapy in Orthopedic Surgery
Gene therapy has great potential for the treatment of musculoskeletal injuries in the future
Phase I of the first clinical trial in orthopedics was successfully completed for human joints
Further tissue engineering with muscle-derived stem cells and gene therapy will lead to the development of
new treatment strategies for tissues with low healing capacities such as articular cartilage
REFERENCES
1.
Adachi, N., Sato, K., Usas, A., Fu, F.H., Huard, J. et al., J Rheumatol. 2002 Sep;29(9):1920-30.
2.
Chu, C.R., L.D. Kaplan, F.H. Fu, J.P. Bradley, and R.K. Studer. AOSSM, 28th Annual Meeting. 2002.
Orlando, FL.
3.
Evans, C. and P. Robbins, J Bone Joint Surg Am, 1995. 77: p. 1103-1114.
4.
Gillis, A., A. Bashir, B. McKeon, A. Scheller, M. Gray, and D. Burstein, Investigative Radiology, 2001.
36: p. 743-748.
5.
Huard, J., G. Ascadi, A. Jani, and et. al., Human Gene Therapy, 1994. 5: p. 949-958.
6.
Kocher, M., J. DiCanzio, D. Zurakowski, and L. Micheli, Am J Sports Med, 2001. 29: p. 292-296.
7.
Lee, J.Y., D. Musgrave, D. Pelinkovic, K. Fukushima, J. Cummins, A. Usas, P. Robbins, F.H. Fu, and J.
Huard, J Bone Joint Surg Am, 2001. 83-A(7): p. 1032-9.
8.
Martinek, V., F.H. Fu, J. Huard, et al., J Bone Joint Surg Am. 2002 Jul;84-A(7):1123-31.
9.
Woo, S.L.-Y., K. Hildebrand, N. Watanabe, J.A. Fenwick, C.D. Papageorgiou, and J.H. Wang, Clinical
Orthopaedics & Related Research, 1999(367 Suppl): p. S312-23.
10.
Youn, I., F. Fu, and J. Suh, The Pittsburgh Orthopaedic Journal, 1999. 10: p. 159-160.
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A large number of basic science studies and pre-clinical trials have to be completed to reach the necessary
efficiency and safety for orthopedic applications
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ICL #10
MANAGEMENT OF THE POST MENISCECTOMY KNEE AND DECISION-MAKING
Wednesday, March 12, 2003 o Aotea Centre, Kaikoura Room
Chairman: Giancarlo Puddu, MD, Italy
Faculty: Christopher Harner, MD, USA, Annunziato Amendola, MD, USA and Philippe Neyret, MD, France
1. Meniscal Allografts – Chris Harner
2. High Tibial Osteotomy – Ned Amendola
3. HTO and the post meniscectomy ACL deficient knee – Philippe Neyret
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4. HTO and posterior instability – Chris Harner
5. Antivalgus Osteotomies – Gian Carlo Puddu
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ISAKOS 2003
Auckland, New Zealand
March, 2003
Top 10 Orthopaedic Procedures:
10) Debride skin/muscle/fracture 11012
Christopher D. Harner, MD
Medical Director
Center for Sports Medicine
University of Pittsburgh
Total knee replacement
Open repair of femur fracture 27236
27447
7)
ACL reconstruction
6)
Open repair of femur fracture 27244
5)
Subacromial decompression
4)
Removal of support implant
20680
3)
Carpal tunnel surgery
64721
•
1)
1)
Chondral debridement
Meniscectomy
Meniscectomy
29877
29881
29881
29888
29826
Source: ABOS, 2002
Rationale
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Indications and Techniques
9)
8)
Practice Profile - CDH
Time: 14 years
#1 goal:
Type: Academic
Preserve the
meniscal and
articular cartilage
Sports Medicine / Knee
Meniscus Transplantation:
• 10 yr experience
• 15-20 cases / yr (>175
total)
Save the
Meniscus!
Selection Criteria
Harner &
Annunziata 2000
• Publications:
–
–
–
1st 30 cases (2-10 yr f/u)
Lateral transplants
ACL + transplant
Selection Criteria
• Age
• Pain (localized)
• Previous surgery
• Status of articular cartilage
45° PA FWB x-ray
Arthroscopic findings
• Alignment
(long cassette)
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Selection Criteria
Graft Choice
Surgical Technique
• Fresh-frozen,
non-irradiated
allografts
• Arthroscopic assisted
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Selection Criteria
(donor age 15 - 35)
• Single tissue bank
• “Small” arthrotomy incisions
• Meniscus sutured with
combined arthroscopic and
open techniques
• Size match
• Standardized post-op rehab
L’Insalata, 1996
Surgical Technique
History
• 26 y.o. male soccer player
• twisting injury (5/97)
– partial medial meniscectomy (6/97)
– subtotal medial meniscectomy (1/98)
– persistent medial joint line pain
+ ADLs/sports
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History
J.F.
• 40 y/o male physician
• Previous lateral meniscectomy
x2
• +ADL/work
Post-operative Management
Results
• Bracing
Demographics
• Motion: CPM 0 - 90° X 4 wks
• Partial to full weight bearing over 4
wks
• Return to ADLs: 8 wks
• Return to Sports: 9 - 12 mo
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• Lateral joint line pain
• 34 meniscal transplants in 31
patients
• Average f/u 36 mo (24 - 72)
• 18 male, 13 female
• Average age 28 (15 - 42)
Subjective Rating Scales
• Previous surgery
1 - 4 (avg 2.4 / pt)
• 11 isolated meniscal
involvement
• 20 combined with ligament
instability
• 100 point scale
• Knee outcome survey
ADL - avg 86 (79 - 92)
Sports - avg 78 (64 - 88)
• Lysholm - avg 84 (82 - 92)
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IKDC Results (n = 31)
Function
al Rating
Activity
Rating
Normal
11
16
Nearly
Normal
19
14
1
1
0
0
Abnormal
•No joint
space
narrowing
over time (p
= 0.31)
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Severely
Abnormal
Results - Lateral Meniscus
Conclusion
n = 20, 2 - 8 yr f/u:
• IKDC:
18% normal, 73% near normal, 9% abnormal
Remains a viable
option in:
•Select patients
• Knee Outcome Score
ADLs
79 ± 13
Sports
75 ± 17
•Joint line pain
• Lysholm:
•Near “neutral”
alignment
•Previous
meniscectomy
81 ± 16
• No joint space narrowing over time
• 18/20 would do again
•“Intact articular
cartilage”
AAOS, 2001
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P.B.
9 yr s/p
T.B.
2nd look
1 1/2 yr s/p
High Tibial Osteotomy
A. Amendola, MD
University of Iowa Hospitals and Clinics
The Post Meniscectomy Knee
1. Presentation
•
Compartment pain
•
± deformity
•
± thrust
3. Indications – The Importance of Alignment
Malalignment
Malalignment
Malalignment
+
+
+
Arthrosis
Instability
Arthrosis
+
Instability
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2. Goals of Treatment
•
Pain reduction
•
Improvement of functional stability – not passive laxity
•
Reduction of thrust / instability
•
Improve the likelihood of success post ligamentous/cartilage or meniscal reconstructive procedures
Malalignment
+
Cartilage / Meniscal Transplantation
4. Contra-indications
- Severe degeneration of opposite tibio-femoral compartment
- Gross loss of motion, 70°
- Usual medical contra-indications
7. Pre-Operative Planning
- Detailed history and physical exam
- Assessment of instability
- In-office gait analysis
Radiographs:
- Routine Series :
- standing AP
- standing tunnel
- lateral
- intra-patellar
- Standing hip to ankle x-ray (target area is weight-bearing axis) – most important for preoperative planning
8. Assessment of Alignment
a) Femorotibial angle: (5 – 7° valgus ) measured on single weight-bearing x-rays
b) Mechanical axis (author’s preference): measures deviation in weight-bearing line
- Advantages and disadvantages to both methods
- Neither is entirely accurate
- Compare to other knee if normal
- Intra-operative measure with fluro is important
9. Posterior Tibial Slope
- Bony slope is 1 – 10°
- Soft tissue (articular slope ) is less
- Increasing slope is similar to flexing knee
- Keep in Mind: - Increasing posterior tibial slope increases tendency for anterior tibial translation
- Increasing posterior tibial slope worsens ACL deficit; helps PCL deficit
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10. Opening vs. Closing Wedge - Advantages / Disadvantages
•
Tibial Opening Wedge
Advantages
- Avoids proximal tib-fib joint & peroneal nerve
- Easier to perform 2 plane osteotomy in sagittal and coronal plane
i.e. correction of varus and hyperextension
i.e. dealing with ACL or PCL insufficiency patterns
- Easier operation (1 cut)
- Does not violate anterior compartment of the leg
Disadvantages
Most often requires graft
? union rate
- Not appropriate for huge ( > 2cm) corrections
•
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Tibial Closing Wedge
Advantages
- No graft
Disadvantages
Alters shape of upper tibia Æimplications for TKA
Difficult to control tibial slope
Most often slope is unintentionally decreased
Difficult to adjust correction intra-operatively
Proximal tib-fib joint violated
Not appropriate for huge ( > 2cm) corrections
11. Authors Preferred Surgical Technique
Opening wedge
Puddu plate fixation
Autograft or allograft
Tibial Valgus Producing Osteotomy Technique
Medial incision
Superficial MCL retracted
Patellar tendon retracted
Drill guide pin under fluoroscopic control
slight obliquity to orientation
- start approximately 4cm below medial joint line
- directed across superior aspect of tibial tubercle at patellar tendon insertion
- to 1 cm distal to lateral joint
- tip of fibular head helpful reference point
- Reposition guide pin as necessary until placement is optimal (1,2 )
- Always perform osteotomy below guide pin (3)
Osteotomy should be oblique but not excessively (1)
- Cortical cut made with small sagittal saw
- Osteotomy completed with osteotome
- thin, flexible osteotomes are better than traditional ones
- leave 1cm lateral cortex as hinge
- osteotomy should stop at least 1cm distal to lateral joint
Technique continued
- continuous or frequent imaging to prevent violation of lateral cortex
- make sure both anterior and posterior cortices are penetrated
- Gradually and carefully open osteotomy to desired width (4 )
- Bone grafting:
7.5mm gap or less, local or none
> than 7.5mm, allograft or autograft (6)
12. Alternate Fixation Options for Opening Wedge Osteotomy
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-
Other plate and screw systems
Bone graft only
External fixator / spatial frames more appropriate for huge corrections
14.
Combined ACL Deficiency / Malalignment
Treatment Algorithms
i)
LATTERMAN and JAKOB Knee Surg Sports Traumatol Arthrosc 1996
Group
1
Age
>40
Pain
+++
Instability
+
Arthroscopy
Subchondral bone
Treatment
HTO alone
2
25-40
+-++
+-++
Severe fissuring
and fragmentation
Staged
3
<20-35
+
+++
Fissuring
Combined
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13. Complications
- Haematomas
- Failure of fixation / non-union
- Hardware
ii) CLATWORTHY and AMENDOLA, Clin Sports Med. 18, 1, January 1999
Primary Symptoms and Examination Findings
15. SURGICAL TECHNIQUE
ACL Reconstruction With High Tibial Osteotomy
Perform hamstring reconstruction in the arthritic knee.
i.
Hamstring tendon graft harvest through osteotomy incision
ii.
Arthroscopy, debridement , prepare notch
iii
Perform opening or closing wedge HTO + fixation (author’s technique – medial opening wedge with
Puddu plate fixation. Operative Techniques in Sports Medicine January 2000, Volume 8, Number 1)
iv.
Drill tibial and femoral tunnels proximal to osteotomy if possible
v.
Pass ACL graft + graft fixation
CAUTION:
•
Be very careful to maintain or decrease posterior tibial slope in ACL deficiency
•
DO NOT INCREASE TIBIAL SLOPE
16. SUMMARY
a) The natural history of arthrosis in the isolated ACL deficient knee with or without reconstruction is
uncertain. However, if malalignment is present it must be corrected.
b) Arthrosis. Alignment. Instability. Separate but related problems with separate or
combined solutions.
REFERENCES
1. Brown, G., Amendola, A., Radiographic evaluation and pre-operative planning for high tibial osteotomy;
Osteotomies About the Knee: Operative Techniques in Sports Medicine. David Drez Jr., Jesse C. Delee
Editors; Giancarlo Puddu, Guest Editor. Volume 8. Number 1. January 2000
2. Clatworthy, M., Amendola, A., The anterior cruciate ligament and arthritis: Clinics in Sports Medicine,
Volume 18. Number 1. January 1999
3. Naudie D, Roth S, Dunning C, Amendola AS, Giffin JR, Johnson JA, Chess D, King GJW., The effect of
opening wedge high tibial osteotomy in the posterior cruciate ligament deficient knee. To be presented at
the 56th Annual Meeting of the Canadian Orthopaedic Association. London, Ontario. June 1 – 4th 2001
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4. A. Amendola, J. R. Giffin, D.W. Sanders, J. Hirst, J.A. Johnson Osteotomy for Knee Instability: The Effect of
Increasing Tibial Slope on Anterior Tibial Translation. Presented at American Orthopaedic Society for
Sports Medicine Specialty Day, San Francisco, California . March 3, 2001
The Post Meniscectomy Knee
Ph. Neyret, T. Aît Si Selmi, T. Lootens, N.Bonin
1/ The role of Medial Meniscus in ACL Deficient knee.
1a/ Natural history of the ACL deficient knee.
We know that ACL rupture leads to Osteoarthritis over time particularly if an isolated Medial Meniscectomy
without ACL Reconstruction has been performed.
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With Henri Dejour Pierre Chambat and Deschamps, we underlined, in the past the links between ACL
Deficient Knee and Osteoarthritis due to some biomechanical factor, particularly the status of the medial
meniscus and the amount of the Anterior Tibial Translation.
1b/ Osteoarthritis after ACL reconstruction
But ACL Reconstruction can also lead to Osteoarthritis and sometimes to early and severe osteoarthritis in
young patients.
We reported with Henri Dejour and G Walch in 1988 that Previous Medial Meniscectomy, a delay InjuryOperation superior to 5 years or pre-operative degenerative changes are liable to lead to early post-operative osteoarthritis.
After ACL Reconstruction, what are the radiological results at long term follow-up. reported
Three very similar lyonnais series reported by T. Aitsiselmi, Chotel and Selva evaluated the clinical and
radiological outcome after ACL reconstruction combined to an extra-articular tenodesis at 10 years followup. They also found a relationship between the medial meniscal status and radiological outcome.
Normal
Sutured
Partial MM
Total MM
Previous MM
10%
20%
30%
60%
If the medial meniscus was preserved it means normal of sutured at time of ACL Reconstruction, the rate
of pre-OA or OA was 10% at 11.5 years mean follow-up.
But if the medial meniscus was partially removed at the time of ACL reconstruction the rate of pre OA or
OA increased to 20% and 30% in case of total meniscectomy. A previous medial Meniscectomy before the
ACL Reconstruction was the worst eventuality : the risk of pre-OA or OA reached to 60%.
The influence of post-operative medial meniscectomy after ACL Reconstruction in the onset of OA is still
unknown because its frequency was very low.
According to Shelbourne, in order of importance, articular cartilage damage, partial or total medial meniscectomy, and partial or total lateral meniscectomy affect the objective and subjective results from5 to 15
years after ACL Reconstruction.
Wu very recently, in the last issue of the American Journal of Sport Medicine, reported that at 10 years followup radiographic abnormalities were more common in the subgroups that had undergone meniscectomy.
2/ The combined operation
Henri Dejour did the Hypothesis that "ACL Deficient Knee with monopodal stance imbalance that appears
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on monopodal stance cannot be compensated for by a simple ligamentous ACL graft ". We try to better
define the relationship between Instability and Osteothritis in a chapter of the book directed by the
Pittburg’s team.
Our early results at 3 years follow-up were published in the CORR in 1994.
But some surgeons (Jakob…) during the 90ies recommand a two stage-surgery, and the debate is still
opened. Let me give a short overview of the publication we did in 1994.
It was a series of 50 patients with symptoms of ACL insufficiency and varus malalignment. 44 were available at follow-up.
At 3.5 years Follow-up we noted improved clinical symptoms, particularly objective and subjective stability.
Moreover Osteoarthritis seemed to be stabilized.
Nevertheless only one patient was able to return to competitive sport activities.
In this series Varus malalignment was either due to medial narrowing mainly after Medial Meniscectomy, or
due to lateral opening in case of lesions of the lateral collateral ligament.
These two situations are completely different. In this short presentation we shall concentrate on the medial
narrowing subgroup and then we shall discuss our present indications of the combined operation.
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2a/ Results at 10 years
2b/ Results at 10 years
What is the long term outcome of the combined operation, ACL graft combined with a Valgus High Tibial
Osteotomy, in one stage surgery ?
•
1983-1999: 47 MedialFTA
grade B: 20
grade C: 27
•
At FU:
35 knees (75%)
Delay Injuy-op: 8y (1-33)
Age at Operation: 32y (18-49)
Previous medial M.: 21 (66%)
FU: 11 years (1-16)
- Material – Method
The inclusion criteria were very strict. Only 47 knees with mild or moderate radiological preoperative
changes, it means grade B or C in the IKDC classification, were operated on between 1983 and 1999. At follow-up, 35 knees were avalaible.The mean delay Injury-Operation was 8 years with a large standard deviation. In 66% of cases a previous medial meniscectomy had been performed.
A closing wedge Osteotomy was performed at the beginning of our experience and progressively we preferred to combine an opening wedge Osteotomy.
- Results :
The IKDC subjective score depends on symptoms, functional evaluation and sport activities. The average is
79 at 11 years follow-up.
Considering the index of satisfaction, 96% of patients considered their knee as normal or almost normal
At follow up 42% of patients practised recreational sports and only 6% continue competitive sports.
The final evaluation allows to underline that 60% of patients belong to the grade A or B, 34% to the grade
C and only 6% to the grade D.
Mean
Closing
Opening
Tibial
Pre-op
10.5
10.9
8.9
Slope
FU
9.4
9.5
9.3
Radiologically we notice a tendancy to decrease the tibial slope in case of closing wedge osteotomy and a
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tendancy to increase the tibial slope in case of opening wedge osteotomy, but the difference is not statiscally significative, in this short series.
We found that the residual, differential, anterior tibial transltion,
on monopodal stance is directlty correlated with the objective
score. In the Groups A and B the residual differential postoperative translation on is 2.5 mm and 5.5 mm in the groups C and D.
It is interesting to know there is a direct relationship between the
Anterior Tibial Translation and the tibial slope. So it is crucial
not to increase the tibial slope when performing the Osteotomy..
The mean valgus correction measured on the long leg films at
one year follow-up was 7°.
At follow-up a loss of 2° was observed in the amount of the valgus correction.
Usually we try to obtain a 2 to 4 valgus alignment.
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a
Pre-op
b
14
c
d
20
3
Follow-up
11
2
21
2
A progression of Osteoarthritis in the medial compartment was noted in 5 Knees, 15% of cases. We do not
establish a direct correlation between the amount of valgus correction and the progression of the
Osteoarthritis.
a
Pre-op
b
30
c
d
4
18
2
Follow-up
10
22
2
A progression of Osteoarthritis in the lateral compartment was noted in 20 Knees. Severe lateral degenerative changes were observed in only two cases.
We do not establish a direct correlation between the amount of valgus correction and the progression of
the Osteoarthritis.
2c/ Indications et technique
What is nowadays the place of the combined operation in our practice ?
•
Firstly in case of medial narrowing without lateral opening.
Example 1 : This patient had had an ACL Reconstruction with a good result.
On the left knee there is a medial narrowing, grade C. Note the large amount of anterior tibial translation
on the radiological lachman and the disappearance of the posterior clear triangle corresponding to the
posterior horn of the medial meniscus.
At 2 years follow-up the progression of OA seemed to be stopped and the left lower limb is well aligned
Example 2 : This patient had undergone a previous ACL reconstruction using a synthetic ligament and a
medial meniscectomy. You can see there was an asymmetrical varus malalignment. At follow-up we can
measure a 2° valgus alignment and a stabilization of the progression of Osteoarthritis. Note the complete
control of the anterior tibial translation on the post-operative profile Xrays in monopodal stance.
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Technically this operation is very simple. We harvest the Bone-Patellar tendon-Bone graft, then drill the two
tunnels and before to pass the graft we perform an opening wedge tibial Osteotomy and then we calibrate
again the tibial tunnel.
To perform a combined Osteotomy is easy if one elevates the Pes Anserinus. The superficial medial collateral ligament is transversally cut. Two parallele pins show the direction of the future Osteotomy.
A fluoroscopic control is absolutely necessary.
The osteotomy is fixed with two or three staples.
. The problem is very different in case of asymmetrical lateral opening without medial narrowing.
In case of asymmetrical lateral opening due to an intersticial rupture of the lateral collateral ligament we
recommand to perform, during the same surgery, The ACL Reconstruction, The opening wedge HTO and a
Lateral Collateral Ligament graft, using a 6mm Bone-Patellar tendon-Bone graft harvested on the contralateral knee. The role of the Osteotomy is to protect the grafts and a small amount of valgus, 2 or 3 degrees is
enough. In the absence of LCL graft an obvious hypercorrection would be required.
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Example 1 : In this patient, during the same operation we performed a combined operation and a fixation
of the bone block of the femoral insertion of the lateral collateral ligament.
Example 2 : This patient had a mild asymmetrical lateral opening, but the long leg film shows a valgus
alignment. In this situation we decide to reconstrut the LCL and the ACL witout HTO. The result is excellent at 4 Years F-U.
. The place of deflexion High Tibial Osteotomy combined with ACL Reconstruction. This option must be
discussed when there is a grade B or C radiological changes without frontal malalignment.
Conclusions :
In the young athletic Acl deficient knee, one must take into account not only the symptoms (mainly instability, rarely pain) but also the long term outcome.
The pre-operative clinical examination and radiological check-up allow to detect:
- Previous Medial Meniscectomy
- Degenerative changes or Imbalance
- Delay Injury- Operation > 5 Years
In such a case don’t forget to discuss the "combined operation"… Thank You.
Bibliography
BONIN N, AIT SI SELMI T, DEJOUR H, NEYRET Ph,
Association Reconstruction du LCA et ostéotomie tibial de valgisation. A 11 ans de recul in « Le Genou du
Sportif », Sauramps Medical, Montpellier 2002 : 225-235.
BOSS A, STUTZ G, OURSIN C, GACHTER A. Anterior cruciate ligament reconstruction combined with valgus
tibial osteotomy (combined procedure). Knee Surg. Sports Traumatol Arthrosc 1995: 3: 187-91.
DEJOUR H, NEYRET P, BOILEAU P, DONELL ST.
Anterior cruciate reconstruction combined with valgus tibial osteotomy. Clin Orthop 1994: 220-8.
DEJOUR H, NEYRET P, BONNIN M.
Instability and osteoarthristis. Knee surgery, Volume 1, 1994, Chap N° 42, "Soft Tissue Injury", Section VII, p.
859-875.
DEJOUR H, WALCH G, NEYRET P, ADELEINE P.
Résultats des laxités chroniques antérieures opérées. A propos de 251 cas revus avec recul minimum de 3
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ans. Rev. Chir. Orthop. 1988: 74: 622-636.
DEJOUR H, DEJOUR D, AIT SI SELMI T, Chronic anterior laxity of the knee treated with free patellar graft
and extra-articular lateral plasty : 10 year follow-up of 148 cases, Rev. Chir. Orthop. 1999: 85: 777-89.
LATTERMANN C, JAKOB RP.
High Tibial osteotomy alone or combined with ligament reconstruction in anterior cruciate ligament-deficient knees. Knee Surg. Sports Traumatol Arthrosc 1996: 4: 32-8.
LERAT J.L., CHOTEL F, BESSE J.L., MOYEN B.
Les résultats après 10 à 16 ans du traitement de la laxité chronique antérieure du genou par une reconstruction du ligament croisé antérieur avec une greffe de tendon rotulien associée à une plastie extra-articulaire externe. A propos de 138 cas. Rev. Chir. Orthop. 84: 712-727, 1998.
NEYRET P, DONELL ST, DEJOUR H.
Results of partial meniscectomy related to the state of the anterior cruciate ligament. Review at 20 to 35
years. J.Bone Joint Surg (Br) 1993: 75: 36-40.
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NEYRET P, WALCH G, DEJOUR H.
Intramural internal meniscectomy using the Trillat technic. Long term results of 258 operations. Rev. Chir.
Orthop. 1988: 74: 637-46.
NOYES FR, BARBER-WESTIN SD, NEWETT TE.
High tibial osteotomy and ligament reconstruction for varus angulated anterior cruciate ligament-deficient
knees. Am.J.Sports Med 2000: 28: 282-96.
SELVA O, CHAMBAT P, TELOS WG, CASALONGA D, BONNIN M.
Reconstruction du LCA avec un recul moyen supérieur à 10 ans. Rev. Chir. Orthop. 1997: 83.
SHELBOURNE KD, GRAY T.
Results of anterior cruciate ligament reconstruction based on meniscus and articular cartilage status at the
time of surgery : five to Fifteen-year evaluations. Am.J. Sports Med. 2000 vol 28 (4): 446-452.
WU WM, HACKETT T, RICHMOND JC.
Effects of meniscal and Articular Surface Status on knee Stability, Function and Symptoms after anterior
cruciate ligament reconstruction. A long term Prospective Study. Am.J.Sports Med. 2002 vol 30(6): 845-850.
Antivalgus Osteotomies.
Giancarlo Puddu MD
Clinica Valle Giulia. Roma
I. Introduction: very often degenerative arthritis of the lateral compartment in the young or middle age
active patient is due to a lateral meniscectomy and or to a femoro tibial malalignement in valgus that can
be corrected with a high tibial or a distal femoral osteotomy.
II. Indications: congenital valgus, early lateral compartment cartilage deterioration after a lateral meniscectomy, initial lateral arthrosis due to overweight, sport abuse and congenital valgus.
III. Preoperative planning: can be made trough a standing radiography of both limbs which includes the
femoral heads and the ankles. For the diagnose and indication it is very useful the P.A radiograph at 45
degrees of knee flexion (fig. 1) and in the doubtful cases an MRI can help the decision (fig. 2). To provide a
satisfactory clinical result, femoral or tibial osteotomy must restore the alignment of the lower extremity
moving the mechanical axis to the 48-50% of the tibial plateau widht from medial to lateral (fig. 3).
IV. Distal femoral osteotomy: we prefer the opening wedge lateral osteotomy, since it is easier and more
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precise technique, using special femoral plates (Arthrex) with the same spacer of the HTO plates, but with
seven holes, three distal and four proximal (fig. 4). .
V. Surgical technique: a longitudinal skin incision is made on the lateral aspect of the distal third of the
tigh, then the fascia lata is splitted longitudinally. An Homan retractor is inserted posteriorly and a special
retractor anteriorly (fig. 5-6). Under fluoroscopy a guide pin is inserted obliquely four to six cm above the
lateral joint line and directed medially toward the femoral origin of the medial collateral ligament (fig. 7).
Preserving an hinge of intact cortical bone on the medial side, the osteotomy cut is open forcing the knee
in adduction and with the wedge opener in site (fig. 8) or with a new tool "the osteotomy Jack". The chosen
plate is positioned and fixed under a fluoroscopic control (fig. 9). Once the plate is secured to the femural
cortex (fig. 10), the defect is filled with an autologous graft, allograft or bone substitute according with the
preferences of the surgeon (fig. 11-12).
VII. Post-operative care: the knee is immobilized with a ROM brace in full extension that allows full range
of motion when unlocked. Passive flexion extension in a CPM, quadriceps setting and straight leg raising
exercises are begun the day after surgery.
After the opening wedge distal femoral osteotomy partial weight bearing is allowed after 45-60 days and
full weight bearing after 60-75 days. After the medial closing wedge HTO partial weight bearing is allowed
after 30 days and full weight bearing after 45 days.
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VI. Medial closing wedge HTO: The correction can be obtained trough a medial closing wedge HTO if the
resulting joint line has an obliquity not greater than 10 degrees (fig. 13-14).
VIII. Conclusions: dealing with degenerative arthritis in the young or middle age active patient with a valgus knee, prior any type of surgical treatment for the degenerated cartilage, it is a "must" to correct the
femoro-tibial alignment. The Author generally prefers the opening wedge distal femoral osteotomy and in
some special cases it is possible to make a closing wedge medial high tibial osteotomy.
Bibliography:
1. Brown GA, Amendola A : Radioghraphic evaluation and properative planning for high tibial osteotomies.
In Operative Techniques in Sports Medicine W. B. Saunders. 2000, 8: pp2-14.
2. Chambat P, Selmi TAS, Dejour D, et AL : Varus tibial osteotomy. In Operative Techniques in Sports
Medicine. W.B. Saunders. 2000. 8: pp 44-47.
3. Coventry MB: Proximal tibial varus osteotomy for osteoarthritis of the lateral compartment of the knee. J
Bone Joint Surg 1987, 69A:32-38.
4. Miniaci A, Grossmann SP, Jacob RP: Supracondylar femoral varus osteotomy in the treatment of valgus
knee deformity. American J of Knee Surg. 1990. 2:65-73
5. Puddu G, Franco V: Femoral antivalgus opening wedge osteotomy. In Operative Techniques in Sports
Med. W.B. Saunders 2000. 8: pp56-60
6. Rosenberg TD, Paulos LE, Parker RD et Al: The forty-five degree posteroanterior flexion weight-bearing
radiograph of the knee. J Bone Joint Surg. 1988. 70A: 1479-1483.
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ICL #11
TOTAL KNEE ARTHROPLASTY – NEW PERSPECTIVES ON DESIGN
Thursday, March 13, 2003 • Aotea Centre, ASB Theatre
Chairman: Paolo Aglietti, MD, Italy
Faculty: David Barrett, MD, United Kingdom, Timothy Wright, PhD, USA, Kelly Vince, MD, USA, Johan Bellemans,
Belgium, William Walsh, PhD, Australia, Mark Pagnano, MD, USA, and Fred Cushner, MD, USA
New Perspectives on Design in Total Knee Arthroplasty
Materials and Wear
Timothy Wright, PhD
Laboratory for Biomedical Mechanics and Materials
Hospital for Special Surgery, New York, NY
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Wear is now recognized as a major threat to the longevity of metal on polyethylene total knee replacements. Retrieval, simulator, clinical, and numerical studies have taught us much about the modes of wear,
the factors that affect them, and the stress conditions under which they occur. While this understanding
should lead us to rational choices for alternate bearing materials aimed at improving wear resistance, the
lack of a direct correlation between the amounts and type of wear and clinical performance hampers the
process. Nonetheless, sufficient evidence exists to suggest the rationale and efficacy of several materials
and fabrication techniques:
• Hard bearing materials (ceramics, hard coatings, oxidized zirconium);
• Elevated cross-linked ultra high molecular weight polyethylenes; and
• Direct compression molded ultra high molecular weight polyethylene
These alternatives must be considered in light of the problem that they are intended to address, the design
and performance conditions under which they would be expected to be advantageous, and the disadvantages they may possess. Hard bearings, for example, would be expected to influence abrasive and adhesive
wear mechanisms, but not markedly affect pitting and delamination types of wear. Similarly, elevated crosslinked polyethylenes should also improve abrasive and adhesive wear resistance (as has been shown when
these material are used in THR acetabular components), but concern about their reduced fracture toughness has raised questions about their suitability. Direct compression molding has a long record of performing well clinically, and recent data suggest that thermal conditioning such as occurs with molding may
provide improved wear resistance. More research is warranted, however, to create a more direct link
between material properties and wear. Even with such research, long-term clinical use remains the only
reliable method for assuring efficacy.
General Reference: Wright TM and Goodman SB: Implant Wear in Total Joint Replacement: Clinical and
Biologic Issues, Materials and Design Considerations. American Academy of Orthopaedic Surgeons,
Rosemont, IL, 2001.
Extraarticular tendon bone healing
W.R. Walsh, PhD, Australia
Biology of extraarticular tendon – bone healing
•
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How does time influence the following factors
o Mechanical properties
o Growth factors and BMPs expression
o Signal transduction - Smads
•
Can we improve tendon-bone healing
o Gene therapy
o Non invasive stimuli
•
Rehabilitation
•
Ultrasound
•
Magnetic fields
Whether to retain, sacrifice, or substitute for the posterior cruciate ligament remains controversial. There
are theoretical advantages to each technique and the excellent long-term clinical results of each ensures
that this controversy will continue. We will review the indications, technique, and results of cruciate retaining fixed bearing total knee arthroplasty.
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Fixed Bearing Cruciate Retaining Total Knee Arthroplasty
Mark W. Pagnano, MD
Department of Orthopedics
Mayo Clinic
Rochester, MN
INTRODUCTION
The controversy over retention or substitution of the posterior cruciate ligament continues. The excellent long-term results of total knee arthroplasties done with cemented condylar components of cruciatesacrificing, cruciate-substituting, and cruciate-retaining designs ensures that this debate will continue. An
assessment of the theoretical issues and clinical results of knee arthroplasty assists in analyzing this controversy. Important new data from the fields of biomechanics, histology, gait analysis, radiology, and from
the operating room have sharpened the posterior cruciate ligament debate. The interested reader can find
a recent review article that extensively explores each of those issues.11 Historically, the potential advantages of posterior cruciate ligament preservation are seen as maintenance of the joint line, femoral rollback, proprioception, maintenance of a central contact point of articulation, and low shear stress on the
bone-cement interface of the tibial component. The disadvantages of posterior cruciate ligament preservation are higher polyethylene stresses, a seesaw effect from femoral glide, difficulty in soft tissue balance,
worse range of motion in some series, and the fact that posterior cruciate ligament retention is not always
possible. 1 This review article will discuss the indications, technique, results, and complications of fixedbearing cruciate-retaining total knee arthroplasty.
INDICATIONS
There are certain situations where it is definitely advantageous to sacrifice the posterior cruciate ligament. The indications for a posterior cruciate ligament-preserving total knee arthroplasty are fixed flexion
of less than 30∞, varus less than 20∞, and valgus less than 25∞; joint subluxation of no more than 1 cm;
structurally intact posterior cruciate ligament; and technical ability of the surgeon. For patients with large
fixed deformities, soft tissue balance may require sacrifice of the posterior cruciate ligament to facilitate
proper soft tissue balancing. A surgeon's technical ability to balance the posterior cruciate ligament is
important. A lax posterior cruciate ligament will not be functional but is preferable to an excessively tight
posterior cruciate ligament. A tight posterior cruciate ligament will limit knee motion and may be a source
of pain and abnormal polyethylene wear patterns. Contraindications to posterior cruciate ligament preservation are severe fixed deformities, technical inability to balance the posterior cruciate ligament, and
anatomic abnormality of the posterior cruciate ligament, such as severe ligamentous degeneration and
absent patella.
TECHNIQUE
Preservation and balance of the posterior cruciate ligament must be combined goals of surgery. The
tibial attachment of the posterior cruciate ligament is located posterior and distal to the tibial plateau.
The tibial attachment of the posterior cruciate ligament is vulnerable to injury during the tibial resection
for total knee arthroplasty. Excessive bone resection from the proximal tibia (>1 cm) or a large posteriorly
sloped cut may jeopardize the tibial attachment of the posterior cruciate ligament. The posterior cruciate
ligament may be injured with a correct tibial resection by excessive posterior travel of the saw blade.
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Placing an osteotome anterior to the posterior cruciate ligament during tibial resection will protect it.
Once the tibial plateau bone has been removed, any remaining bone island anterior to the posterior cruciate ligament can be trimmed to allow placement of the tibial component.
Balancing the posterior cruciate ligament can be difficult. A slightly lax posterior cruciate ligament is
probably preferable to one that is excessively tight. Balance of the posterior cruciate ligament should be
assessed after correction of any varus or valgus ligamentous imbalance. Varus or valgus imbalance can
affect assessment of posterior cruciate ligament tension. Soft tissue balance always should be tested in
extension and in flexion. The gap or space between the femoral and tibial cut surfaces should be within 1
to 2 mm of each other in flexion and extension. Posterior cruciate ligament tension is assessed best with
the trial total knee prosthesis in place. An excessively tight posterior cruciate ligament will result in (1)
anterior translation of the tibia from beneath the femur; (2) anterior lift-off of the trial polyethylene from
the tibia tray in flexion; and/or (3) displacement of the femoral component in flexion. A useful test of the
relative balance of the posterior cruciate ligament is the POLO (for Pull-Out, Lift-Off) test introduced by
Scott.2 In this test, a trial reduction is done with a stemless tibial trial and a curved tibial insert. The pullout portion of the test is done at 90∞ of flexion and confirms that the posterior cruciate ligament is not too
loose if the tibial insert can not be subluxed (pulled-out) anteriorly from beneath the femur. The lift-off
portion is done while putting the knee through a range of motion as much as 120∞ and ensuring that the
tibial insert does not book open (lift-off) in flexion and indicate that the posterior cruciate ligament is too
tight. Scott postulates that if the posterior cruciate ligament is not too loose and not too tight then it
must be just right.
If the posterior cruciate ligament is excessively tight, the tension can be decreased by several techniques. Increased tibial bone resection only is appropriate if the knee is tight in flexion and extension. If
the knee is tight only in flexion, increasing tibial bone resection will leave the knee lax in extension, resulting in symptomatic instability. If the knee is tight only in flexion, the posterior slope of the tibial cut
should be assessed. The tibia normally has a 3∞ to 7∞ posterior slope. The amount of posterior slope cut
on the tibia will be dependent on the prosthetic design. Some implants have an inherent posterior slope
in the articular geometry and will require less posterior slope than knees with a flat geometry in the sagittal plane. Increasing posterior slope for the tibial resection will relax the posterior cruciate ligament.
Posterior tibial slope should not exceed 10∞ to avoid risk of injury to the tibial attachment of the posterior
cruciate ligament. Posterior cruciate recession consists of selective release of the anterior fibers of the
posterior cruciate ligament from their tibial attachment. Release of the anterior 10% to 20% of the posterior cruciate ligament will result in correct soft tissue balance. If greater than 75% of the posterior cruciate
ligament is released, a posterior cruciate ligament-substituting prosthesis should be considered. The
remaining 25% of the posterior cruciate ligament fibers may rupture with activity, leading to late instability.12 If the posterior cruciate ligament is released or absent, the tibial tray should be more conforming
because rollback does not occur. Therefore, the surgeon should match the constraints of the soft tissue
with the inherent constraints of the knee system being used.
RESULTS AND COMPLICATIONS
Early ligament-retaining prostheses, such as the polycentric and geometric designs, were not able to
provide predictable results.
The Miller-Galante I prosthesis had a relatively flat articular geometry and multiple sizes. The objective
was to reproduce normal knee kinematics. A study of 116 cemented prostheses at 3.5 years found 88%
good or excellent results.16 The range of motion was 105∞. Reoperation was required in 9% of the knees,
with revision in 6%. When inserted without cement the results with MG-I prosthesis have been termed
problematic. Berger et al. recently reported the 11 year followup of 113 consecutive cementless MillerGalante I total knees.3 Cementless femoral fixation in that study was deemed excellent while tibial components had a 6% rate of revision. The cementless metal-backed patella used in that series was poor with a
30% rate of revision. Those authors now have abandoned cementless fixation in total knee arthroplasty.
The posterior cruciate-sparing modification of the Total Condylar prosthesis was the Cruciate Condylar
prosthesis. The same femoral component was used for the Total and Cruciate Condylar implants. The tibial component of the Cruciate Condylar differed from that of the Total Condylar by having a posterior cruciate recess posteriorly. One objective of the cruciate condylar was to encourage femoral rollback and
motion.14 The long-term results of this design have been reported by multiple groups.5,8,13 A 9-year
study of 144 knees found 95% good or excellent results.10 Mean knee motion was 106∞. Tibial radiolucent
lines were present in 41%, of which 12% were progressive. Eight of the knees were failures. A review of 78
knees in 63 patients followed for a mean of 10 years at the Mayo Clinic was done.13 Good or excellent
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results were achieved in 93% of knees. Mean flexion was 102∞. Radiolucent lines were present adjacent to
57% of the knees. Using an end point of revision, survivorship was 96% at 10 years. There were no significant differences in survivorship, radiolucent lines, or knee scores between knees with an all-polyethylene or
metal-backed tibial component. Complications consisted of deep sepsis in 1%, loosening in 1%, and
supracondylar fracture in 3%. In yet another study of 42 knees followed at 11 years, 93% good or excellent
results were achieved.5 The range of motion was 104∞. Incomplete radiolucent lines were observed in
75%. The complication rate was 17% and the reoperation rate was 19%.
The Kinematic condylar prosthesis had metal backing of the tibial component and separate right and
left femoral components. The tibial plateau was flattened in the sagittal plane in an attempt to improve
motion by encouraging femoral rollback. A study of 192 knees followed for a mean of 6 years found 88%
good or excellent results.18 Mean knee motion was 109∞. Radiolucent lines were present adjacent to 40%
of the tibial and 60% of the patellar components. Reoperation was done in 11 knees, of which four were for
patellar loosening and one was for patellar fracture. In a study from the Mayo Clinic, 119 knees were evaluated at 10 years.9 Good or excellent results were achieved in 87%. Mean knee motion was 105∞. Joint line
height was changed a mean of 1 mm. A 2-mm radiolucent line was identified adjacent to two patellar, one
femoral, and one tibial component. Patellar component loosening was identified in six knees. Aseptic
loosening of the tibial and femoral component occurred in two knees. Using an end point of revision, survivorship was 96% at 10 years.
The Press Fit Condylar prosthesis was introduced with a keeled tibial component that was designed to
resist offset loading while preserving tibial bone stock. A recent survivorship analysis of 1000 consecutive
posterior cruciate retaining Press Fit Condylar knees revealed a 10-year survivorship free of mechanical failure of 98.7%.4 The Press Fit Condylar design is available in both cemented and cementless versions. A
comparison of 51 cemented and 55 cementless Press Fit Condylar knees was done at 10 years.6
Survivorship with revision as the end point was 96% for the cemented knees and 88% for the cementless
knees. Knee Society scores for pain and function were 92 and 72 for the cemented knees and 88 and 66
respectively for the cementless knees. Another 10-year followup study included 155 knees from an initial
study group of 235 knees.17 Cementless fixation was used in more than half of the femoral components
and less than 10% of the tibial components. Knee Society pain and function scores were 95 points and 84
points, respectively. Survivorship to revision was reported as 92% at 10 years.
The Anatomic Graduated Component prosthesis includes a one-piece metal-backed component with
direct compression molded polyethylene. A multicenter study of 2001 Anatomic Graduated Component
knees was done.15 The predominant diagnosis was osteoarthritis (91%) and the followup was from 3 to 10
years with 71 knees having 10-year data. Knee Society pain and function scores were 75 and 86 respectively
at last followup. A survivorship analysis (that excluded metal-backed patellar failures) predicted a 98% 10year survivorship free of revision. A consecutive series of 387 knees done with the Anatomic Graduated
Component design and using thin (4.4 mm) tibial polyethylene was reported at an average of 10 year followup. Survivorship with revision or loosening as the endpoint was 98.7% at 5 years, 95.4 percent at 10
years and 94.3% at 15 years.10
The Mayo Clinic experience with 11,606 primary total knee arthroplasties was presented at the 2002
American Academy of Orthopaedic Surgeons annual meeting (Dallas). Of 8052 posterior cruciate-retaining
total knee arthroplasties with a metal-backed tibial component, a 91% survivorship at 10 years was predicted. Therefore, the results of posterior cruciate-retaining prostheses appear durable. There appears to be
little difference between metal-backed and all-polyethylene tibial components or between meniscal and
fixed bearing implants. A longer duration of experience will be required to determine if these design differences affect long-term results.
References
1. Andriacchi TP, Galante JO: Retention of the posterior cruciate in total knee arthroplasty. J Arthroplasty
3:S13-S19, 1988.
2. Martin SD, Scott RD, Thornhill TS: Current concepts of total knee arthroplasty. J Orthop Sports Phys
Therap 28:252-261, 1998.
3. Berger RA, Jacobs JJ, Rosenberg AG, Barden RM, Galante JO: Problems with cementless total knee
arthroplasty at eleven years follow-up (Abstract). J Arthroplasty 16:251, 2001.
4. Berry DJ, Whaley A, Harmsen WS: Survivorship of 1000 consecutive cemented cruciate-retaining total
knee arthroplasties of a single modern design: results at a mean of 10 years (Abstract). J Arthroplasty
16:252, 2001.
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5. Dennis DA, Clayton ML, O'Donnell S, et al: Posterior cruciate condylar total knee arthroplasty. Clin
Orthop 281:168-176, 1992.
6. Duffy GP, Berry DJ, Rand JA: Cement versus cementless fixation in total knee arthroplasty: Results at 10
years of a matched group. Clin Orthop 356:66-72, 1998.
7. Insall JN: Historical Development, Classification, and Characteristics of Knee Prostheses. In Insall JN,
Windsor RE, Scott WN et al (eds). Surgery of the Knee. Ed 2. New York, Churchill Livingstone, 677, 1993.
8. Lee JG, Keating EM, Ritter MA, Faris PM: Review of the all-polyethylene tibial component in total knee
arthroplasty. Clin Orthop 260:87-92, 1990.
9. Malkani AL, Rand JA, Bryan RS, Wallrichs SL: Total knee arthroplasty with the kinematic condylar prosthesis: A ten-year follow-up study. J Bone Joint Surg 77A:423-431, 1995
10. Meding JB, Ritter MA, Keating EM, Faris PM: Total knee arthroplasty with 4.4 millimeters of tibial polyethylene: Average ten year follow-up study (Abstract). J Arthroplasty 16:252, 2001.
11. Pagnano MW, Cushner FD, Scott WN: Whether to preserve the posterior cruciate ligament in total knee
arthroplasty. J Am Acad Orthop Surg 6:176-187, 1998.
12. Pagnano MW, Hanssen AD, Lewallen DG, Stuart MJ: Flexion instability after primary posterior cruciate
retaining total knee arthroplasty. Clin Orthop 356:39-46, 1998.
13. Rand JA: A comparison of metal-backed and all polyethylene tibial components in total knee arthroplasty. J Arthroplasty 8:307-313, 1993.
14. Ritter MA, Gioe TJ, Stringer EA, Littrell D: The posterior cruciate condylar total knee prosthesis: A fiveyear follow-up study. Clin Orthop 184:264-269, 1984.
15. Ritter MA, Worland R, Saliski J: Flat-on-flat, non-constrained compression molded polyethylene total
knee replacement. Clin Orthop 321:79-84, 1995.
16. Rosenberg AG, Barden RM, Galante JO: Cemented and ingrowth fixation of the Miller-Galante prosthesis. Clin Orthop 260:71-79, 1990
17. Schai PA, Thornhill TS, Scott RD: Total knee arthroplasty with the PFC system: results at a minimum of
ten years and survivorship analysis. J Bone Joint Surg 80B:850-853, 1998.
18. Wright J, Ewald FC, Walker PS et al: Total knee arthroplasty with the kinematic prosthesis. J Bone Joint
Surg 72A:1003-1009, 1990.
Posterior Stabilized Knee Prostheses
Kelly Vince MD
General Principles
Posterior stabilized (PS) prostheses were first introduced at the Hospital for Special Surgery in New York in
1978 by John Insall and Al Burstein. The PS design featured a prominent tibial spine that articulated
against a transverse cam on the femoral component. This prevented posterior dislocation in flexion (especially for the patellectomy patient) and mechanically enabled femoral "rollback". It eliminated"kinematic
conflict", that resulted from retention of the posterior cruciate ligament with conforming articular surfaces.
The PS design should be regarded as "semi-constrained" as it provides no stability to varus or valgus
forces.
New perspectives
Three complications with early PS designs have largely been eliminated. Patellar fractures, complicated 7%
of early cases. Modification of the trochlear groove and improved surgical technique have decreased this
dramatically. Entrapment of rubbery scar on the deep surface of the quadriceps tendon, against the anterior edge of the trochlear groove with extensor, the so-called patellar clunk, has also largely been eliminated.
Dislocation of the spine and cam mechanism occurred after a design modification in 1989. Attention to the
flexion gap and design eliminated this problem.
Two recent studies identified wear on polyethylene spine, It is unlikely however that this is a significant
source of debris. The spine can also impinge on the anterior edge of the femoral component with hyperextension and may even break off producing late instability. Some of this data has probably been misinterpreted.
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In several closely followed groups of PS implants, osteolysis was not observed in either the earliest, nonmodular PS designs, or in the early modular version. An isolated group with severe osteolysis has emerged.
In some cases, with bilateral arthroplasty only one side has been affected. Shelf life and sterilization
method have not been implicated.
Posterior stabilization can be provided by highly conforming articulations (deep dished) or exaggerated
anterior "lipped" polyethylene. These have the advantage of easy surgical conversion and decreased
expense, but without the advantage of femoral rollback. As the complexity of femoral rollback, especially in
deep flexion, is appreciated, mobile bearing, PS implants have been developed.
Although most surgeons agree that the functional results obtained with modern total knee arthroplasty are
acceptable, it is clear that even with the most recent designs it is still impossible to duplicate the behaviour and functional performance of a normal knee.
ICLs
The Influence of Kinematics on Maximal Flexion after TKA
Prof. Dr. J. Bellemans
University Hospital Pellenberg
Katholieke Universiteit Leuven
Belgium
Recent kinematic studies have shown that modern TKA designs consistently provoke aberrant kinematics
compared to the normal knee, mainly due to the absence of the ACL and the inability to maintain a functional PCL.
With regard to roll-back, PS cam-post designs appear to perform better than PCL retaining knees, but only
in deeper degrees of flexion, usually only beyond 90 degrees.
Whether it is strictly necessary to try to obtain normal kinematics with our TKA designs, is still an open
debate.
It is clear however that the aberrant kinematics we have noted with the current designs, are the direct
cause of the flexion limit we see in many of our patients.
Furthermore they probably also are the basis for many of the discomforts associated with modern TKA,
such as difficulties in stair descent, chair rise, pivoting activities, frust instabilities, etc.
With regard to these issues, I believe there are two potential directions to improve our current TKA
designs; (1) by introducing the concept of guided-motion (intrinsic mechanism), or (2) by maintaining or
restoring the (extrinsic) determinants of kinematics, i.e. the cruciate ligaments, the joint configuration, and
the extraarticular structures.
Patella Design in TKA
Fred Cushner, MD
ISK Institute, New York, N.Y. USA
The complication rate in TKA from the resurfaced patella is well described in the literature. In fact, many
authors will leave the patella unresurfaced in an attempt to avoid patella complications following TKA. This
presentation will focus on not only the complications but also the design issues that can decrease the
occurrence of these complications. Design Issues for both primary as well as revision cases will also be
reviewed.
The initial discussion will focus on the complications that may be related to design issues. Studies
describing synovial entrapment as well as "patella clunk" will be discussed as well as the modifications that
have occurred with the PS design to eliminate these complications. Failure of metal backed patella will
also be reviewed and some attention will be given to the newer metal backed designs. Optimal patella
thickness and shape will also be reviewed.
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Current options in regards to the patella will be presented. The success of onset versus inset patella will
be reviewed as will the research looking at the benefits of a central peg versus the three-lug design.
Optimal patella thickness of the component will be reviewed as will proper patella placement as it pertains
to design features.
Design features of the trochlea will also be reviewed. The benefits of symmetrical versus asymmetrical
designs will be discussed as will other design features such as built in external rotation, trochlea depth,
trochlea alignment, and overall component alignment,
The revision setting with it’s inherent bone loss presents the surgeon with a difficult problem. Surgical
options with new patella designs that compensate for bone loss will be discussed
New Perspectives on Design in Total Knee Arthroplasty
Materials and Wear
Paolo Aglietti, MD
First Orthopaedic Clinic,
University of Florence, Italy
ICLs
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Balance between conformity and constraint is crucial to allow kinematics freedom maintaining good wear
properties. The emergence of the mobile-bearing articulating poly surfaces in TKR reflects the efforts to
optimised wear while dealing with complex function. Mobile bearing designs have not yet proven to provide better results and increased function but long-term clinical experience and laboratory data from knee
joint simulators seem to suggest that mobile bearing designs have an advantage in reducing polyethylene
wear (particularly pitting and delamination). Laboratory wear studies investigated correlations between
pattern of motion of articular surfaces and wear. New mobile bearings with conforming "low-stress" articular geometries and motion at the undersurface create an additional challenge in minimizing top-surface
and back-surface wear. Comparative clinical an laboratory data on wear and stresses in fixed and mobile
bearings are showing a trend toward less amount of wear, in particular delamination, for mobile bearings.
Errors in rotational component positioning may affect many functions of TKR especially the patello-femoral
tracking. Mobile bearing tibial designs may be more forgiving than fixed bearing designs to minor rotational malalignments.
ICL #12
Tendinopatia Rotuliana –
Aquiliana en deportista.
Dr Sergio Montenegro
Clínica Arauco– Clínica Dávila
Santiago-Chile
Patellar-Achilles
Tendinopathy in soccer placer.
Sergio Montenegro MD.
Arauco Clinic-Davila Clinic
Santiago-Chile
Diapositiva 2:
Slide 2.
TENDÓN
• Estructura anatómica de tejido conectivo fibroso
denso y regular que ancla el músculo al hueso.
• Funciones:
–Transmite fuerza muscular al esqueleto con mínima pérdida de energía, absorbiendo golpes bruscos para evitar el daño muscular.
–Rol de propiocepción.
Tendon
Anatomic structure made of connective, fibrous,
dense tissue, which anchors muscle to bone.
Functions:
- It transmits muscular force to the skeleton with
minimum loss of energy, absorbing abrupt blows
to avoid muscular damage.
- Propioceptive roll.
Diapositiva 3
TENDÓN: TIPoS
• Intrasinoviales
–Tendones flexores
• Extrasinoviales
–T. Cuadricipital, rotuliano, aquiliano.
Slide 3
Tendon Types
• Intrasinovial
-Flexing Tendons
• Extrasinovial
-Quadricipital tendon, Patellar tendon, Achilles
tendon.
Diapositiva 4.
Tendón
• Tejido compuesto:
–Colágeno tipo I ( 85% peso seco del t.)
–Colágeno tipos III, IV, V, VI, XII
• Proteoglicanos: (polisacáridos proteicos)
• Decorina (principal.)
• Biglicano
• Lumicano
• Fibromodulina.
• PGs : compuestos por glicosaminoglicanos
(polímeros disacáridos.
Slide 4
Tendon
Composition of the Tissue:
- Collagen type I (85% dry weight of the total)
- Collagen types III, IV, V, VI, XII
- Proteoglycan: (polysaccharide proteins)
- Decorin (principal)
- Biglicane
- Lumican
- Fibromodulin
- Proteoglycan (PGs): made up of glicosaminoglicans (polymeric disacharides.
Diapositiva 5:
Tendón : Bioquímica
• PGs en tendón:
-Rol importante en las fibras de colágeno.
-Rol en separar las bandas de fibras
-Así disminuir el stress de ruptura.
• Fibronectina (composición de la matriz celular)
Slide 5:
Tendon: Biochemistry
• Proteoglycans (PGs) in tendon:
- Important Roll in collagen fibers.
- Roll in separating the fiber bands
- Thus to diminish stress of rupture
• Fibronectin (composition of the cellular matrix)
ICLs
TENDON INJURIES IN FOOTBALL (SOCCER)
Thursday, March 13, 2003 •` Carlton Hotel, Carlton I
Chairman: Alberto Pienovi, MD, Argentina
Faculty: Ramon Cugat, MD, Spain and Sergio Montenegro, MD, Chile
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ICLs
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-Rol importante en la adherencia de la matriz celular
• Fibras elásticas: (dentro del Tendón)
-Capacidad de absorción de golpes.
-Mantención del patrón ondulante del colágeno.
- Important roll in the adhesion of the cellular
matrix.
• Elastic Fibers: (within the tendon)
- Capacity of absorption of traumas.
- Maintaining of the wave pattern of collagen.
Diapositiva 6:
TENDÓN
BIoLoGÍA Y BIoMECÁNICA
• Las propiedades MECÁNICAS están determinadas principalmente. por el colágeno:
–Resistencia tisular: (directamente proporcional):
• Contenido total de colágeno
• Densidad de uniones (cross-links) estables.
• organización del colágeno.
• Diámetro fibrilar.
–Fuerzas de Tensión: (inversamente proporcional.):
• Contenido de colágeno tipo III.
• Radio PG/colag.
Slide 6:
Tendon
BIOLOGY And BIOMECHANICS
The mechanical properties are determined mainly
by collagen:
-Tissue Resistance:(directly proportional)
-Total contents of collagen
-Density of unions (cross-links) stable
-Organization of the collagen
-Fibrillar Diameter:
-Force Tension: (inversely proportional.)
Contents of collagen type III.
- Ratio Proteoglycan /collagen
Diapositivas: 7
TENDINoPATIAS
Slide: 7
TENDINOPATHIES
• Causas : carga de entrenamiento excesivo.
–Con relación a:
• Biotipo atlético.
• Capacidad metabólica.
• Correcta ejecución de ejercicios.
• Apoyo correcto del pié.
• Zapatilla adecuada.
• Balance muscular (evaluación isokinética)
• Superficie de entrenamiento.
• Clima.
Causes: excesive training load.
-In relation to:
- Athletic Biotype.
- Metabolical Capacity.
- Correct performance of exercices.
- Correct leaning of the foot
- Adequate sport shoe.
- Muscular Balance (isokinetic evaluation)
- Training Surface
- Climate
Diapositiva 8:
LESIÓN TENDINoSA
• Directa
- Contusión
- Laceración
• Indirecta
- Sobrecarga x tensión aguda
- Lesión unión M-T.
- Fractura por avulsión.
• Lesiones por sobreuso:
- Microtrauma repetitivo
Slide 8:
Tendon Injury:
Direct:
-Contusion
-Laceration
Indirect: overloading by acute tension.
M-T union injury.
Fracture by avulsion
Injuries caused by overuse:
-Repetitive microtrauma
Diapositiva 9:
LESIÓN TENDINoSA
• Degenerativa:
- Tendinosis:
• T. De Aquiles porción libre.
• T. Patelar
• Entesopatía : (más frecuente. T. Aquiles)
- Haglund
• Rotura (parcial o completa).
• Inflamatoria : Peritendinitis o paratenonitis.
• Bursitis: traumática, séptica, Enfermedad
Slide 9
Tendon Injury:
• Degenerative:
-Tendinosis:
• Achilles Tendon free portion
• Patellar Tendon
• Enthesopathy: (more frequent Achilles Tendon)
-Haglund
Rupture (partial or complete).
Inflammatory: Peritendinitis or paratenonitis.
Bursitis: traumatic, septic,
Systemic disease
Diapositiva 10:
LESIoNES X SoBREUSo
• Más frecuente en deportes de alta exigencia:
–Carrera, ciclismo, remo, natación.
• Deportes que requieren aplicación de movimientos explosivos:
–Volleyball, Raquetball, Basquetball, Golf, Tenis.
Slide 10:
INJURIES CAUSED BY OVERUSE
More frequent in high demanding sports:
Racing, cycling, rowing, swimming;
sports that require applying explosive movements:
-Volleyball, Raquetball, Basquetball, Golf, Tennis.
Diapositiva: 11
LESIoNES X SoBREUSo
Slide: 11
Injuries by overuse.
• LESIoNES Centro Alto Rendimiento (20012002): 1320.
–Lesiones tendinosas
:355 (26.9%)
High Performance Center injuries (2001-2002):
1320.
-Tendon Injuries:
355 ( 26.9%)
–Lesiones musculares
:291 (22.1%)
-Muscular Injuries :
–Fracturas por stress
:22
( 1.6%)
-Fractures caused by stress:
22 (1.6%)
–Periostitis
:54
( 4.1%)
-Periostitis:
54 (4.1%)
(45.3%)
-Others:
–otras
598 (54.7%
291 (22.1%)
ICLs
Sistémica.
(45,3%)
598(54.7%)
Diapositiva 12:
LESIoNES x SoBREUSo
• 50 - 60% de todas las lesiones deportivas.
• Se deben a una falla en la adaptación de las
células y la matriz extracelular al uso repetitivo y
cargas submáximas.
• La capacidad adaptativa y reparativa del T. se
puede sobrepasar cuando es estirado repetidamente más de 4 - 8% de su longitud original.
Slide 12:
Injuries by overuse.
• 50 - 60% of all the sport injuries.
• They are due to a fault in the adaptation of the
cells and the extra cellular matrix to the repetitive
use and submaximal loads.
• The adaptive and repairing capacities of the tendon can be exceeded when it is stretched repeatedly more than 4 - 8% of its original length.
Diapositiva 13:
LESIoNES TENDINoSAS
• MECANISMoS:
–1.- Stress aplicado al tendón dentro de su capacidad de carga fisiológica, y que excede la capacidad
adaptativa basal de las estructuras, o, es tan frecuente que no hay tiempo suficiente para que el
tejido tenga la capacidad de lograr una reparación
intrínseca.
Slide 13:
Tendon Injuries:
• Mecanisms:
-1. - Stress applied to the tendon within its physiological lifting capacity, and that exceeds the basal
adaptive capacity of the structures, or, it is so frequent that there isn’t enough time for the tissue to
have the ability to obtain an intrinsic repair.
Diapositiva: 14
LESIoNES TENDINoSAS
• MECANISMoS:
–2.- Aplicación brusca de carga única pesada que
produce una lesión inicial, que debilita la estructura del tendón y subsecuentemente, cargas fisiológicas repetitivas, no permiten la maduración
de la cicatrización del tejido.
Slide: 14
Tendon Injuries:
• Mecanisms:
2. -Abrupt application of heavy unique load that
produces an initial injury, that weakens the structure of the tendon and that, subsequently repetitive physiological loads, do not allow the maturation in the healing of the tissue.
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ICLs
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Diapositiva 15:
HISToPAToLoGÍA
• TENDINITIS
• TENDINoSIS
• PARATENDINITIS
• RUPTURAS PARCIALES
• oTENDINoPATÍA: término genérico, para lesiones
en o alrededor del tendón por sobreuso
Slide 15:
HISTOPATHOLOGY
• TENDINITIS
• TENDINOSIS
• PARATENDINITIS
• PARTIAL RUPTURES
• TENDINOPATHY: generic term, for injuries in or
around the tendon by overuse
Diapositiva 16:
TENDINoSIS
• Degeneración intrínseca tendinosa sin signos
clínicos o histológicos de INFLAMACIÓN intratendinosa.
• No siempre es sintomática (30% personas > 35
años).
• Puede debutar con la ruptura del tendón.
• ¿Porqué en algunas personas produce dolor,
que llegue a una indicación operatoria?
• ¿Por qué en otras es tan asintomático, que
llega a causar ruptura?
Slide 16:
TENDINOSIS
• Intrinsic tendinose degeneration without clinical
or histological signs of intratendon INFLAMMATION.
• It not always is symptomatic (30% people > 35
años).
• Can make a debut with the rupture of the tendon.
• Why is it so painful, in some people that it leads
to a surgical recommendation?
• Why in others, it’s so painless, that it leads to
rupture?
Diapositivas 17:
-SoBRECARGA REPETITIVA SoBRE TENDÓN
-Alteración Función celular
-Alteración Actividad Metabólica
- Respuesta reparativa no efectiva
-INFLAMACIÓN
-Liberación de: PGs, citoquinas
enzimas citolíticas
Slide 17:
-REPETITIVE OVERLOAD ON THE TENDON:
-Alteration of Celular Function
-Alteration of Metabolic Activity
-Non-efective repairing answer
-INFLAMMATION
-Liberation of: Proteoglycans, cytokines cytolitical
enzimes.
Diapositiva 18:
TENDINoSIS
• Afecta todos los componentes del tendón:
(colágeno, fibroblastos, matriz extracelular).
• Colágeno:
– Lisis de fibras de colágeno.
– Pérdida de orientación paralelismo fibras. de
colágeno.
– Disminución de la densidad del colágeno.
– Microrupturas con depósitos de: Glóbulos Rojos,
fibrina, fibronectina.
– ondulaciones irregulares de fibras. de colágeno.
– Aumento. Colágeno tipo III (reparación).
– Disminución. birefrigencia ( Mo con luz polarizada).
– Áreas de proliferación angioblástica (hiperplasia
angiofibroblástica (Nirschl, 1979):
• Neovascularización y aumento de celularidad.
Slide 18:
TENDINOSIS
• It afects all the components of the tendon: (collagen, fibroblasts, extracelular matrix).
• Collagen:
- Lysis of collagen fibers.
- Loss of parallel direction in fibers of collagen.
- Diminution of the density of the collagen.
- Microruptures with deposits of: Red globules,
fibrin, fibronectin.
- Irregular fiber waves of collagen.
- Increase collagen type III (repair).
- Diminution birefrigerence (Optic Microscope
with polarized light).
- Areas of angioblastic proliferation (angiofibroblastic hyperplasia (Nirschl, 1979):
• Neovascularization and increase of cellularity.
Diapositiva 19:
TENDINoSIS
• Patrones de degeneración del colágeno:
– Hipóxica
– Hialina
– Mucoide o mixoide
Slide 19:
TENDINOSIS
• Patterns of degeneration of collagen:
- Hypoxemia
- Hyaline
- Mucoid or mixoid
- Fibrinoid
- Lipomatous
- Calcifications, fibrocartilaginous and bone metaplasia.
Diapositivas 20:
TENDINoSIS
• Es el resultado final de un Nº de sutiles procesos patológicos con diferentes manifestaciones
histológicas.
• Se puede asociar a paratenonitis.
Slide 20:
TENDINOSIS
• It is the final result of a number of subtle pathological processes with different histological manifestations.
• It can be associated to paratenonitis.
Diapositiva 21:
TENDINoSIS
FACToRES ETIoLÓGICoS
• Hipoxia tisular: Trauma repetitivo --> lesión
microvascular.
• Radicales libres de oxígeno --> lesión tisular.
• Ejercicio --> aumento de temperatura intratendón (43-45ºC) es > que la que soportan los
fibroblastos.
• Edad.
• Inmovilización
• Hormonas (E2).
• Drogas (corticoides, ATB fluoroquinolonas)
alteran la matriz.
Slide 21:
TENDINOSIS:
ETHIOLOGICAL FACTORS
• Tissue Hypoxemia: Repetitive trauma --> injury
in the microvascular structure.
Free Radicals of Oxygen --> tissue injury.
• Exercise --> increase of the intratendon temperature (43-45ºC) is > than the one that supports
fibroblasts.
• Age.
• Inmovilization
• Hormones (E2).
• Drugs (corticoids, antibiotics fluoroquinolones)
alter the matrix.
Diapositiva 22:
TENDINoSIS
FACToRES EXTRÍNSECoS
• Inestabilidad articular: (hombro - m. rot.).
• Mal alineación:
– pronación de el tobillo
– genu valgo
– Aumento anteversión femoral.
• Disminución de flexibilidad.
• Debilidad muscular. o desbalance muscular.
• Sobrepeso.
• Tipo de carga (tensión, compres.,etc).
• Patrón de carga (concéntrico, excéntrico)
• Magnitud de la fuerza (única, repetida).
Slide 22:
TENDINOSIS.
EXTRINSECAL FACTORS
• Articular Instability to: (shoulder - patellar
movement.)
• Bad alignment:
- pronation of the ankle
- genu valgo
- Increase in femoral anteversion.
• Diminution of flexibility.
• Muscular Weakness or muscular inbalance.
• Overweight.
• Type of load (tension, compression, etc).
• Pattern of load (concentric, excentric)
• Magnitude of the force (unique, repeated).
Diapositiva 23:
TENDÓN EFECTo DE INMoVILIZACIÓN
• Disminuye su fuerza tensil.
• Disminuye resistencia.
• Disminuye peso total.
• A un mes:
– Disminución de:
• la celularidad
• organización de fibras. de colágeno
• Diámetro de las fibras. de colágeno.
• Uniones de colágeno.
• Contenido de agua y de PGs se altera.
• No está claro el mecanismo por el cual ocurre y
si está o no mediado por células.
Slide 23:
TENDON INMOVILIZATION EFECT
• Diminishes its tensile force.
• Diminishes resistance.
• Diminishes its total weight.
• To a month:
- Diminution of:
• cellularity
• Organization of collagen fiber.
• Diameter of the fibers of collagen.
• Unions of collagen.
• The contents of water and proteoglycans is
altered.
• The mechanism by which it happens is not clear
ICLs
– Fibrinoide
– Lipomatosa
– Calcificaciones, fibrocartilaginosa y metaplasia
ósea.
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and if it is or not mediated by cells.
ICLs
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Diapositiva 24:
TENDoN
EFECTo DE REMoVILIZACIoN
• Recuperación de las propiedades bioquímicas. y
biomecánicas.
• Aceleración de la síntesis de colágeno y de las
uniones.
Slide 24:
Tendon
REMOVILIZATION EFECT
- Recovery of biochemical and biomechanical
properties.
- Accerelation of the synthesis of collagen and of
the unions
MoVILIZACIÓN PRECoZ MUY IMPoRTANTE PARA
MINIMIZAR EFECToS ADVERSoS.
EARLY MOVILIZATION IS VERY IMPORTANT TO
DIMINISH ADVERSE EFFECTS.
Diapositiva 25:
TENDÓN
CAMBIoS CoN LA EDAD
• Aumenta contenido de colágeno insoluble.
• Aumento. maduración de uniones de colágeno.
• Aumento. diámetro de fibras de colágeno.
• Disminuye. turn over del colageno.
• Disminución contenido de agua y PGs.
• Disminución. Celularidad y vascularización.
• Desde 3a década (¿disminución? Actividad física?).
• Si se agregan calcificación. o degeneración.
Mucoide.
• > susceptibilidad de lesión y < capacidad. de
cicatrización.
Slide 25:
TENDON
Aging Changes
• The contents of insoluble collagen increases.
• Increasing in the maturation of the unions of collagen.
• Increasing in the diameter of the fibers of collagen.
• The turn over of collagen decreases.
• The contents of water and Proteoglycans
decreases.
• Diminution of cellularity and vascularization.
• From the 3rd decade (diminution of physical
activity?).
• Calcification and Mucoid degeneration are
added.
• There is more susceptibility of injury and less
capacity of healing.
Diapositiva 26:
TENDÓN
CAMBIoS CoN LA EDAD
• Estudios experimentales sugieren que el mantener el ejercicio hace más lenta estas alteraciones
bioquímicas.
Rodeo S.A, Isawa K. (oKU, AAoS, Sp Med 2)
Slide 26:
TENDON
Ageing Changes
• Experimental researches suggest that maintaining exercise make these biochemical alterations
slower.
Rodeo S.A., Isawa K. (OKU, AAOS, Sp Med 2)
Diapositiva 27:
LESIoNES TENDINoSAS CLASIFICACIÓN
• 1.-Según sitio anatómico:
– Unión M-T
– osteotendinoso (tenoperiostal)
(tendinopatías de inserción).
– En el tejido. Tendinoso.
• 2. - Patrón histopatológico.
• 3. - Nivel funcional.
Slide 27:
TENDON INJURIES: CLASIFICATION
• 1-According to anatomical site:
- Muscular –tendon union
- Osteotendinous (tenoperiostal) (tendinopathies
of insertion).
- In the tendinose tissue.
• 2. - Histopathological Pattern.
• 3. - Functional Level.
Diapositiva 28:
LESIoNES TENDINoSAS CLASIFICACIÓN
• 3. - Nivel funcional:
INTENSIDAD DEL DEPoRTE NIVEL
SINToMAToLoGÍA. DEPoRTE
Leve
1
Sin dolor Normal
2
Dolor en ejerc. extremo,
desaparece sin actividad.
Slide 28:
TENDON INJURIES CLASIFICATION
• 3. - Functional Level:
SPORTS
INTENSITY LEVEL SYMTOMATOLOGY.
Mild
1
No pain
2
Pain in extreme sport,
disappears without activity
3
4
Severo
5
6
Duele 1-2 hrs. post-ejercicio
Dolor aumenta. con cualquier
Actividad y dura 4-6 hrs.
Dolor inmediato dura 12-24 hrs.
Dolor actividad. diaria
Moderate
3
4
Severe
5
6
It hurts for 1-2 hrs. after exercise
Pain increases with any activity
and lasts 4-6 hrs.
Immediate pain lasts 12-24 hrs.
Pain in daily activity
Diapositiva 29:
LESIoNES TENDINoSAS DIAGNoSTICo
• Rx.
• Ecotomografía
• TAC
• RNM
Slide 29:
TENDON INJURIES DIAGNOSIS
• RADIOGRAPH
• ULTRASONOGRAPHY
• CT scan
• MRI
Diapositiva 30
PAToLoGÍA TENDINoSA ECoGRAFÍA
-Ventajas
Desventajas
** bajo costo
** alta inversión inicial
** acceso a cualquier tend. ** experiencia
** estudios superficiales ** resultados operador** dinámico e interactivo
dependiente
** permite comparar
** artefactos (simulan
** uso Doppler-color
pato-logía)
y angio de poder ("Powerangio")
Slide 30:
TENDON PATHOLOGY ULTRASONOGRAPHY
Advantages
Disadvantages
** low cost
** high initial investment
** access to any tendon ** experience
** superficial studies
** results operating** dynamic and interactive dependant
** allows to compare
** artifacts (simulate
** use Doppler-color and pathology)
“Power-angio”)
Diapositiva 31:
Tendinosis Rotuliana
• Rodilla del saltador.
• Típica lesión por sobrecarga.
• Atletas que someten aparato. extensor a
movimiento. intensos y repetidos : (carreras explosivas)
– Volleyball, Basquetball, Salto alto y largo.
• Más frecuente. en hombres entre 18 y 25 años.
• Localización: (Ferretti A, 1986)
– Inserción proximal T. rotuliano:
65%
– Inserción distal cuádriceps: 25%
– Inserción distal T. rotuliano :
10%
Slide 31:
Patellar Tendinosis
• Jumping knee
• Typical injury by overload.
• Athletes who put the extensor apparatus under
intense and repeated movements: (explosive
races)
- Volleyball, Basquetball, High Jump and Long Jump.
• Its more frequent in men between 18 and 25
years old.
• Location: (Ferretti To, 1986)
- Proximal Insertion of the patellar tendon.: 65%
- Distal insertion of quadriceps: 25%
- Distal insertion of Patellar Tendon: 10%
Diapositiva 32
TRATAMIENTo GENERAL
• AINE / AIES
• Fisio - KNT
• Crioterapia post-ejercicio.
• ondas de choque
• Brace de tendón rotuliano.
• Rodillera con refuerzo infrapatelar.
Slide 32:
Patellar Tendinosis
GENERAL TREATMENT
• NSAID/SAID
• Physical therapy
• Post-excercise Cryotherapy
• Shock wave therapy
• Patellar tendon Brace.
• Knee protector with infrapatellar reinforcement.
Diapositiva: 42
TENDÓN RoTULIANo
TRATAMIENTo QUIRÚRGICo
• PASoS: video artroscopia asociada–Resección
paratendón.
–Liberación tendón e incisiones de descarga
(tenotomías longitudinales) y escarificación (resec-
Slide: 42
PATELLAR TENDON
SURGICAL TREATMENT
• Steps: knee arthroscopy associated
Paratendon resection.
-Releasing of the tendon and incisions of unloading (longitudinal tenotomies) and scrafication
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Moderado
3.93
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ción áreas degenerativas).
–Resección peritenon y adherencias.
–Resección sinovial alterada.
–Perforaciones rótula o tibia, resección ósea–
(resection of degenerative areas).
-Peritenon removing and adhesion removals.
-Synovial resection altered.
-Drillings in patella or tibia, bone resection
Diapositiva 47
RESULTADoS
• 40 Pacientes - 44 tendones.
• Seguimiento X: 25 m (rango 3 - 60 meses)
• Sexo: H: 36
M: 4
• Edad : X: 28 años (rango: 17 - 46).
• Intervenciones previas:
–Abierta
:
0
–Artroscópica
:
4
Slide 47
RESULTS
• 40 patients - 44 tendones.
• Follow up durring: 25 months (rank 3 - 60 months)
• Sexo: M: 36
W 4
• Edad: X: 28 years (rank: 17-46)
• Previous surgeries:
-Open:
0
-Arthroscopics:
4
Diapositiva 48
RESULTADoS
• Localización:–Polo proximal de rótula: 3 (
6,8%)
–Polo distal de rótula: 33 (75,1%) –
tercio medio del tendón: 5 (11,3%)
–Inserción distal en tibia: 3 (6,8%)
Slide 48
RESULTS
• Localization:- Proximal Pole of patella: 3 (6,8%)
- Distal Pole of patella: 33
(75,1%) – Third middle portion of the tendon: 5
(11,3%)
- Distal insertion in tibia: 3 (6,8%)
Diapositiva 49:
RESULTADoS
• Deportes :
–Fútbol
:
–Atletismo
:
–Basketball
:
–Rugby
:
–Patín carrera :
–Pesas
:
–Ciclismo
:
–Tenis
:
–Volleyball
:
–Hockey
:
–Sin deporte :
11 (1 árbitro)
5 ( 2 maratón)
4
3
4
4
2
3
3
1
4
Slide 49:
RESULTS
• Sports:
-Soccer: 11 (1 umpire)
-Athletics: 5 (2 marathon)
-Basketball: 4
-Rugby: 3
-Roller skate racing: 4
-Weights: 4
-Cycling 2
-Tennis: 3
-Volleyball: 3
-Hockey: 1
-Without sports: 4
No:
:
:
:
:
Slide 50:
RESULTS
• Sports Return:
-YES : 34 (T) 85% NO: 6 (T)
- Average Time
: 4.7 Months
-Competitive level:
• Equal
: 30
• Minor
: 4
Diapositiva 50:
RESULTADoS
• Retorno deportivo:
–SÍ:
34 (T) 85%
–Tiempo promedio
–Nivel competitivo
• Igual
• Menor
Diapositiva 51:
- RESULTADoS
- Complicaciones :
- Precoces :
- Hematoma herida: 3
- Infección superficial: 0
- Infección profunda: 0
- Tardías :
- Disestesias zona opuesta.:12
- Dolor anterior en cuclillas: 0
3.94
6 (T)
4,7 meses.
30
4
Slide 51:
RESULTS
- Complications:
- Early:
- Hematoma of the surgical incision: 3
- Superficial Infection: 0
- Deep Infection: 0
- Late complications :
- Dysesthesia opposite zone.:12
- Ventral Pain in haunches: 0 -
Reoperaciones:
0
Frame 56:
REINTEGRo ACTIVIDAD FÍSICA
• Ausencia total de dolor
• Movilidad articular de rodilla normal.
• Flexibilidad muscular-tendinosa mejor que antes
de la cirugía.
• Equilibrio isokinético Fuerza 1-extensores de
rodilla.
• Déficit isokinético < al 10% con el segmento contralateral.
• Capacidad. aeróbica normal para enfrentar la
actividad. Física.
• No sentir ningún tipo de temor al realizar actividad física.
Diapositiva 68:
LESIÓN TENDINoSA PREVENCIÓN
• Acondicionamiento físico.
• Calentamiento previo al ejercicio.
• Elongación pre y post actividad.
• Evitar ejercicios unidireccionales repetidos.
• Adaptación al terreno.
• Equipo adecuado.
- Reinterventions: 0
Slide 56:
PATELLAR Tendinosis
RETURN TO FISICAL ACTIVITY
• Total absence of pain.
• Articular mobility of knee normal
• Muscular- tendinose flexibility better than before
the surgery.
• Isokinetic balance strength F1- knee extensors.
• Isokinetic deficiency < at 10% with the opposite
segment.
• Normal aerobic capacity to do physical activity.
• No to feel any kind of fear while doing physical
activity.
Slide 68:
TENDON INJURY PREVENTION
• Physical Conditioning.
• Previous warming before excercises.
• Pre and post stretching related activities.
• Avoid unidirectional repeating excercises.
• Accomodating to surface.
• Adequate equipment.
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-
ARTHROSCOPIC TREATMENT OF THE FIRST PATELLA DISLOCATION
Alberto Pienovi MD
Centro de Traumatología y Ortopedia San Isidro. ARGENTINA
Web page: www.ctosanisidro.com
Purpose The purpose of this study was to perform a prospective non-randomized evaluation of arthroscopic
treatment of first patella dislocation.
Introduction: The treatment of the first patella dislocation is still a controversial matter.
Several papers evaluate the results of non-operative treatments and of different surgical techniques, reaching several conclusions.
In this study we present and analyze the results of arthroscopic treatment using our technique in 29 cases.
Method: Twenty-nine cases were evaluated in 28 patients. One patient was bilateral. Six of these cases
referred a previous sensation of patella instability or laxity. The average age was 20,3 (range l6 to 36) 6 were
men and 3 women. All patients had a previous MRI and underwent a clinical and radiographic evaluation of
the contra lateral knee, looking for conditions that predispose this pathology. The average period between
the accident and the surgery was of 15 days (3/32 days). The arthroscopic treatment consisted in the reparation of the medial retinaculum with absorbable suture plus shrinkage with radio frequency and lateral
retinacular release using an electrobistoury. In one case the anterior tibial tubercle was transferred using a
miniopen technique, as the patient presented a high patella
The knee was immobilized with a brace for 3 weeks, and afterwards rehabilitation started immediately. The
practice of contact sports was authorized 5 to 6 months postoperative.
Results: From the 29 cases of this group, 56% presented conditions predisposing this pathology in the contra lateral knee.
3.95
The average follow-up was 26.7 months (8 lo 44), obtaining 86.21 % of excellent or very good results
according to the UCLA evaluation table. No recurrent dislocations occurred in this group, 13.79% of the
results were regular, corresponding to those cases presenting, after surgery, some pain or sense of instability when practicing sports.
Discussion:
Acute patella dislocation occurs mainly in young athletes, most of them presenting conditions predisposing this pathology. In these cases we expect the best results using this technique.
Arthroscopic treatment of the first patella dislocation presents low morbility and allows an efficient and
early recovery of its normal anatomy. We present a technique that repairs the injured tissues associated to
an arthroscopic realignment of the patella, with predictable results.
Arthroscopic Treatment for Patellar Tendinitis in Soccer players
Alberto Pienovi MD
Centro de Traumatología y Ortopedia San Isidro. ARGENTINA
Web page: www.ctosanisidro.com
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INTRODUCTION
Patellar tendinitis or "jumper’s knee" is an injury frequently occurring in athletes performing eccentric
strengths of the patellar tendon. It mainly involves kicking or jumping activities, such as volleyball, basketball, hockey, soccer and athletics. This lesion may also be related to any physical activity that requires an
effort of the lower extremities.
The use of "hard" surfaces in sports fields and the wide practice of soccer have also influenced the increase
of this pathology.
The lesion presents micro-traumas and micro-lesions in the tendinous tissue and its osseous insertion,
where small degenerative and necrotic areas are presented. It may resemble other tendinitis, such as those
of the Achilles tendon or tennis elbow.
The pathogenesis of the lesion has been poorly defined, and the physiopathology has been related to the
clinical aspect.
It clinically appears as spontaneous and intense pain related to physical activity, usually in the upper area
of the tendon or in the lower pole of the patella. It may eventually be bilateral.
X-rays may exceptionally show calcifications or an increase of density in the area. Echographies are useful
and present an hypoechoic image, edema and peri-tendinous irregularities. The MRI allows to evaluate the
stages and to compare images with the contralateral knee.
The treatment is controversial even nowadays among specialists in sports medicine. It greatly depends on
the athlete’s requirements, the sport and whether the athlete is professional or amateur.
We consider that a pathology not responding to conservative treatment should be surgically treated, therefore avoiding the progression of the affection to more severe levels.
CLASSIFICATION
We used the clinical 4-stage classification of Blazina et al.
Stage I: Pain after practicing sports. It does not alter the performance.
Stage II: Pain before practicing sports. It partially decreases while practicing sports and appears again after
finishing the effort. It decreases the athlete’s performance.
Stage III: Pain remaining before, during and after the effort. The athlete is unable to compete.
Stage IV: Partial or complete rupture of the tendon.
MATERIAL AND METHOD
Twenty-one cases are presented corresponding to twenty-one patients who underwent an arthroscopic
treatment. Seventeen were male and four female, showing a high predominance of men.
The cases presented here were all Stage III, being the athletes unable to practice sports normally. They all
had undergone several previous treatments.
The average age was twenty-three point seven years (range nineteen to thirty-two)
They were all athletes, twelve amateur and nine collegiate.
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The average duration of symptoms was eight months (range five to twenty-three months)
During the postoperative period, a brace is placed in extension position only as protection.
Physiotherapy with active and passive mobility is indicated as tolerated. The rehabilitation program must
be prompt and aggressive but avoiding inflammation.
Training under resistance and strengths and return to sports vary in each patient between one to two
months.
We consider that the keys of the surgical technique are:
"The creation of a conformable pre-tendinous cavity"
"The decompression of the tendon through a wide opening of the pre-tendinous fascia"
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SURGICAL TECHNIQUE
We performed the arthroscopic surgery with local anesthesia and without tourniquet.
Initially, an intra-articular arthroscopy allows the diagnosis and treatment of associated injuries, exploring
the distal pole of the patella that occasionally presents hypertrophic bursitis that is debrided.
With an eighteen needle, the maximum pain area is marked, which generally coincides with the lower pole
of the patella.
Two longitudinal portals, slightly oblique to allow movements, twenty-five mm over and under the area are
enough to work at ease. A pre-tendinous cavity is created with blunt instruments.
A wide debridement is performed until the peri-tendon is arthroscopically observed. The anterior decompression of the tendon is achieved by cutting longitudinally the peri-tendinous fascias with a retractile
knife. They are generally three layers that may be independent or forming an only fascia.
With the exposed tendon, a new debridement is performed, if necessary, and with a knife wide longitudinal
cuts are carried out over the tendon on the same direction of its fibers.
RESULTS
The average follow-up was two point four years (range fourteen to thirty-seven months).
The evaluation method was the one established by Popp et. al. with modifications.
Excellent: full return to sports.
Good: Sporadic symptoms
Fair: Less competitive level
Poor: no improvement
Fifteen patients (seventy-one point four percent) presented excellent and very good results; four patients
(nineteen point oh five percent) fair results with return to sports with poorer performance and two patients
(nine point fifty-two percent) poor results.
CONCLUSIONS
Patellar tendinitis is a pathology that presents great clinical variations and histological degeneration of the
patellar tendon and its osseous insertions.
This pathology extremely disables the athlete. It initially appears unimportant, but it progressively decreases the athlete’s performance or leads to the interruption of sporting activities.
The arthroscopic treatment shows good results and is indicated in stage III cases or in those cases in which
conservative treatments have failed, therefore, preventing the progression of the pathology.
The surgical treatment together with rehabilitation allows quicker healing and tissue regeneration.
Arthroscopy opens a new field in the minimum invasive surgical treatment of these affections.
3.97
ICL #13
KNEE MENISCUS REPAIR
Thursday, March 13, 2003 • Carlton Hotel, Carlton II
Chairman: Prof. Dr. med. Dieter Kohn, Germany
Faculty: Andrew Amis, DSc, United Kingdom, Romain Seil, MD, Germany, and Uffe Joergensen, Denmark
The questions
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Meniscus reconstruction is a routine procedure in orthopaedic sports medicine. It has been shown that
suturing a meniscus back to the capsule will restore knee function and prevent degenerative changes at
least for 10 years. Some studies suggest that reconstruction of the more frequent intrasubstantial tears is
able to prevent the knee from changes as seen after meniscectomy. The reputation of partial meniscectomy
has suffered during the past years because we have become aware that this procedure is followed by early
degenerative changes of the joint as well. But the long term prognosis after reconstruction of intrasubstantial meniscal tears is still unsecure. The scientific basis of this procedure is still weak. Lots of questions
have remained:
Does the reconstructed meniscus function similarly or equal to an intact meniscus?
Which types of meniscus reconstruction can prevent or delay early degenerative arthritis?
Which lesions do better with partial resection compared to reconstruction?
How strong must the reconstruction be to allow healing?
How can we enhance healing if this is really necessary?
What are the complications with the "innovative" devices?
What are the long-term effects and side-effects of the biodegradable materials?
Which procedures are dangerous for the hyaline cartilage. Because injury to the cartilage during reconstruction procedures is very common but has hardly ever been evaluated scientifically?
Does the benefit of ease of insertion justify the costs and possible side-effects of "innovative devices"?
ICL 13 will not solve all these problems, but we will address the following questions:
-
What is our contemporary biomechanical knowledge about meniscus function?
What does laboratory testing tell us about actual techniques of meniscus reconstruction?
What are the most effective techniques today to suture a meniscus?
What the are the actual techniques of non-suture meniscus repair?
LABORATORY TESTING OF MENISCUS REPAIR
Romain Seil, M.D.
University Hospital
University of Saarland
Homburg / Saar, Germany
The purpose of laboratory testing is to evaluate and to improve the mechanical factors of meniscus healing, either for meniscus sutures or for new devices for meniscus repair. In order to be as close as possible
to the clinical setting, the biomechanical analysis of meniscus repairs can be performed at different time
points:
1. Immediately after repair (t = 0) in so-called time-zero cadaver studies.
2. During the healing period (t = 0 – 12 weeks). Such studies have been performed either in tissue-culture
models or in animal studies.
3.98
3. After the initial healing phase (t > 12 weeks). So far, the biomechanical properties of meniscus repair at
this period have only been addressed in animal studies.
T=0
The tensile fixation strength is analyzed on a materials test system (INSTRON®, ZWICK®, MTS®). A uniaxial load is applied in tension to the repaired meniscus in an axis parallel to the long axis of the suture or
the implant to be tested. The ultimate tensile load is recorded on a load-displacement curve. In most of
the studies a complete vertical tear was created at the entire periphery of the meniscus in order to prevent
any load transfer other than at the repair site. Usually 1 suture / device was analyzed per test. The tears
were standardized in each study, allowing for a comparison within one study.
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Most of the studies dealing with laboratory testing of meniscus repair have been performed as time-zero
studies, testing the tensile fixation strength of either sutures (KOHN D, 1989; RIMMER MG, 1995; POST
WR, 1997; SEIL R, 2000) or sutures compared to fixation devices (ALBRECHT-OLSEN PM, 1997; ASIK M,
1997 & 2002; DERVIN GF, 1997; BARBER FA, 2000; BECKER R, 2001 & 2002; BELLEMANS, 2002; BOENISCH
UW, 1999; SEIL R, 2000; SONG EK, 2000; ARNOCZKY SP, 2001; RANKIN CC, 2002; WALSH SP, 2001; FISHER
SR, 2002).
The first laboratory study on meniscus repair was published in 1989 (KOHN & SIEBERT). The authors compared open meniscus repair techniques to arthroscopic techniques. They incriminated the circumferential
horizontal collagen fiber orientation for the higher ultimate failure strengths (UFS) for vertical sutures compared to horizontal sutures. They further showed the importance of the superficial, dense fibers which
increased the UFS of mattress sutures compared to sutures including only deeper collagen layers. Post
(POST WR, 1997) showed that the UFS of meniscus sutures were strongly dependent on the suture material. In a recent study (SEIL R, 2000) we did not find any difference between horizontal and vertical PDS 2-0
mattress sutures, whereas vertical sutures became increasingly stronger with increasing strength of the
suture material. The UFS of horizontal sutures was limited at approximately 100 N. This suggests that the
maximum UFS of horizontal sutures is limited by the tissue quality of the meniscus and the strength of the
suture material, whereas the failure strength of vertical sutures depends mainly on the strength of the
suture.
Regarding the testing conditions there were several factors which varied from study to study and which
might have influenced the results. There is no common agreement concerning the design of the tests,
which makes comparisons between different studies more difficult. These variables include the type of tear,
the age and origin of the specimen (human, bovine and porcine menisci have been used) and the crosshead speed (displacement rate) at which the tests were performed, varying from 50 to 750 mm/min in different studies. With the new fixation devices laboratory testing becomes even more complex as the UFS
may be affected by the insertion angle of the device and the number of barbs engaged in the meniscal tissue (BOENISCH UW, 1999). This might explain the large variations encountered with some devices in different studies. These variations were especially apparent for the Meniscus Arrow® (BionX Implants Inc.,
Blue Bell, PA, USA) and the BioStinger® (Linvatec Corp., Largo, FL, USA). ARNOCZKY found a mean UFS of
57.7 N (+/- 13.8) for the Meniscus Arrow® and 35.1 N (+/- 6.7) for the BioStinger®, whereas BARBER et al.
found a mean UFS of 33.4 N (+/- 8.4) and of 78.3 N (+/- 30.6) respectively. Some of these devices reached
values which were close to 2-0 UPS sutures. However, the mean UFS of new devices were generally inferior
to sutures.
T = 0 – 12 WEEKS
This period corresponds to the postoperative healing phase. During this phase the operated knee may be
protected by a brace and a specific rehabilitation program is generally applied. Two mechanical factors
have been analyzed during this phase: the evolution of tensile fixation strength of the sutures / devices
over time (ARNOCZKY SP, 2001; DIENST M, 2001) and the effect of repetitive loading on meniscus repairs
(SEIL R, 2000 and 2001).
The effect of hydrolysis time on sutures / devices has been analyzed in a tissue culture model. In these
studies, the menisci were incubated after the repair over a defined period, after which the UFS were evalu3.99
ated. Using PDS sutures DIENST et al. (2001) found a significant decrease of the UFS of nearly 50%, whereas the UFS of nonabsorbable suture material did not change. ARNOCZKY & LAVAGNINO (2001) found no
decrease in UFS for the BioStinger®, the Meniscus Arrow® and the Clearfix Screw® (Mitek Products Inc., A
Division of Ethicon, Inc., Westwood, MA, USA) over a period of 24 weeks. However, the SD staple®
(Surgical Dynamics, Inc., Norwalk, CT, USA) and the Mitek Meniscal Repair System® (Mitek Products Inc., A
Division of Ethicon, Inc., Westwood, MA, USA) showed a complete loss of fixation strength after 24 and 12
weeks respectively.
Repetitive, cyclic loading of meniscus sutures showed the appearance of a gap of 3-4 mm with a load of 40
N between the 2 parts of the meniscus (SEIL, 2000). Furthermore, failures of the sutures occurred. Cyclic
testing of new devices showed failures as well. No failures were noted with the Meniscus Arrow®. This was
incriminated to the large head of the device. Compression of the repair site lead to an increase of the UFS
of 60% (STÄRKE, 2002).
T > 12 WEEKS
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During this phase laboratory testing of meniscus repair has essentially been performed in animal studies
analyzing the failure strength of the scar tissue (Tab.1). Even if KAWAI (1989) found UFS after 3 months of
up to 80 % of the intact control meniscus in dogs, most other authors found data which were far from normal. This shows that meniscal scar tissue does not reach its initial biomechanical properties after a period
of 3 to 4 months. KOUKOUBIS et al. (1997) observed an increase in UFS of repaired dog menisci over a 1year-period.
Port J, 1996
Kawai Y, 1989
Roeddecker K, 1994
Animal model
Goat
Dog
Rabbit
Time after surgery (months)
4
3
3
Koukoubis TD, 1997
Guisasola I, 2002
Dog
Sheep
12
1,5
Ultimate failure strength
30 % of normal tissue
Up to 80 % of normal
Fibrin glue: 42 %
Suture: 26 %
No therapy: 19 %
SD staple > suture
< 50 % of normal
Tab. 1
FORCES ACTING IN VIVO
In vitro-testing of meniscus repair has been performed with tensile forces only. The tensile forces acting on
meniscal repairs in vivo are unknown. Furthermore, there are not only tensile, but also compressive and
shear forces acting on the meniscus. These complex forces are difficult to reproduce in vitro. Only few studies tried to analyze this important question. KIRSCH and KOHN investigated the tensile forces acting on
posterior horn sutures of the medial meniscus in a cadaver model. They were lower than expected as they
never exceeded 10 N.
NEW COMPLICATIONS
New complications have been described with the new fixation devices, among which rail-shaped chondral
lesions on the femoral condyle after meniscus repair with Meniscus Arrows®. In a biomechanical cadaver
study we analyzed whether meniscus sutures and different types of devices induced meniscofemoral contact areas and contact stresses (SEIL, 2001). We found no contact areas / stresses with conventional mattress sutures. However, using the Meniscus Arrow®, the Clearfix Screw® and the Meniscal Dart®, contact
areas / stresses could be found in 89%, 54% and 29% of the analyzed cases respectively. They were significantly smaller / lower for those devices with a small head.
CONCLUSIONS
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1. The maximum failure strength of horizontal sutures is limited by the tissue quality of the meniscus AND
the strength of the suture material, whereas the failure strength of vertical sutures depends mainly on the
strength of the suture.
2. The maximum failure strength of new meniscus fixation devices is generally inferior to the failure
strength of sutures.
3. The varying results of failure strengths for a given type of suture / fixation device between different studies indicates that a standardized testing model is needed.
4. The biomechanical properties of meniscus sutures / fixation devices after meniscus repair may vary over
time, depending on the material’s properties of the suture / fixation device.
5. In vivo forces acting on the repair site are not completely known, but they might be lower than expected.
6. The exact biomechanical properties of the scar tissue of a healed meniscus are unknown.
7. The complication potential of new devices must be evaluated further.
ARNOCZKY SP, LAVAGNINO M. Tensile fixation strengths of absorbable meniscal repair devices as a function of hydrolysis time. An in vitro experimental study. Am J Sports Med, 29 (2): 118-123, 2001
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LITERATURE:
ALBRECHT-OLSEN, P.; LIND, T.; KRISTENSEN, G.; FALKENBERG, B.: Failure strength of a new meniscus
arrow repair technique: biomechanical comparison with horizontal suture. Arthroscopy., 13 : 183-187, 1997.
ASIK M, SENER N, AKPINAR S, DURMAZ H, GÖKSAN A. Strength of different meniscus suturing techniques. Knee Surg Sports Traumatol Arthroscopy, 5: 80-83, 1997
ASIK M, SENER N. Failure strength of repair devices versus meniscus suturing techniques. Knee Surg
Sports Traumatol Arthrosc 2002; 10 (1): 25-9
BARBER FA; HERBERT MA: Meniscal repair devices. Arthroscopy 2000; 16 (7): 754-6
BECKER R, STARKE C, HEYMANN M, NEBELUNG W. Biomechanical properties under cyclic loading of
seven meniscus repair techniques. Clin Orthop 2002; (400): 236-45
BECKER R, SCHRODER M, STARKE C, URBACH D, NEBELUNG W. Biomechanical investigations of different meniscal repair implants in comparison with horizontal sutures on human meniscus. Arthroscopy 2001;
17 (5): 439-44
BELLEMANS J, VANDENNEUCKER H, LABEY L, VAN AUDEKERCKE R. Fixation strength of meniscal repair
devices. Knee. 2002; 9(1):11-4
BOENISCH, U.W.; FABER, K.J.; CIARELLI, M.; STEADMAN, J.R.; ARNOCZKY, S.P.: Pull-out strength and stiffness of meniscal repair using absorbable arrows or Ti-Cron vertical and horizontal loop sutures. Am.J
Sports Med, 27: 626-631, 1999.
DERVIN, G.F.; DOWNING, K.J.; KEENE, G.C.; MCBRIDE, D.G.: Failure strengths of suture versus biodegradable arrow for meniscal repair: an in vitro study. Arthroscopy., 13: 296-300, 1997.
DIENST M, SEIL R, KUEHNE M, KOHN D. Cyclic testing of meniscal sutures after in vitro culture. 20th
Annual Meeting Arthroscopy Association of North America, Seattle, Washington, 2001
FISHER SR, MARKEL DC, KOMAN JD, ATKINSON TS. Pull-out and shear failure strengths of arthroscopic
meniscal repair systems. Knee Surg Sports Traumatol Arthrosc 2002; 10 (5): 294-9
GUISASOLA I, VAQUERO J, FORRIOL F. Knee immobilization on meniscal healing after suture: an experimental study in sheep. Clin Orthop 2002; (395): 227-33
KAWAI, Y.; FUKUBAYASHI, T.; NISHINO, J.: Meniscal suture. An experimental study in the dog. Clin.Orthop.,
286-293, 1989.
KIRSCH L; KOHN D; GLOWIK A: Forces in medial and lateral meniscus sutures during knee extension – an
in vitro study. J Biomech, 31 (Suppl.1): 1041999.
KOHN, D.; SIEBERT, W.: Meniscus suture techniques: a comparative biomechanical cadaver study.
Arthroscopy., 5: 324-327, 1989.
KOUKOUBIS, T.D.; GLISSON, R.R.; FEAGIN, J.A.J.; SEABER, A.V.; SCHENKMAN, D.; KOROMPILIAS, A.V.;
STAHL, D.L.: Meniscal fixation with an absorbable staple. An experimental study in dogs. Knee.Surg.Sports
Traumatol.Arthrosc., 5: 22-30, 1997.
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PORT J; JACKSON DW; LEE TQ; and SIMON TM: Meniscal repair supplemented with exogenous fibrin clot
and autogenous cultured marrow cells in the goat model. Am J Sports Med, 24: 547-555, 1996.
POST, W.R.; AKERS, S.R.; KISH, V.: Load to failure of common meniscal repair techniques: effects of suture
technique and suture material. Arthroscopy., 13: 731-736, 1997.
RANKIN CC, LINTNER DM, NOBLE PC, PARAVIC V, GREER E. A biomechanical analysis of meniscal repair
techniques. Am J Sports Med 2002; 30(4): 492-7
RIMMER, M.G.; NAWANA, N.S.; KEENE, G.C.; PEARCY, M.J.: Failure strengths of different meniscal suturing
techniques. Arthroscopy., 11: 146-150, 1995.
ROEDDECKER, K.; MUENNICH, U.; and NAGELSCHMIDT, M.: Meniscal healing: a biomechanical study.
J.Surg.Res., 56: 20-27, 1994.SEIL, R., RUPP, S., KOHN, D. Cyclic testing of meniscus sutures. Arthroscopy 16
(4), 1-8, 2000.
SEIL R; RUPP S; DIENST M; MÜLLER B; BONKHOFF H; and KOHN D: Chondral lesions after arthroscopic
meniscus repair using meniscus arrows. Arthroscopy, 2000.
SEIL R; RUPP S; JURECKA C; REIN R; and KOHN D: Der Einfluß verschiedener Nahtstärken auf das
Verhalten von Meniskusnähten unter zyklischer Zugbelastung. Unfallchirurg, 2000.
ICLs
SEIL, R.; RUPP, S.; and KOHN, D.: Cyclic testing of meniscal sutures. Arthroscopy, 16: 505-510, 2000.
SEIL R, RUPP S, JURECKA C, KOHN D. Biomechanical evaluation of new meniscus fixation devices.
ISAKOS, 14th -18th may 2001, Montreux, Switzerland
SEIL R, RUPP S, MAI C, PAPE D, KOHN D. The footprint of meniscus fixation devices on the femoral surface
of the medial meniscus: a biomechanical cadaver study. ISAKOS congress Montreux, 2001
STÄRKE C, BERTH A, BECKER R. Der Einfluss axialer Kniebelastung auf die biomechanische Stabilität von
Meniskus-Refixationstechniken. 19th Kongress der Deutschsprachigen Arbeitsgemeinschaft für
Arthroskopie (AGA), october 11-12th, Innsbruck 2002
SONG EK, LEE KB. Biomechanical test comparing the load to failure of the biodegradable meniscus arrow
versus meniscal suture. Arthroscopy 15 (7): 726-732, 1999
WALSH SP, EVANS SL, O’DOHERTY DM, BARLOW IW. Failure strengths of suture vs. biodegradable arrow
and staple for meniscal repair: an in vitro study. Knee, 2001; 8(2): 129-33
Treatment of Meniscus Tears in ACL-Reconstructed Knees
K. Donald Shelbourne, MD
Methodist Sports Medicine Center
Indianapolis, IN
I. Factors to consider
• ACL intact or ACL deficient knee
• Medial versus Lateral
• Degenerative versus Nondegenerative
• Stable versus Unstable
• Treatment choices
• Remove
• Repair
• Leave alone
• Postoperative Rehabilitation – does it matter?
II. Meniscus tears
• Mensicus tears observed at the time of ACL reconstruction are different than tears that occur in ACLintact knees
• In general, meniscus tears in ACL-intact knees have extensive degeneration
• Meniscus tears after an acute ACL tear are traumatic and occur mostly in the posterior and peripheral
part of the meniscus
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•
•
•
Meniscus tears in chronic ACL-deficient knees can be degenerative or nondegenerative depending on
the number and severity of instability episodes
There is no correlation between joint line tenderness and meniscus tears with an acute ACL injury
(Shelbourne et al. AJSM 1995)
My research and experience is mostly with patients who have ACL insufficiency
This presentation of my algorithm for treatment applies to meniscus tears in conjunction with ACL
reconstruction
III. History of treatment
• Before arthroscopy was available, most of the meniscus tears associated with ACL instability were not
observed or treated
• 82-83 before using arthroscopy consistently with ACL reconstruction--35% had either a LMT or MMT
• Expected patients to return because of meniscal symptoms at some time after ACL reconstruction –
didn’t happen!
• When arthroscopy was used (from 1984 on), many meniscus tears were observed
• 67%of patients had either LMT or MMT
• Felt compelled to either repair or remove the tears even though the tears were not symptomatic
• Leaving the tear alone was not considered
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•
IV. Lateral Meniscus Tears
• Usually incidental findings, especially with acute injury
• Acute injury – 62% have LMT
• Chronic – 49%
• Found that many LMTs will heal if left in situ (FitzGibbons and Shelbourne, AJSM 1995)
• Peripheral, posterior, or posterior horn avulsion tears
V. Peripheral Stable Medial Meniscus Tears
• With acute ACL injury, common tear is a peripheral undersurface tear (tension side)
• They can be missed easily
• Adding sutures above the tear caused the tear to "pucker" forward
• Added vertical sutures
• 2nd look revealed that most vertical sutures did not remain but meniscus healed
• Current treatment is to leave the tear in situ and treat with trephination
VI. Study by Shelbourne/Rask (Arthroscopy 2001)
• To determine the long-term clinical sequelae of salvageable, non-degenerative, peripheral vertical
MMTs seen at the time of ACL reconstruction
• Meniscus tears – Stable > 1 cm but < 2 cm in length treated with abrasion and trephination
• Meniscus tears – Unstable > 2 cm in length, treated with suture repair (> 50% of the circumference
Subsequent arthroscopy
Group
Left in Situ
Abrade/Trephine
Suture
No Tear
•
•
N
139
233
176
526
Subsequent scopes
N
(%)
15
(10.8)
14
(6)
24
(13.6)
14
(2.9)
Time Post-op (years)
2.5
2.3
4.3
5.0
Subsequent scopes performed at a mean of 3.7 years after ACL reconstruction
Of patients who had subsequent arthroscopy, 45% of the AT and SITU groups and 75% of the
SUTURE group had the procedure at > 2 years after ACL reconstruction
Conclusions
• Of unstable peripheral vertical MMTs treated with suture repair, 13.6% failed, with most re-tears
occurring at greater than 2 years after repair
• Of stable peripheral vertical MMTs treated with abrasion and trephination alone and no direct
fixation, most (94%) remain asymptomatic at a mean of 3.6 years after treatment
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VII. Bucket-Handle Meniscus Tears
• Occur mostly in patients who have chronic ACL instability
• When the meniscus becomes locked, the patient seeks treatment because of pain and lack of function
• Found that patients who had flexion contractures from locked bucket-handle tears and then underwent
ACL reconstruction and treatment for the locked meniscus had a high rate of arthrofibrosis
(Shelbourne/Johnson, AJSM 1993)
• Began doing two-staged procedures
• Meniscus treatment followed by rehabilitation to regain full range of motion
• ACL reconstruction as an elective procedure
• Gave us an opportunity to evaluate meniscal healing when patients had an unrestricted rehabilitation
program after meniscus repair
• Initially used 8-10 sutures for the repair because we knew patients would be weight bearing quickly
after surgery
• Believe that weightbearing stabilizes the meniscus by pushing it to the capsule
• Follow-up arthroscopy at the time of ACL reconstruction
• Meniscus is healed but very few sutures present
• Realized that the vascular access channels created from placing the sutures were key
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•
•
•
•
Approach to Repair of Bucket-Handle Meniscus Tear
Used a rasp and multiple needle sticks to stimulate bleeding
Began using 4-6 sutures in the anterior half of the meniscus
Left the posterior section in situ because we know these tears can heal
Basically converted an unstable tear to a stable tear
•
•
•
Study by Shelbourne/O’Shea (AJSM, In Press)
Between 1987 and 1999, 1470 chronic ACLs performed
Eighty-eight patients had a locked bucket-handle meniscus tear that severely limited knee extension
The average amount of knee flexion contracture at evaluation was 20 + 10 degrees
Results: 52 patients with 55 repairs
Healed
N
N
(%)
Meniscus Zone
White/white
43
21
(49)
White/Red
11
8
(73)
Red/Red
1
1
(100)
Total
55
30
(54.5)
•
•
•
•
•
•
•
Partially Healed
N
(%)
17
(40)
2
(18)
0
(0)
19
(34.5)
No Healing
N
(%)
5
(11)
1
(9)
0
(0)
6
(11)
At an average follow-up of 4.3 + 3.1 years, 4 additional menisci (7%) were symptomatic and required
meniscectomy
At final follow-up, 36 of 43 (83.7%) of meniscus repairs in the white/white zone remained asymptomatic
All repairs in the red/white and red/red zone remained asymptomatic
At a mean of 60 months, the average modified Noyes score was 89.9 + 8.6 (range 67-100)
No patients had difficulty regaining full range of motion
In the short-term after meniscal repair, bucket-handle tears, even in the white/white zone, appear
healed or partially healed.
Only 1 of the 19 menisci that were partially healed at the time of ACL reconstruction became symptomatic and required removal
VIII. Now what?
• We know that stable peripheral MMTs can heal in situ without suture repair treatment
• We know that repairs of unstable locked MMTs can heal well
• Now we need to know, does the repair of large BH MMTs give better results than removal? (do they
function like a normal meniscus)
Repair vs. Meniscectomy: Assumptions
• Need to "Save the mensicus" at all costs
• Meniscectomy dooms the knee to future degenerative changes
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•
•
•
Meniscus repair has to be better than meniscectomy
Performed two separate studies – Bucket Handle MMT and BH LMT
To determine the level of superiority meniscus repair had above partial meniscectomy for isolated,
unstable, bucket-handle meniscus tears with regard to objective and subjective results
•
•
•
•
•
•
•
•
•
Methods
Patients did not have any other meniscus tears, chondral damage, or other ligamentous injury
56 patients underwent meniscus repair (REP group)
• 30 nondegenerative tears
• 26 degenerative tears
99 patients had a tear that was felt to be unsalvageable (REM group) –
• 4 nondegenerative
• 95 degenerative
Subjective Results
REM group – 87/99 patients available at 7.8 years after surgery (range 2 to 19 years)
REP group – 51/55 patients available at a mean of 8.9 years after surgery (range 3 to 15)
Total Score: Repair vs. Removal
• REM group: 90.9 + 16.7 points
• REP group: 90.9 + 11.6 points
Further evaluation for the REP group based on whether the tear was degenerative or nondegenerative
Not enough numbers in the REM group – almost all degenerative
REP group
• Deg tear: 87.1 + 12.9 points
• Non-deg tear: 93.9 + 9.8 points (P=0.0123)
IKDC Results: Overall Grade
Normal
N
(%)
Group (N)
Repaira (24)
20
(83)
Nondegenerative (12) 11
(92)
Degenerative (12)
9
(75)
Removal (52)
41
(79)
•
•
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IX. Bucket-Handle Medial Meniscus Tears (Shelbourne/Carr, AJSM, In Press)
• Between 1982 and 1995, 155 patients met the inclusion criteria
• Unstable BH MMT
• Meniscus tear > 2 cm extending in more than half of the meniscus
• The meniscus, when probed, could be pulled into the intercondylar notch or was displaced in the notch
Nearly Normal
N
(%)
3
(13)
1
(8)
2
(17)
8
(15)
Abnormal
N
(%)
1
(4)
0
(0)
1
(8)
3
(6)
Severely Abnormal
N
(%)
0
(0)
0
(0)
0
(0)
0
(0)
Available for
• REP group – 25 patients at 7.1 years p.o.
• REM group – 56 patients at 6.0 years p.o.
Graded as
• Normal
• Nearly normal
• Abnormal
• Severely abnormal
IKDC overall grade: (No patient had a grade of Severely Abnormal)
Remove Group
Repair Group
N
(%)
N
(%)
Grade
Normal
26
(46)
13
(52)
Nearly Normal
25
(45)
9
(36)
Abnormal
5
(9)
3
(12)
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Radiographic Grade: No Patient had a grade of Severely Abnormal; one patient refused x-rays)
Remove Group
Repair Group
Grade
N
(%)
N
(%)
Normal
41
(79)
20
(83)
Nearly Normal
8
(15)
3
(13)
Abnormal
3
(6)
1
(4)
•
•
•
•
•
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•
•
Results
All but one of the 15 patients who did not have a normal radiographic grade had > 5 years f/u
5 patients in REP group and 1 patient in REM group required second surgery on the meniscus
4 of 5 patients in the REP group had a degenerative type tear at the time of the initial treatment
Discussion
Study by O’Shea showed "healing" of the meniscus or at least a low incidence of symptoms requiring
removal (9%)
However, no statistically significant difference between meniscus repair and partial meniscectomy, at
least with the follow-up of 6 to 8 years
Further sub-analysis based on type of tear
Results of degenerative tears worse than nondegenerative tears (87 vs. 94 points)
X. Bucket-Handle Lateral Mensicus Tears (Shelbourne/Dersam)
• Between 1982 and 1995, 91 patients had isolated, unstable bucket-handle lateral meniscus tears
• "Isolated" means the patient did not have a medial meniscus tear or any articular cartilage damage
•
•
•
•
•
•
•
•
•
•
Methods
67 tears were seen as repairable
Repaired with an inside-out technique
Usually, 2-3 vertical sutures were used
24 tears were felt to be irreparable
Tears usually had complex vertical and horizontal tears
Postoperative rehabilitation was the same program for both the repair and removal groups
Subjective follow-up – Modified Noyes Knee Survey
Objective follow-up
• IKDC
• Standing PA 450 weightbearing view
Results
Minimum two year subjective follow-up:
• Repair group - 57 patients, mean 7 years post-op
• Remove group - 21patients, mean 11.1 years post-op
Minimum 2 year objective follow-up:
• Repair group - 30 patients, mean 5.9 years post-op
• Remove group - 12 patients, mean 8.1 years post-op
Subjective scores
Category
Total Score
Pain
Swelling
Stability
Activity
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Repair Group
Mean ± SD
92.5 ± 9.4
16.8 ± 3.1
8.9 ± 1.5
19.2 ± 2.l2
18.8 ±3.1
Remove Group
88.7 ± 13.2
14.0 ± 4.0
9.0 ± 1.3
19.0 ± 2.2
17.7 ± 3.9
P-value
0.2014
0.0478
0.8078
0.5083
0.0732
IKDC Results: (No patient had a grade of Severely Abnormal)
Overall Grade
Radiographic Grade
Repair
Remove
Repair
Remove
N (%)
N (%)
Grade
N (%)
N (%)
Normal
16 (53)
2 (11)
26 (87)
10 (83.3)
Nearly Normal
11 (37)
8 (42)
3 (10)
1 (8.3)
Abnormal
3 (10)
2 (40)
1 (3)
1 (8.3)
•
•
Subsequent symptoms after repair: Only 2 of 67 patients (3%) required a subsequent arthroscopy
because of symptoms of locking or catching
Discussion
Although statistical significance was not found between groups for most factors, we believe the data
indicate a trend toward worse clinical results with partial meniscectomy
• Overall IKDC grade
• Subjective pain score
These clinical differences may indicated a degenerative changes in that joint that do not appear on
radiographs
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•
XI. Summary
• This group of studies looked at the results that were specific to one type of meniscus tear
• Patients who had other types of intraarticular damage were eliminated so that the specific results could
be reported
• Other reports in the literature seldom are this specific
• Many types of meniscus tears can heal or remain asymptomatic with repair
• Many tears can be left in situ after treatment with abrasion and trephination
•
Posterior horn avulsions
•
Peripheral medial or lateral meniscus tears
•
Most of these tears are associated with acute ACL injury
• Many bucket-handle meniscus tears (even in the white/white zone) can be repaired without causing
symptoms in the future
• Fewer repaired BH lateral meniscus tears cause subsequent symptoms than BH medial meniscus tears
• 3% lateral
• 9% medial
• Clinically, patients who underwent meniscectomy (lateral or medial) appeared to have inferior results
than patients who had meniscus repair
• Not sure how well some repairs function
• For BH medial meniscus repairs, degenerative tears resulted in lower subjective scores than nondegenerative tears
• Difficult to observe statistically significant superior results with repair versus removal, even with 8-10
year follow-up
• Further follow-up studies need to be specific with regard to meniscus tear type and ACL-intact or ACL
deficient knees
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ICL #14
COMPLEX ISSUE IN ACL RECONSTRUCTION
An International Perspective
Thursday, March 13, 2003 • Aotea Centre, Kupe/Hauraki Room
Chairman: Kai-Ming Chan, MD, Hong Kong
Faculty: Freddie Fu, MD, USA, Savio Woo, PhD, DSc, USA, James Lam, FRCS, Hong Kong, Hans Paessler, Germany,
Masahiro Kurosaka, Japan, Christer Rolf, United Kingdom and Hsiao-Li Ma, MD, Taiwan
The ACL graft…A biological and biomechanical perspective
Savio Woo (15 minutes)
2.
My preferred method of ACL reconstruction…Graft choice and technical pearls
Hans Paessler (8 min)
Masahiro Kurosaka (8 min)
KM Chan (8 min)
Christer Rolf (8 min)
3.
Combined ACL plus repairable meniscal injury – My preferred approach
James Lam (8 min)
Ma Hsiao-Li (8 min)
4.
Revision ACL surgery
Freddie Fu (15 min)
5.
Questions and Answers
All (10 min)
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1.
INTRODUCTION:
Approximately 250,000 ACL reconstructions/year in the USA alone
80-90% success rates
Approximately 25,000 revision ACL reconstructions/year
Misplaced tunnels in 10-40% [4-6]
Purpose of this Instructional Course Lecture
Review current clinical experience, indications, techniques, results and controversies with revision
ACL reconstruction.
Clinical experience
20 years
200 ACL reconstructions/year
30 revisions/year
INDICATIONS
Subjective
Instability (ADL’s, Sports)
Pain
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Objective
Evidence of increased laxity on physical exam
Evidence of increased laxity on instrumented knee testing (KT 1000)
ETIOLOGY OF FAILURE
1. Surgical technique
Technical errors
Tunnel location
Graft impingement
Graft tension
Mechanical properties of the graft [2]
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Classification
Surgical technique
Biological failure
Biomechanical failure
2. Biological failure
Avascularity
Immunology
Stress shielding
Bone to bone and bone to tendon healing
3. Biomechanical failures
Trauma (re-injury)
Aggressive rehabilitation
PREOPERATIVE EVALUATION
Determine etiology, classify primary and secondary causes of graft failure, revise preoperative plan.
History
Symptoms (pain vs. instability)
Previous surgical procedures (i.e. graft type, associated pathology)
Physical exam
Laxity patterns (assess secondary restraints)
Anterior vs. posterior drawer
Rotational stability
Pivot shift test
Varus/valgus
Posterolateral corner
Radiographs
Tunnel position, size, fixation type, Fairbank’s changes
AP, lateral
45∞ PA FWB
Special examinations
MRI
Bone scan
CT scan
Gait analysis
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TECHNICAL CONSDERATIONS
Principe of treatment is not the same as in primary ACL reconstruction!
Pre-operative planning
Set realistic goals with patients
Return to sports vs. ADL’s
Beware of "knee abuser"
Staged procedure:
1 vs. 2 stages (bone grafting)
Secondary restraints:
Collaterals
Meniscus (role for transplantation)
Cartilage (role for osteotomy)
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Graft selection:
Autograft vs. allograft [1]
Computer-assisted vs. traditional planning
Removal of hardware
Pre-operative planning
Leave in place if possible
Remove hardware only with appropriate tools
Prosthetic ligament removal in one piece
Tunnel placement
Femoral tunnel:
Anterior:
re-drill tunnel in correct position
Correct:
larger graft with bone graft or over-the-top position
Posterior:
convert to over-the-top position
Tibial tunnel:
Anterior:
Correct:
Posterior:
re-drill tunnel in correct position
larger graft with bone graft
two stage bone grafting, large allograft
Graft fixation
Generally interference screws
Alternatives (i.e. suture post, staple)
REVISION GRAFT SELECTION
Graft types
Allograft (bone-patella tendon-bone, Achilles tendon)
Autograft (bone-patella tendon-bone, hamstring tendons, quadriceps tendon)
Graft selection
Autograft:
For failed allograft without technical failures
If patient refuses allograft
Allograft:
For failed autografts
For complex revision cases
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REHABILITATION
Avoid aggressive rehabilitation! [3]
Special considerations
Complex cases (secondary restraints)
Delayed allograft incorporation
General rules
Respect graft healing
PWB 6-8 wks
Return to sports after >12 month
Follow up study [4]
35 patients (25 autografts/10 allografts)
Revision with allografts (21 PT/14 AT)
Average follow up, 18-40 month
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PITTSBURGH EXPERIENCE
Results
Subjective (U Pittsburgh Subjective Knee Rating)
Mean 73 (7-90), max 100
Would have surgery again
Yes: 83%, No 17%
Objective (IKDC)
B
14%
C
50%
D
36%
KT-1000 laxity
<3mm 43%
3-5mm 43%
>5mm 14%
SUMMARY
1. Careful pre-operative evaluation (gather all data)
2. Counsel your patient
3. Address the whole knee – not only the ACL
4. Have different techniques available
5. Revision is technically demanding
6. Results are not as good as in primary reconstructions
REFERENCES
1.
2.
3.
4.
5.
6.
Harner, C.D., E. Olson, J.J. Irrgang, S. Silverstein, F.H. Fu, and M. Silbey, Clin Orthop, 1996(324): p. 134-44.
Höher, J., S.U. Scheffler, J.D. Withrow, G.A. Livesay, R.E. Debski, F.H. Fu, and S.L.-Y. Woo. Journal of
Orthopaedic Research, 2000. 18(3): p. 456-61.
Irrgang, J.J. Clinics in Sports Medicine, 1993. 12(4): p. 797-813.
Johnson, D.L., T.M. Swenson, J.J. Irrgang, F.H. Fu, and C.D. Harner, Clinical Orthopaedics & Related
Research, 1996(325): p. 100-9.
Kohn, D., T. Busche, and J. Carls. Knee Surgery, Sports Traumatology, Arthroscopy, 1998. 6 Suppl 1: p. S13-5.
Musahl, V., T. Cierpinski, H. Hornung, and P. Hertel, 63. Jahrestagung der DGU, November 1999,
Berlin, Germany, 1999.
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ICL #15
ELBOW ARTHROSCOPY (LIGAMENT INJURIES AND TENDINOPATHY)
Thursday, March 13, 2003 • Aotea Centre, Kaikoura Room
Chairman: Luigi Pederzini, MD, Italy
Faculty: Gary Poehling, MD, USA, Gregory Bain, FRACS, Australia and Champ Baker, Jr., MD, USA
Arthroscopic technique is becoming more and more useful in the treatment of elbow pathologies.
Degenerative stiff elbow (DSE) and post-traumatic stiff elbow (PSE) must be considered.
In DSE patients complain pain more than ROM deficit,while in PSE patients complain ROM deficit more
than pain.
ICLs
Several surgical steps are described:Arthroscopic release of the posterior fossa,resection of the tip of the
olecranon, arthroscopic release of the anterior capsule ,resection of the ipertrophic coronoid process,ulnar
nerve release.,arthroscopic O.K. procedure, arthroscopic resection of the radial head.The Rom in DSE and
PSE after arthroscopic treatment was evidenced in the Morrey functional arch.DSE patients at 3 years follow up show some mild pain and some decreased ROM.PSE patients mantain a good ROM at 3 years follow up.Time from trauma can influence the results.
Elbow Osteochondral Lesions - The Role of Arthroscopy
Poehling, Gary
Definitions
1. Osteochondrosis - Panner's Disease: This is a disease of the ossification center that occurs in the first
decade of life. It is generally a self limited problem that reconstitutes itself over a year's period of time
with very few long term problems. Observation and rest is the treatment of choice.
2. Osteochondritis Dissecans: This is an inflammatory process effecting the articular surface. It has a peak
incidence in 10-15 years of age. It is most commonly seen in throwing athletes and female gymnasts.
Evaluation
1. Range of motion
2. Radiographs
a. Loose bodies
b. AVN entire capitellum - Panners age 4-10
c. Superficial defect - OCD age 10-15
3. Indications
a. Failure of conservative treatment
b. Fixed contracture greater than 10 degrees.
c. Mechanical symptoms, locking and catching.
Surgical Technique
1. Anterior joint - 5 mm arthroscope
a. Proximal medial portal
b. Anterolateral portal
2. Posterior joint - 2.7 mm scope
a. Mid lateral portal
b. Adjacent portal
3. Posterior portal - best to visualize the defect in 75% of cases.
4. Debridement and loose body removal is treatment of choice
5. Alternatives
a. Headless screw
b. Biodegradable pin
c. Allograft
3.112
Elbow Arthroscopy: Set-Up/Portal Anatomy and Diagnostic Arthroscopy
Gary G. Poehling, M.D.
Wake Forest University Health Sciences
Winston-Salem, North Carolina
Operating Room Set-Up & Instrumentation
Figure 3a
Figure 3b
Figure 1
Figure 2
ICLs
I. Patient Positioning (Figure 1)
A. Lateral position with arm support
B. Prone or supine position-alternative
C. General anesthesia (preferred)
II. Instrumentation
A. Non-sterile upper arm tourniquet (optional)
B. Fluid pump with pressure monitoring,
4.5 mm/30º & 2.7/30º mm arthroscopes
C. Motorized shaver, grasping forceps
D. Suction basket
E. OR set up (Figure 2)
Figure 3c
III. Technique
A. Portals-anterior compartment
1.
Proximal medial portal (Figures 3)
2.
Anterio-lateral portal (inside out)
3.
Joint distension through mid-lateral "soft spot" using 18 ga. Spinal needle with 30-50 cc sterile
Ringer’s Lactate solution
Diminished joint laxity and volume with diagnosis of contracture
4.
Establish proximal medial portal, anterior to intermuscular septum along anterior humeral shaft
(brachialis protects anterior neurovascular structures)
5.
Arm flexion helps protect anterior neurovascular structures
Figure 4a
Figure 4b
Figure 5
3.113
B. Portals-posterior compartment (Figures 4a and 4b)
1.
2.7 mm arthroscope through mid-lateral or adjacent lateral portals (see Figure 5)
2.
Use of posterior (posterior lateral or trans-triceps) portals for evaluation/instrumentation of posterior joint and olecranon fossa (see Figure 6)
3.
Trans-triceps portal is made with a longitudinal incision 1.5-2.0 cm proximal to olecranon process
with elbow flexed 90º
Figure 6a
Figure 6b
Figure 6c
ICLs
IV. Indications
A. Loose bodies
B. Osteochondritis Dessicans (OCD)
C. Rheumatoid Arthritis - Synovectomy
D. Contracture/Arthrofibrosis
E. Pigmented Villinodular Synovitis (PVNS)
F. Lateral Epicondylitis
G. Radial Head Fractures
H. Radial Head Resection
I. Synovial Chondromatosis
J. Infection/Septic Arthritis
K. Posterolateral Instability
V. Contraindications
A. Advanced degenerative joint disease
B. Previously transposed ulnar nerve prevents any medial approaches
C. Excessive heterotopic bone
D. Reflex Sympathetic Dystrophy (RSD)
E. Soft tissue compromise
References
1.
Poehling GG, Ekman EF, Ruch DS. Elbow Arthroscopy, in Oper Arth, p 821-28
2.
Menth-Chiari WA, Poehling GG, Ruch DS. Arthroscopic resection of the radial head. Arthroscopy
1999 Mar; 15(2):226-30
3.
Moskal MJ, Savoie FH, III, Field LD. Elbow arthroscopy in trauma and reconstruction. Orthop Clin
North Am 1999 Jan;30(1):163-77
4.
Ruch DS, Poehling GG. Anterior interosseous nerve injury following elbow arthroscopy.
Arthroscopy 1997 Dec;13(6):756-8
5.
Day B. Elbow arthroscopy in the athlete. Clin Sports Med 1996 Oct;15(4):785-97
6.
Baker CL, Brooks AA. Arthroscopy of the elbow. Clin Sports Med 1996 Apr;15(2):261-81
7.
Ekman EF, Poehling GG. Arthroscopy of the elbow. Hand Clin 1994 Aug;10(3):453-60
8.
Gallay SH, Richards RR, O’Driscoll SW. Intraarticular capacity and compliance of stiff and normal
elbows. Arthroscopy 1993;9(1):9-13
9.
Verhaar J, van Mameren H, Brandsma A. Risks of neurovascular injury in elbow arthroscopy: starting anteromedially or anterolaterally. Arthroscopy 1991;7(3):287-90
10.
Lynch GJ, Meyers JF, Whipple TL, Caspari RB. Neurovascular anatomy and elbow arthroscopy: inherent risks. Arthroscopy 1986;2(3):190-7
* Illustrations by Annemarie B. Johnson, CMI
3.114
It has been recognised for some years that elbow arthroscopy has a much higher incidence of nerve injury
than arthroscopy involving other joints. This is largely due to the close proximity of the three major nerves
to the elbow joint.
The ulnar nerve is at risk when introducing the medial portal particularly if the patient has a subluxating
ulnar nerve or the patient has had a surgical anterior transposition. Injury to the ulnar nerve can occur during debridement of the medial gutter (Figure 1).
The radial nerves and the posterior interosseous nerves are at risk during lateral portal placements. The
nerves are less likely to be injured if the joint is distended and a proximal lateral portal is used. The radial
nerve is at risk when performing an anterior capsular release, synovectomy or a radial head excision (Figure
2).
The median nerve passes anterior to the brachialis muscle and therefore tends to be protected during
elbow arthroscopy (Figure 2).
The details of the anatomy of each of the nerves with relation to the elbow joint will be presented.
ENDOSCOPIC ULNAR NERVE RELEASE
We have performed a cadaveric study to assess the safety and efficiency of performing an endoscopic ulnar
nerve release at the level of the elbow with the Agee single portal endoscopic device. In a cadaveric model
we were able to reproducibly perform a release of the arcade of Struthers, decubital retinaculum and
Osborne’s FCU fascia. In cadaveric models there were no injuries to the ulnar nerve, its motor branches or
articular branches. By setting the trocar into the radial side of the cubital tunnel the chance of injury to the
motor branches is significantly reduced.
We have been using this technique in clinical cases and found the technique to be safe and associated with
a much more rapid rehabilitation and smaller morbidity than conventional open approaches that we had
used previously.
Figure 1
ICLs
Elbow Arthroscopy and Nerves
Gregory Bain, Adelaide, South Australia.
www.gregbain.com.au
Figure 2
Elbow Arthroscopy: A Long Term Follow-Up
Champ L. Baker, Jr., MD
The Hughston Clinic
Columbus, Georgia
Introduction
•
Burman reports that the elbow is unsuitable for arthroscopic exam – 1931 JBJS
•
Japanese credited for renewed interest in elbow arthroscopy with publications in the 1970’s
•
Increased popularity in the mid 1980’s
3.115
•
•
Accounts for 11% of arthroscopies at Mayo Clinic
7.6% of orthopedists perform elbow arthroscopy
Indications
•
Loose body/Foreign body
•
OCD
•
VEO
•
Posterior impingement
•
Synovitis
•
Arthrofibrosis
•
Diagnostic
•
DJD
•
Fracture
•
Lateral Epicondylitis
•
Radial Head Excision
•
Evaluate competency of Ulnar Collateral Ligament
•
Septic arthritis
ICLs
Contraindications
•
Severe ankylosis
•
Distortion of normal anatomy (e.g. ulnar nerve transposition)
•
Local skin infection
Procedure
•
General Anesthesia
•
Prone position
•
Portal Placement
– Superomedial
– Superolateral
– Direct lateral
– Posterocentral
•
2.7mm 30° arthroscope
Post-op
•
Outpatient
•
F/U 1 week
•
Post op rehab depends on procedure
– Regain motion #1 priority in all procedures
Materials and Methods
•
Query of elbow arthroscopy by Champ Baker, MD
•
February 1984 – February 2001
•
Chart Review
•
Patients contacted by phone
– Clinic Visit
– Phone survey
Chart Review
•
Date of birth
•
Date of surgery
•
Sex
•
Hand dominance
•
Side of procedure
•
1º, 2º, and 3º diagnosis
•
1º, 2º, and 3º procedures
•
Complications
•
Prior surgery
•
Repeat surgery
3.116
Concomitant surgery
Workman’s comp
History of injury
Preop range of motion
Occupation
Deleted patients
•
Concomitant open procedures (e.g. ulnar nerve transposition)
•
Diagnostic scopes
•
Deceased
Patient Follow-up
•
Phone contact
– Clinic visit
•
Andrews elbow scoring system
– Subjective and objective
•
Visual analog pain scale
•
Much better, Better, Same, or Worse
– Phone survey
•
Modified Andrews elbow scoring system
– Subjective
•
Analog pain scale
•
Much better, Better, Same, or Worse
ICLs
•
•
•
•
•
Questionnaire
Results
•
324 elbows, 311 patients
•
44 elbows deleted
– 36 open
– 5 diagnostic
– 3 deceased
•
•
Ages - 11.5yo to 73.5yo (38.5 avg)
•
Sex – 206 M (74%) and 74 F (26%)
•
Hand dominance – 194 right (69%), 20 left (7%), 66 no documentation (23%)
•
Procedure side – 187 right (67%) and 93 left (33%)
•
Workman’s comp – 218 no and 62 yes
Primary Diagnosis
Prior Surgery
•
Prior surgery – 21 patients (7%)
– Open procedures - 13
– ORIF – 7
– Scope - 1
Concomitant surgery
•
Concomitant surgery – 20 (7%)
– Shoulder scope – 9
– Olecranon bursectomy – 4
– Lateral release – 3
– Carpal tunnel release – 2
– CMC arthroplasty – 1
– Ankle scope - 1
Complications
•
Total complications – 15 (5%)
3.117
•
– Transient numbness – 6
– Arthrofibrosis – 3
– Neuroma – 2
– Post-operative drainage – 2
– Cellulitis – 1
– Heterotopic bone – 1
No permanent neurovascular compromise
Repeat Surgery
•
Repeat surgery – 26 (9%)
– Open procedure – 17
– Scope – 8
– Total elbow replacement – 1
•
4/26 patients VEO – open resection olecranon osteophyte or UCL recon
•
3/26 open lateral release after scope release
•
3/26 unrelated repeat procedures (e.g. radial tunnel release 1 year after loose body removal)
ICLs
3.118
Results
•
•
26 elbows deleted from f/u due repeat surgery
•
254 elbows in 242 patients possible for f/u
•
82 elbows in 79 patients contacted
– 52 phone interview
– 30 clinic visit
•
82 follow up elbows
•
Ages 11.5 - 71yo (avg. 42yr)
•
Follow up 17 – 155 mos (avg. 64.5 mos)
•
Sex, hand dominance, procedure side, workman’s compensation cases, and primary
diagnosis analogous to total surgical population
•
Visual analog scale (0-10)
– Daily pain avg. 1.39 (range 0-9)
– ADL pain avg. 2.18 (range 0-8)
– Work pain avg. 2.98 (range 0-10)
•
Andrews criteria - subjective
– Pain avg. 18.29 (range 5-25)
– Swelling avg. 23.17 (range 5-25)
– Locking avg. 22.44 (range 5-25)
– Activity limitation avg. 20.85 (range 5-25)
•
Subjective score avg. 84.76 (range 25-100)
•
71% (58/82) elbows with good and excellent results
•
80% (65/82) elbows better and much better
•
74% (48/65) non-WC patients with good and excellent results
•
75% (49/65) non-WC better and much better
•
59% (10/17) WC patients with good and excellent results
•
100% (17/17) WC patients better and much better
•
Good and Excellent Results
– VEO 100% (6/6)
– OCD 83% (5/6)
– Loose body 75% (9/12)
– Lateral epicondylitis 74% (23/31)
– Synovitis 71% (5/7)
– DJD 57% (4/7)
– Posterior impingement 50% (1/2)
– Arthrofibrosis 45% (5/11)
•
Better and Much Better
– OCD 100% (6/6)
– DJD 86% (6/7)
Literature
•
Retrospective (1979-95)
•
47 pts
•
age 3.5 – 17yo (avg age 14 yr)
•
min 2yr f/u (avg. 4.7yrs)
•
Modified Andrews elbow scoring system
•
85% good to excellent results, 90% return to sport
– Micheli, LJ, et. al.
– Boston, Mass
– Journal of Arthroscopy 2001
•
Retrospective (1977 – 1996)
•
103 patients, mean f/u 6.2 yrs, 3 – 72yo
•
Figgie score increased from 49.3 to 89.1
•
Age didn’t affect the results
•
Pain showed the greatest improvement
•
Loose bodies, rheumatoid and septic arthritis improved the most
•
Limited improvement in degenerative arthritis
– Jerosch, J. et al
– Munster, Germany
– Arch orthop trauma surg 1998
•
Retrospective (1980-1998)
•
414 elbows with >6 week f/u
•
Chart review, survey, telephone contact (37/96 pts)
•
Major complications – permanent neurovascular injury, compartment syndrome, postop joint infection, loss of motion >30º
•
Minor complications – transient nerve palsy that completely resolves, drainage >5 days, superficial
infection, loss of motion <30º
•
Major complications – 4 (.8%)
– Joint space infection
•
Minor complications – 50 (11%)
– Prolonged drainage – 22
– Transient nerve palsies – 12
– Superficial infection – 11
– Loss of motion – 5
•
Risk factors for temporary nerve palsy were RA and a contracture
– O’Driscoll, S., et al
– Rochester, MN
– JBJS 2001
ICLs
– Synovitis 86% (6/7)
– Lateral epicondylitis 84% (26/31)
– Loose Body 75% (9/12)
– Arthrofibrosis 73% (8/11)
– VEO 67% (4/6)
– Posterior impingement 50% (1/2)
Conclusion
•
Elbow arthroscopy is predictably (>70% good or excellent and better or much better results) a good
procedure for OCD, loose body, synovitis, and lateral epicondylitis
•
Less predictable results for DJD, VEO, arthrofibrosis, and posterior impingement
•
Neurovascular injury can be minimized with complete knowledge of the regional anatomy of the
elbow and careful attention to detail
3.119
Treatment of Lateral Epicondylitis and Soft Tissue Impingement
Champ L. Baker, Jr., M.D.
The Hughston Clinic
Columbus, Georgia
Lateral Epicondylitis Definition
"Painful overuse tendinosis at the lateral aspect of the elbow"
Henry J. Morris (Lancet 1882) "Lawn Tennis Arm"
ICLs
Mechanism
Traumatic or non-traumatic mechanisms
Often repetitive use injury
Poor blood supply to tendon
Insufficient healing
Vicious cycle
Inflammation ‡ microtear ‡ frank rupture
Pathoanatomy
Initially thought to be inflammatory process (tendonitis) of ECRB and
aponeurosis at lateral epicondyle (Goldie, 1964)
Later described by Nirschl as "Angiofibroblastic tendinosis"
•
Degenerative process
•
Granulation tissue
•
No inflammatory cells
ECRB involved 100%
•
ECRL, EDC less commonly
97% tendinosis
35% gross rupture
common extensor
Diagnosis
Pain and tenderness over lateral epicondyle and common extensor tendon origin
Pain with resisted wrist extension and supination
Pain with passive wrist flexion with elbow extended
Radiographs usually normal
Non-operative Treatment
Rest
Ice
NSAID’s
Counterforce brace
Physical therapy
Modalities
Corticosteroid injection
75% to 90% of pts do well
Efficacy of Nonoperative Treatment for Lateral Epicondylitis
Bowen, Dorey and Shapiro (American J. Orthopedics, August 2001)
•
84 patients
•
2.8 year follow-up
•
25% required surgery
•
Multiple injections prognostic
Surgical Treatment
10-25% of patients are recalcitrant to non-op treatment
Operative
3.120
•
•
•
Open
Percutaneous
Arthroscopic
Open
Identification of pathology
Excision tendon (ECRB)
Decortication epicondyle
Repair common extensor origin
Arthroscopic Lateral Release
Preserves common extensor origin
Speeds rehabilitation
Allows intra-articular examination for chondral lesions, loose bodies, etc.
ICLs
Percutaneous
Release ECRB with #11 blade
Local anesthesia / office or outpatient
21 elbows in 17 patients
20/21 normal function at 31 months follow-up
Arthroscopic Release for Lateral Epicondylitis: A Cadaveric Model
Kuklo, Taylor, Murphy, Islinger, Heekin and Baker
(Arthroscopy 1999; 15(3);259-64)
Arthroscopic resection of the ECRB and decortication of the lateral epicondyle
10/10 successfully debrided / decorticated from 20-27mm as demonstrated by post-arthroscopic dissection
1/10 cases over resected into subcutaneous fat
Conclusions:
•
LCL not harmed - posterior
•
Technically feasible
•
Technically reproducible
Arthroscopic Classification
Type I- Deep fraying to ECRB
Type II- Linear tears on undersurface of ECRB
Type III- Complete avulsion of ECRB
Arthroscopic Technique
Prone position
General anesthetic
Tourniquet optional
Equipment
•
2.7, 4.0, 30º /70º arthroscope
•
3.5/4.5 full radius resector / burr
•
Hand instruments / radiofrequency – monopolar 2.0
Proximal Medial Portal
•
2 cm proximal to the medial epicondyle
•
Adjacent to the intermuscular septum
•
Avoid the medial antebrachial cutaneous nerve
Proximal Lateral Portal
•
2 cm proximal and 1 cm anterior to the lateral epicondyle
•
Visualization of the anterior joint and capsule
Operative sequence
•
Intra-articular inspection
•
Identification of ECRB origin after resection of capsule at lateral epicondyle
•
Debridement of pathologic tissue at ECRB origin
3.121
•
Decortication of lateral epicondyle and lateral epicondylar ridge
ICLs
Arthroscopic classification and treatment of lateral epicondylitis: Two year clinical results
Baker, Murphy, Gottlob and Curd
(J Shoulder Elbow Surg 2000; 9;475-82)
Patient Follow Up
1991-1997, 42 elbows (40 patients)
•
26 males, 14 females
•
Mean age: 42.7 yrs (18-59yrs)
Prevalence
•
Type I Lesion: 15 (36%)
•
Type II Lesion: 15 (36%)
•
Type III Lesion: 12 (28%)
Average length of subjective follow up: 2.04 years (1 to 5.9 years)
Patient Follow Up - Morrey (Mayo Clinic) Elbow Evaluation
•
Pain
•
Motion
•
Strength
•
Instability
•
Function
Results Morrey / Mayo Score (100 Points possible)
•
Overall 95
•
Type I 96
•
Type II 87
•
Type III 99
Function Score (12 Points possible)
•
Overall 11
•
Type I 10.8
•
Type II 10.6
•
Type III 11.6
Patient Response: 37/39 better or much better
Arthroscopic Release for Lateral Epicondylitis
Owens, Murphy and Kuklo (Arthroscopy 2001 Jul;17(6):582-7)
16 patients
•
5 Type I
•
5 Type II
•
6 Type III
3 with concurrent pathology
Return to work – 6 days
Arthroscopic Treatment of Lateral Epicondylitis- The 4-Step Technique
Romeo and Fox (Orthopedic Technology Review Vol 4 No. 5 Sept/Oct 2002)
1. Resect anterior lateral capsule
2. Resect ECRB proximal and posterior to ECRL
3. Resect anterior to LCL
4. Decorticate origin of ECRB
Follow-up
•
14 patients
•
2 years
•
13 of 14 extremely satisfied
•
Strength symmetrical
Current study
Evaluate the long-term results of arthroscopic treatment of lateral epicondylitis in terms of:
•
Patient satisfaction
•
Pain relief
3.122
ICLs
•
Return to function
Demographics: Chart Review
•
111 patients
•
120 elbows
•
Male:Female ratio: 52%:48%
•
Age Range: 19-76yrs., Average age: 46 yrs.
Mechanism:
•
Acute / Traumatic : 22%
•
Chronic / Overuse: 71%
•
Unknown: 7%
Hand Dominance:
•
Dominant: 66%
•
Non-dominant: 24%
•
Bilateral: 10%
Worker’s Comp:
•
Yes: 27%
•
No: 73%
Conservative Treatment
Non-op duration:
• <6 mo: 13%
• 6-12 mo: 50%
• >12 mo: 29%
• Unknown: 8%
Number of Injections:
• 0: 7%
• 1: 22%
• 2: 18%
• 3+: 45%
• Unknown: 8%
Preop Findings
Tenderness Lateral Epicondyle
Pain with resisted wrist extension and supination
ROM:
• FROM: 72%
• Lacks Ext: 5%
• Lacks Flex: 7%
• Lacks both: 12%
• Unknown: 4%
Intraoperative Findings
Baker Type:
• Type I: 32%
• Type II: 37%
• Type III: 19%
No correlation between lesion type and age, sex, etiology, length of nonoperative treatment, or arm
dominance.
Associated Pathology:
• None: 41%
• Synovitis: 34%
• Degenerative changes: 21%
• Loose body: 4%
Follow Up Interval
1-2 years: 29 pts
2-3 years: 14 pts
3-4 years: 22 pts
4-5 years: 16 pts
>5 years: 39 pts
Average: 49 months
3.123
Results
ICLs
44 pts contacted
Average F/U 43 months
3 failures which later required open procedure
Visual analog scores (0-10)
• Pain at rest: 1.2
• Pain with ADL: 2.1
• Pain at work: 3.2
Results: Patient response
Compared to pre-op:
• Much better: 61%
• Better: 28%
• Same: 11%
• Worse: 0%
• (89% Better or Much Better)
Results: Andrews Criteria
Subjective score
• Excellent: 56%
• Good: 14%
• Fair: 25%
• Poor: 5%
• (Average 85/100 points)
Objective score
• Excellent: 95%
• Good: 5%
• Fair: 0%
• Poor: 0%
• (Average 98/ 100 points)
Total score:
• Excellent: 69%
• Good: 23%
• Fair: 8%
• Poor: 0%
• (Average 184/200 points)
• (92% Good or Excellent results)
Summary Lateral Epicondylitis
Arthroscopic treatment of lateral epicondylitis is a reliable treatment
•
Results comparable to open procedures
•
Release is feasible and reproducible
•
Arthroscopy allows complete examination and treatment of associated pathology
•
Keeps common extensor origin intact
•
Allows quicker rehabilitation
•
Grip strength maintained
Synovial Fringe
Remnant of confluence of radial ulnar, ulnohumeral and radial humeral joints.
Described as a cause of tennis elbow with excision recommended in open series.
Symptoms
Intermittent catching, locking, loss of motion.
No antecedent trauma.
Pain with flexion/extension of the elbow.
Pain localized to radial head.
Signs
3.124
Pain may be present on forced hyperextension.
Pain on forced pronation, localized to lateral radial capitellar joint.
Pain relieved with intra-articular Xylocaine injection.
Studies
Treatment
Arthroscopic release
•
Proximal medial viewing portal
•
Proximal lateral operating portal
•
Look for anterior band
Posterior arthroscopy
•
Direct lateral portal
•
Look for › synovitis in the posterior RC joint
•
Remove fibrotic synovium
•
Look for radial chondromalacia
ICLs
X-rays negative.
No record of MRI studies.
Conclusions
The presence of synovial plicae in the radiocapitellar joint must be considered in the differential
diagnosis of painful snapping elbow. Arthroscopy confirms the diagnosis and allows excision of the
plica.
Always suspect in "tennis elbow".
Arthroscopic evaluation should always include posterior radial capitellar joint
My Practice: "Tennis Elbow" 2002
First visit
•
History and physical confirm diagnosis
•
Rehab exercises (super seven)
•
Counterforce brace/decrease activities
•
Injection +/Second visit – symptomatic
•
Injection
•
ESWT
Third visit – failed ESWT
•
Arthroscopic release
Thank you!
Bibliography
•
Baker CL Jr, Murphy KP, Gottlob CA, Curd DT. Arthroscopic classification and treatment of lateral
epicondylitis: 2-year clinical results. J Shoulder Elbow Surg. 2000;9:475-82.
•
Baker CL Jr, Murphy KP, Gottlob CA, Curd DT. Arthroscopic versus open techniques for extensor
tendinosis of the elbow. Tech Shoulder Elbow Surg. 2000;1:184-191.
•
Kuklo TR, Taylor KF, Murphy KP, Islinger RB, Heekin RD, Baker CL Jr. Arthroscopic release for lateral
epicondylitis: a Cadaveric model. Arthroscopy 1999;15:259-64.
•
Nirschl RP. Elbow tendinosis/tennis elbow. Clin Sports Med. 1992;11:851-70.
•
Nirschl RP, Pettrone FA. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint
Surg Am. 1973;55:1177-82.
3.125
ICL #16
NEW FRONTIERS IN SHOULDER ARTHROSCOPY
Friday, March 14, 2003 • Aotea Centre, ASB Theatre
Chairman: W. Jaap Willems, MD, Netherlands
Faculty: Stephen Burkhart, MD, USA, George Lajtai, MD, Austria, Anthony Miniaci, MD, FRCS, Canada and Joe De
Beer, MD, South Africa
- Opening – Jaap Willems
- Arthroscopic Treatment of Subscapularis Tendon Injuries – Stephen Burkhart
- Arthroscopic Management of Acromioclavicular Dislocations – Joe De Beer
ICLs
- Arthroscopic Reconstruction of Glenoid Fractures – George Lajtai
- Decision Making in Multidirectional Shoulder Instability – Anthony Miniaci
- HAGL Lesions: Can They be Treated Arthroscopically – Jaap Willems
ARTHROSCOPIC MANAGEMENT OF ACROMIOCLAVICULAR DISLOCATION
DR JOE DE BEER
CAPE TOWN
In our large experience of rugby injuries it was evident that injury to the AC joint is the most common
shoulder injury in rugby. These included Type I – V dislocations.
Grade I Subluxation: these often lead to a painful AC joint. Management is Arthroscopic Mumford procedure, using two superior AC portals. This approach is also used for other forms of isolated AC joint pain
(for e.g. "weight lifter’s shoulder")
Grade II subluxation: Often Arthroscopic Mumford is indicated.
Grade II subluxation: it has to be determined what the cause of the pain is in these cases:
1 AC joint pain – pain relief after injection of local anaesthetic into AC joint.. This cause is rare in Grade III
2 Secondary impingement of rotator Cuff due to tilting of scapula. Diagnosis made by subacromial injection – Arthroscopic Acromioplasty may be indicated.
3 Traction on brachial plexus and scapular stabilisers: the most common problem – diagnosis made by
traction on arm. Reconstruction of AC joint is indicated. (Weaver Dunn procedure)
ARTHROSCOPIC ACROMIOCLAVICULAR RECONSTRUCTION
This is a relatively new procedure and been described by Snyder (done via subacromial route) and Wolfe
(done via intra-articular route). This procedure further developed by using graft material from distal clavicle to coracoid – viewing the coracoid from a posterior gleno-humeral portal
CONCLUSION:
The arthroscopic management of painful AC joint is well established and reproducible. Reconstruction of
the AC joint arthroscopically has been developed and will soon be perfected.
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Arthroscopic reconstruction of glenoid fractures
Georg Lajtai MD
Altis -Center for Sportsurgery
Austria, Europe
http://www.shoulder.org
Introduction:
Fractures of the scapular are relatively uncommon injuries, and most can be treated satisfactorily with nonoperative methods (1-6).
Fractures of the scapula generally occur in high energy setting of vehicular trauma or fall from height. They
are infrequent injuries compromising no more than 5 % of shoulder girdle fractures in most clinical reports.
(2,7,8)
ICLs
Scapula fractures are often associated with multiple traumatic injuries which may take priority, drawing
attention away from a treatment of the scapular fracture (2,3,6).
This is likely because of a thick protective muscular envelope and recoil of the underlying chest wall on
impact. Another factor is the highly mobile shoulder girdle soft tissue and bony suspensory mechanism
where the clavicle and its articulations represent the sites of failure with most accident mechanisms.
Displaced fractures of the acromion, scapular spine and neck have shown poorer outcomes with conservative treatment and for this reason operative reduction and internal fixation are usually recommended (911).
Open reduction and internal fixation of displaced glenoid fractures have shown promising results in previous small series (10, 12, 13)
Classification:
Ideberg proposed a detailed scheme for classification that was based on a review of 338 scapula fractures
in 322 patients (13). This scheme included fractures of the glenoid rim and the glenoid fossa.
Classification of intraarticular glenoid fractures
Type I:
Glenoid rim fractures
Typ I a:
With anterior fracture fragment
Typ I b:
With posterior fracture fragment
Type II:
Inferior glenoid fracture involving part of the neck
Type III:
Superior glenoid fracture extending through the base of the coracoid process
Type IV:
Horizontal fracture involving both scapular, neck and body. Fractureline always runs inferior to the
spine of the scapular
Type V:
Horizontal fracture (as in type IV), with an additional complete or incomplete neck fracture
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Type VI:
Type VI fractures are severely comminuted injuries of the glenoid fossa, caused by violent forces.(14)
Arthroscopic reconstruction of displaced glenoid fractures
Requirements:
1. Trained surgeons in arthroscopic shoulder surgery
2. Experienced surgeons in ostheosynthesis and their complications
3. Well presorted OR-Team
4. Having the possibility to do the reconstruction open if necessary (Instruments…)
5. Arthroscopic pump must be available
6. Arthroscopic instruments
7. Cannulated screws
8. Nurse must perfectly use the C- arm
If there is one point not accomplished, you should not try to do this type of procedure.
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Positioning:
The patient is positioned in the lateral decubitus position with the arm in 45
degrees abduction and 20 degrees anteversion in a shoulder arm holder.
The C-arm must have the possibility to change the position between the
axial and the ap-position, so that surgeons can change the view according to
what they need to see.
Good arthroscopic is well as good. X ray pictures must be guaranteed otherwise the procedure can turn into a disaster.
OR-Technique:
• Standard posterior portal to the glenohumeral joint
• Rinse the glenohumeral joint to get good visibility
• Inspection of the joint
• Remove debris and blood clots out of the joint and the fracture line
• Classify the fracture and additional injuries
• Make an anteriorsuperior and midglenoidal portal with the SPS portal system in correct position to the
fracture fragments
At this point the C- Arm will put in to the OR field so that an axial as well as an AP-view is possible.
•
At the time, when the C- Arm is correct positioned and the arthroscope looks at the fracture, the surgeon
starts to make the reposition manoeuvre with the raspatorium - arthroscopically as well as radiologically
controlled.
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At the beginning of the procedure the aim is to mobilize the fracture parts - to get a perfect reduction later
on.
• Viewing from the anterior portal the next step will be, to put a Steinmann-pin through the posterial
portal into the proximal glenoid fragment.
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When the fracture fragments are mobilized and it is visiable that the reposition will be possible, next step
is to change the portals, so that the arthroscope is viewing from the anterior portal.
This Steinmann-pin will be used as a joystick to direct the proximal fracture in correlation to the distal
fragment.
If the Steinmann-pin is good in place, reduction can be done on the arthroscopic as well on the radiologic
control.
•
Put in an orientation needle
With a K-wire you can hold the reduction and it allows a temporary fixation of the fracture fragments.
If you are happy with the result of your reduction:
•
Make a skin incision at the Neviaser portal where your K-wire is in place and insert a cannulated screw.
•
Control your manoeuvre with x-ray and arthroscope
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Conclusion: Arthroscopic reconstruction of glenoid fractures can be recommended in dislocated two part
glenoid fractures type Ideberg IV and V. It is a technical demanding operative procedure, but minimal invasive and it allows anatomical
reduction under arthroscopical control and stable fixation. Therefore a short postoperative rehabilitation
and a good functional outcome can be expected.
References:
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1. Aulicino, P. L.; Reinert. Charles; Kornberg, Markus; and Williamson, Sterling: Sisplaced intro-articular glenoid fractures treated by open reduction and internal fixation. J. Trauma, 26: 1137-1141, 1986.
2. Imatani, R.J.: Fractures of the scapula: a review of 53 fractures. J. Trauma, 15: 473-478, 1975
3. Mc Gahan, J. P., Rab, G. T.; and Dublin, Arthru: Fractures of the scapula. J. Trauma, 20: 880-883, 1980.
4. Rowe, C. R.: Fractures of the scapula. Surg. Clin. North America, 43 : 1565-1571, 1963.
5. Ruedl, T., and Chapman, M. W.: Fractures of the scapula and clavicle. In Operative Orthopaedics, edited
ba <m. W. Chapman, Vol. 1 pp 197 – 202. Philadelphia. J. B. Lippincott, 1988.
6. Thompson, D. A., Flynn, T. C.; Miller, P. W.; and Fischer, R. P.: The significance of scapular fractures. J.
Trauma, 25: 974-977, 1985.
7. Tscherne H. Christ M: Konservative and operative therapie der Schulterblattbrüche. Hefte Unfallheilkd
126:52-9. 1975.
8. Bauer G. Fleischman W. Dussler B: Displaced scapular fractures: Indication and long term results of open
reduction internal fixation: Arch Orthop Trauma Surg 114:215-219. 1995
9. Gagey O. Cury JP. Mazas F: Recent fractures of the scapula. Apropos of 43 cases: Rev. Chir. Orthop.
Reparatrice Appar Mot 70: 443-447. 1984
10. Hardegger FH. Simpson LA. Weber BG : The operative treatment of scapular fractures. J. Bone Joint Surg
66B:725-731. 1984
11. Jeanmaire E. Ganz R : Le treatment des fractures de l’omoplute. Indications operatoires : Acta Orthop
Belg 30 : 673-678. 1964
12. Aulicino PL. Reinert C. Kornberg M. Williamson S: Dixplaced intraarticular gleonoid fractures retated by
open reduction internal fixation. J. Trauma 26: 1137-1141. 1986.
13. Ideberg: Epidemiology of scapular fractures. Acta Orthop. Scand. 1995; 66 (5:395-397)
14. Goss TP: Factures of the glenoid cavity JBJS, 74 A, No 2, 299-305, 1992
Decision Making in Multidirectional Shoulder Instability
Anthony Miniaci, MD FRCSC
Professor Orthopaedic Surgery
Head Sports Medicine Program
University of Toronto
The Toronto Western Hospital
Objectives
At the end of this presentation the participant will be able to
1. Understand the various clinical patterns and different pathologies that constitute the condition of
Multidirectional instability of the shoulder
2. Have knowledge of the various techniques, both open and arthroscopic, utilized in addressing MDI
3. Understand some of the potential pitfalls of the various surgical techniques
4. Be able to make decisions about types of treatment that can be employed based on the clinical presentation, symptoms and surgical pathology
INTRODUCTION
- Multidirectional shoulder instability is a difficult clinical problem
- Many reasons for confusion
- Lack of definitions regarding definitions of patient population, symptoms, surgical pathology
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- Patient population- type of instability (voluntary, involuntary, habitual), direction (anterior, posterior,
multi), injury pattern (traumatic, atraumatic), laxity (degree, generalized vs. focal, asymmetry)
- Symptom definition- (Pain, Instability-subluxation/dislocation, micro)
- Surgical pathology- capsular laxity, labral or cuff pathology, Bankart lesion, bony defects
- More difficult than AMBRI definition- a spectrum exists even amongst these patients
Treatment Options
Open Inferior Capsular Shift
- traditional, humeral based capsular shift
- glenoid based procedures
- assure shift is in north-south plane, not east-west
- east-west shift results in loss of external rotation and potential recurrent instability
- superior east west shift results in decreased external rotation and inferior instability-(Flask Deformity of
capsule)
- long term surgical results depend on patient and symptoms
- generally the best for MDI with true instability and generalized laxity
- approach from front in most but may want to consider posterior approach in those patients with MD laxity BUT posterior predominance of symptoms
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- Open Inferior Capsular Shift
- Arthroscopic Inferior Capsular Shift and Interval Closures
- Thermal Capsular Modification
Arthroscopic Capsular Shift
- same principles as open shift
- glenoid based shift and therefore amount of shift is less than humeral based shifts
- capsular tuck when labrum is intact
- BE CAREFUL with tucks- tendency is to reduce capsular volumes in all directions which can cause stiffness(loss of rotational motion) or failures
- Interval closure possible and considered important arthroscopically
- Sometimes combined with focal or minor thermal treatment
Thermal Capsular Modification
- thermal energy becoming increasingly popular
- use of laser, radiofrequency
- laser – more expensive to use
- requires specialized training
- more dangerous to use
- radiofrequency – less expensive, easier to use
Techniques
- depends on temperature dependent denaturation of the crystalline triple helix of type I collagen
- time and temperature dependent
- >65∞ causes significant denaturation of collagen
- decrease stiffness and viscolastic behaviour of tissue for 6 weeks then recovery
- remodeling ? is very slow and therefore may require more time to rehabilitation
Clinical Uses
- wide popularity because of ease of use
- indications are not clear!
- most reported series treat patients with mixed clinical picture
- very few guidelines for use
- many questions – indication for use
- length of immobilization
- how to treat capsule
- location of application
- ? complications
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Recent Study (Miniaci et al.)
- 19 patients with MDI with true instability
- 2 year follow-up
- 9/19 failures (47%)
- 5/19 stiffness – reduced rotational motion
- 4/19 – potential axillary nerve irritation
- Failures – surgical revision revealed capsular deficiency in one third
Clinical Results
- Not good in posterior dislocation, MDI or voluntary types of instability pattern
- Better results in anteroinferior instability, More subtle instability (subfluxation vs.Dislocaton)
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Unknown Issues
1. ?
immobilization time – will this improve failure rate or does it increase stiffness rate
2. ? capsular stripes/dots vs. painting – will this reduce capsular damage
3. ? avoid inferior pouch – does this reduce axillary nerve injury or does it not treat
essential lesion of MDI (inferior capsular redundancy)
RECOMMENDATIONS
- need more research to determine technique and indications
- be careful in patient selection (i.e. degrees of instability)
- need classification of patients being treated to determine optimal method of treatment
CLASSIFICATION
1. MDI with true dislocations/instability
2. MDI with PAIN but no or little instability complaints
2a. MD laxity- asymmetric – pain +/- mild instability
2b. MD laxity- symmetric- pain
MDI with true dislocations/instability
- thermal capsular modification not very successful
- open or arthroscopic shift preferred
- beware of other pathology
- with voluntary instability, especially posterior an open procedure still preferred
MDI with no instability complaints but PAIN
- arthroscopic shift excellent
- treat other pathology, often labral tears will give asymmetric laxity
- thermal as an adjunct is questionable/no proof but good reports
- when laxity is symmetric and no other pathology is identifiable may want to consider thermal treatment
References:
1. Altchek DW, Warren RF, Skyhar MJ and Ortiz G: T-Plasty: A Technique for Treating Multidirectional
Instability in the Athlete. Orthop. Trans, 13:569-561, 1989.
2. Bigliani LU: Anterior and Posterior Capsular Shift for Multidirectional Instability. Techniques Orthop, 3
(4): 36-45, 1989.
3. Bigliani LU, Kurzweil PR, Schwartzbach CC, Flatow EL, and Wolfe I: Inferior Capsular Shift Procedure for
Anterior Inferior Shoulder Instability in Athletes Orthop. Trans. 13:560, 1989.
4. Bigliani, LU, Pollock, RG, McIlveen, SJ, and Flatow, EL: The Inferior Capsular Shift Procedure for
Multidirectional Instability of the Shoulder. American Orthopaedic Association, One Hundred and Sixth
Annual Meeting, Coronado, California, June, 1993.
5. Cooper RA and Brems JJ.: The Inferior Capsular Shift Procedure for Multidirectional Instability of the
Shoulder. J. Bone and Joint Surg., 74-A: 1516-1521, Dec., 1992.
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6. Cordasco FA, Pollock RG, Flatow EL, and Bigliani LU: Management of Multidirectional Instability.
Operative Techniques in Sports Medicine, 4:293-300, 1993.
7. Endo H., Takigawa T., Takata K. and Miyoshi S.: A Method of Diagnosis and Treatment for Loose Shoulder
(in Japanese). Cent. Jpn. J. Orthop. Surg. Traumat, 1971, 14:630-2.
8. Harryman DT, Slides JA, Harris SL., and Matsen FA: Laxity of the Normal Glenohumeral Joint: A
Quantitative In Vivo Assessment. J. Shoulder and Elbow Surg., 1:66-76, 1992.
9. Miniaci, A., McBirnie J. L. Thermal Capsulargraphy in the Treatment of Multidirectional Shoulder
Instability. A Prospective Consecutive Series. (submitted publication)
10. Neer CS II: Involuntary Inferior and Multidirectional Instability of the Shoulder: Etiology, Recognition,
and Treatent. IN: Instr. Course Lect. 1985: 34:232-238.
11. Neer CS II, and Foster CR: Inferior Capsular Shift for Ivoluntary Inferior and Multidirectional Instability
of the Shoulder. A Preliminary Report. J. Bone and Joint Surg., 62A: 897-908, 1980.
12. Neer CS II: Shoulder Reconstruction. Saunders, Philadelphia, 1990:273-341.
13. Norris TR, and Bigliani LU: Analysis of Failed Repair for Shoulder Instability – A Preliminary Report. IN:
Bateman JE, and Welsh RP, Eds: Surgery of the Shoulder. Decker, Philadelphia, 1984.
14. Treacy, S. H., Savoie, F. H., Field, L. H. Arthroscopic Treatment of Multidirectional Instability. J. Shoulder
Elbow Surg. 8: 345-350, 1999.
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ICL #17
Knee OCD
Friday, March 14, 2003 • Aotea Centre, Kupe/Hauraki Room
Chairman: Lars Engebretsen, MD, PhD, Norway
Faculty: Anthony Miniaci, MD, FRCS, Canada, Lars Peterson, MD, PhD, Sweden, Jon Karlsson, MD, PhD, Sweden and
Andre Frank, MD, France
TREATMENT OF OCD WITH MOSAIC PLASTY
Professor Jon Karlsson
ICLs
Although the treatment of OCD is controversial and there is no consensus in the literature, mosaic plasty,
using osteochondral grafts is without doubt one option. This form of treatment is especially useful in case
of large OCD, which is still in-situ. In most cases 3-4 osteochondral plugs can be used. This form of treatment is probably widely used today, however, there are several obvious limitations, which are still unsresolved. The risk of complications, including donor-site pain is one of the major draw-backs. In most cases
the mosaic plasty is also performed as an open knee surgery, in which case arthrotomy is needed. It should
also be born in mind that the best treatment is still unknown, as no randomised studies are yet found.
OSTEOCHONDRITIS DISSECANS OF THE KNEE TREATED WITH AUTOLOGOUS CHONDROCYTE
TRANSPLANTATION
Lars Peterson, Gothenburg Universiy, Gothenburg, Sweden.
Introduction: The etiology of osteochondritis dissecans (OCD) is still unknown, but the relations to trauma,
repeated trauma and physical activity are discussed as possible. The treatment however varies with the age
of the patient and the type of lesion and is a challenging clinical problem. Autologous chondrocyte transplantation (ACT) has been used in the treament of OCD of the knee in Gothenburg, Sweden since 1990.
Previous reports on the treatment of OCD with ACT showed promising results. Late results (2-10 year follow-up) will be presented as well as complications.
Methods: Forty-two patients with OCD were treated with ACT between September 1990 and October 1997.
Mean age was 26 years (range 15-50) and the mean duration of symptoms was 7.5 years at the time of
treatment. 83% had a mean of 3.2 prior surgeries. The defects were located on the medial femoral condyle
(n=28), the lateral femoral condyle (n=13) or the femoral trochlea (n=1), the mean defect size was 5.7 cm2
(range 1.5-12.0) and mean depth was 7.7 mm (range 4-15). At a mean follow-up of 4.8 years (range 2-10) 33
patients were assessed clinically and 10 patients were evaluated arthroscopically.
Results: At follow-up the clinical status were graded Good or Excellent in 86% of the patients and 84% considered themselves improved. Tegner-Wallgren activity score increased from mean 6.8 preoperatively to 9.3
at follow-up and mean Lysholm score at follow-up was 73.5, compared to 44.3 preoperatively. BrittbergPeterson functional VAS decreased from a mean 80.4 preoperatively to 31.6 at follow-up. At the arthroscopic assessment the graft was evaluated according to the Brittberg scoring system for the degree of defect
repair, integration to border zone and macroscopic appearance with a maximum of 12 points. The mean
score was 10.2, only one had a score less than 9. In two patients the treatment was considered as a failure,
both of which occurred early postoperatively. Successful and unsuccessful cases will be presented.
Discussion: The outcome after treating OCD with autologous chondrocyte transplantation is successful for
more than 80% of the patients, the clinical status is improved and the patients consider themselves
improved and are able to live a more active life.
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Osteochondritis Dissecans
Clinical Treatment Options
Anthony Miniaci, MD, FRCSC
Professor of Orthopaedic Surgery
Head of Sports Medicine Program
Department of Surgery, University of Toronto
Toronto, Ontario
At the end of this presentation the participant will be able to:
- Understand the history and evaluation of osteochondral knee disorders specifically osteochondritis dissecans
- Identify the efficiency of the various surgical techniques used to treat osteochondral defects and indications for each
- Be able to identify the limitations and strengths of various techniques used to treat chondral and osteochondral pathology
ICLs
Objectives:
Osteochondritis Dissecans
Localised lesion characterised by seperation of a segment of articular cartilage and its underlying subchondral bone
Incidence
-Poorly understood entity with no universally accepted etiology.
-True incidence unknown as often spontaneous resolution without presentation.
-Multiple joints reported but knee accounts for 75% (Pappas)
Male:Female 2:1 (Pappas)
Etiology
2 Types based around physeal closure
- Juvenile OCD
5-15yr
-Adult OCD
15-50yr
-Several factors implicated,
- Trauma
- Ischaemia
- Genetic
- Defects of ossification
-? Hormonal
Direct Trauma- As the posterolateral portion of the medial femoral condyle is affected in 85% of knees,
direct trauma is unlikely (Aichroth)
Indirect Trauma
- Odd facet of patella articulating with area (Aichroth)
- Impingement of tib spine on area in internal rotation (Fairbank)
Ischemia
-Abnormal End-artery theory of subchondral bone susceptible to emboli and ischaemia has been suggested. (Campbell)
-other studies found blood supply of subchondral femur rich in anastomoses & the histology of loose bodies and resected fragments to NOT demonstrate evidence of OCD (Chiroff)
Genetic
-Suggested that OCD may represent a mild subgroup of epiphyseal dysplasia (Ribbing)
-Associations with Perthes & Achondroplasia
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-Familial relationships have been recorded (Stougard)
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Ossification Defects (Juvenile OCD)
-OCD represents irregularity of ossification (Mubarak)
-Multiple OCD lesion maybe due to an irregularity of ossification due to MED (Mubarak)
Presentation
-Symptoms dependent on stage of lesion
-Early - vague pain +/- swelling, activity related
-Late - if flap or loose body, catching & giving way
-Effusion, tenderness, crepitus
-External rotation of leg
-Wilson’s sign (Flex to 90 & extend in IR, pain at 30 degrees)
Investigations
-Plain x-ray – notch/tunnel view required
-Tc 99 Scan – previously described to identify & follow the course/recovery of OCD (Cahill)
-MRI now best modality for diagnosis and following progress of lesion
MRI Classification
Stage I -Thickening of artic. cart. & low signal change
Stage II-Artic. cart. breached & low signal rim behind fragment
Stage III -Artic. cart. breached & high signal changes behind fragment
Stage IV
-Loose body (Dipaola)
MRI
-MRI Arthrogram better to assess breach in cartilage (Kramer)
-Spoil Gradient Sequences for articular cart (SPGR)
Arthroscopy
- Arthroscopic assessment
- Clanton & DeLee
o Grade I
- Depressed subchondral fracture
o Grade II
- OC fragment attached by an osseous bridge
o Grade III
- A detached non-displaced fragment
o Grade IV
- Displaced fragment
Management
-Controversy & confusion in literature as often small numbers, mix juvenile & adult and few prospective trials
-Management dependent on
- Age of patient
- Stage of lesion
Juvenile OCD-Lesions in knees with open physes usually heal with conservative treatment, those that don’t are due to
continued activity. (Cahill)
-Ideal initial management conservative.
- Protected wt bearing/restriction of activities (90 degree casts)
- However, affected children often athletic & difficult to fully restrict.
- Try to avoid impact activities
- Chances of success with non-op treatment decrease as time of physeal closure nears
- 50% heal within 12 months
- Follow progress with serial MRI
Indications for Operative Intervention
-Symptoms persist for 6 – 12 months despite adequate non-operative treatment
- Loose fragment
- Progression of defect radiologically (MRI)
- Predicted physeal closure within 6-12 months
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Adult OCD
- Symptomatic lesions rarely heal with non-operative measures
- Lower tolerance for operative intervention after failure of conservative measures.
Operative Intervention
-Stabilisation/Re-fixation of fragment
(Clanton II, III & selected IV)
-Excision of fragment/Reconstruction of OCD defect
-Clanton Type II/III (IV)
- Principles:
- rigid fixation
- enhance blood supply
- re-establish congruency
Internal Fixation: (open or arthroscopic)
- Pins (Smillie)
- K-wires (Cahill)
- Herbert Screws (Mackie)
- Biodegradable Rods (Dervin)
- Corticocancellous Bone Pegs (Victoroff)
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Arthroscopic Drilling:
- Controversial for most lesions but good results reported in Juvenile
Clanton II lesions(Aglietti)
-Additional bone grafting under articular cartilage (Anderson)
OCD Defect
- Poor results after excising lesion & leaving defect (Cahill)
- Healing fibrocartilage biomechanically less resilient than articular cartilage predisposing to
degenerative changes (Landells)
Fragment Fixation-Technique (Miniaci)
a) Clanton and DeLee type II and III lesions
- Unstable lesions that fail conservative management
- can be used in prepubertal and postpuberty patients
- theoretical considerations
i. stabilize fragment with K-wire, remove after fixed with 1 or 2 plugs
ii. drill holes – stimulates blood supply
iii. press fit 3.5 mm or 4.5 mm plugs
- results in stable fixation
iv. place peripheral plugs between native vascular bone and fragment so that healing of fragment
can occur
v. plug serves as a source of bone graft
vi. cartilage cap on "plug" restores articular surface so end result will have continuous articular
cartilage surface
vii. central plug should be used for ultimate stability. This should be long enough to traverse OCD
fragment into underlying vascular bone.
Measure depth preoperatively.
Ultimately provides- blood supply–drilling
-stability-interference fixation
-bone grafting of fibrous layer
-congruent articular cartilage surface
clinical results > 20 cases of OCD
100% healing rates
no additional fixation
return to activity and sports by 3 to 4 months
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complete healing by 6 to 9 months
viii. Type IV Lesions
-Where suitable for fixation- debride bed
-Initial stabilisation with k-wires is required before plug insertion
b).Chronic lesions- Indications for Treatment
- Symptomatic defect (trial of debridement)
- Stable knee
- Normal biomechanical alignment
- Minimal degenerative changes
Defect Reconstruction
- Large osteochondral grafts
-Autografts (Outerbridge)
-Mosaic Autografts (Hangody, Bobic, Miniaci)
-Allografts (McDermott)
- Chondrocyte culture implantation- ? not as effective as a result of bone defect
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Filling of Defect – Mosaicplasty Reconstruction
Technique – when fragment lost BE CAREFUL
-Aim to recreate joint curvature &congruence
-Fill defect with grafts from the periphery inwards. This allows for assessment of joint curvature and for
central graft support
-Central pegs will need to be longer to account for the greater height of curvature and depth of crater
- need to sit central plugs higher, since you are reconstructing both
a bone and cartilage defect
- if plugs in center are not higher, then reconstruction will be flat
- * measure center of defect on MR preoperatively to determine size
and length of plugs
- graft harvest from edge of patellofemoral joint (Both knees as necessary) (10-12 4.5 mm grafts from
each knee)
-Post-operative treatment
- Allow knee motion but strict non-wt bearing for 6 weeks
- Gradual wt-bearing at 6 weeks
- return to sport 3-4 months
-effusion can last 4 months ( painless )
1. Focal Traumatic Osteochondral Lesions
- similar principles to OCD
- in acute lesions can use plugs to fix osteochondral lesions
- femoral condyles easiest
- tibial lesions difficult, not practical
- trochlear lesions usually require arthrotomy
2. Patellofemoral Lesions
- trochlear and patellar lesions need arthrotomy
- usually combine with Fulkerson osteotomy and lateral release
i. to be sure to reconstruct contour of both femoral trochlea and patella
ii. place plugs close together to increase stability
iii. put knee through repeat range of motion – if incongruency exists, this
needs to be adjusted otherwise the plug heads will SHEAR off
Optimum Surgical Conditions
- many unknown variables at present
- morbidity related to both donor and recipient sites as well as method of delivery
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Recipient Sites
- hole preparation crucial
- preserve bone stock, need stable construct
- drilling holes causes thermal necrosis
- dilating holes preserves bone stock and reduces thermal necrosis
- press fit plug to hole for stable construct
- bottom out hole to avoid
- subsidence
- cyst formation
- fill defect with as much articular cartilage as possible, reduces % of fibrocartilage
- put plugs even with surrounding articular surface
i)too proud- causes loosening and cyst formation
ii)recessed- covered with fibrocartilage
- ? heterotropic transfers
- does thin cartilage become thick or vice versa
- ? cartilage degeneration
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Donor Sites
- plug harvest location important
- keep out tibiofemoral joint
- 5mm on periphery of patellofemoral joint is optimal (less contact), avoids reciprocal arthrosis
- large plugs, > 5mm fill incompletely, with fibrosis tissue
- causes reciprocal OA in areas of weight bearing contact
Graft Harvest and Delivery
Harvest
- do not use power trephine for harvest
- causes cell necrosis
- multiple small plugs allows for better reconstruction of curved surface
- inspect plus after harvest
i) plug integrity
ii) fractures
iii) obliquity
iv) measure depth of plug
Plug Delivery
- press fit plugs, flush with surrounding articular surface, bottom out hole
- manual or light pressure only to insert plugs
- ? impaction causing cell necrosis
- reconstruct curved surfaces, (center higher than periphery)
- tendency is for flat reconstructions
Basic Science/Clinical Results
- early clinical results
good anecdotal
- need to define patient populations
- at present best in patients failing other procedures (i.e. debridement, microfracture, etc.)
- osteochondritis dissecans excellent results
- traumatic lesions good
- patellofemoral – fair to good
- histologically Type II collagen preserved, bone healing of plugs provides solid structure
- subchondral cyst formation a concern
Future
- ? hybrid techniques
- ? donor site reconstruction
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REFERENCES
Buckwalter JA, Mankin H.J. Articular cartilage: Part II: Degeneration and Osteoarthrosis, Repair,
Regeneration, and Transplantation. JBJS- American Volume 1997; 79A:612-618.
Rodrigo JJ, Steadman RJ, Silliman JF, Fulstone HA. Improvement of Full-thickness Chondral Defect Healing
in the Human after Debridement and Microfracture Using Continuous Passive Motion. Am. J Knee Surg
1994; 7:109-116.
O’Driscoll SW, Keeley FW, Salter RB. Durability of Regenerated Articular Cartilage Produced by Free
Autogenous Periosteal Grafts in Major Full-thickness defects in Joint Surfaces Under the Influence of
Continuous Passive Motion. A Follow up Report at one year. JBJS 1988; 70A: 595-606.
Hangody L. Kish G, Karpati Z, Szerb I, Udvarhelyi I, Toth J, et al. Autogenous Osteochondral Graft
Technique for Replacing Knee Cartilage Defects in Dogs. Orthopaedics 1997; 5: 175-181.
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Bobic V. Arthroscopic Osteochondral Autograft Transplantation in Anterior Cruciate Ligament
Reconstruction: Preliminary Clinical Study. Knee Surg. Sports Traumatology, Arthroscopy 1996; 3:262-264.
Garrett JC. Fresh osteochondral Allografts for Treatment of Articular Defects in Osteochondritis Dissecans
of the Lateral Femoral Condyle in Adults. Clinical Orthopaedics & Related Research 1994; 33-37.
Hurtig M, Pearce S, Warren S, Kalra M, Miniaci A. Arthroscopic Mosaic Arthroplasty of the Equine Third
Carpal Bone. Submitted for publication.
Pearce S, Hurtig M, Clarnette R, Kalra M, Miniaci A. Investigation of Two Techniques for Optimizing Joint
Surface Congruency with Mosaic Arthroplasty. Submitted for publication.
Hurtig M, Evans P, Pearce S,Clarnette R, Miniaci A. The Effect of Graft Size and Nimber on the Outcome of
Mosaic Arthroplasty Resurfacing: An Experimental Model in Sheep. Submitted for publication.
References- Osteochondritis Dissecans
Pappas AM. OCD. Clin Orthop 158;1991
Aichroth P. OCD of the knee. JBJS 53-B;1971
Fairbank HA. OCD. British J Surg 21;1933
Campbell & Ranawat. OCD: the question of etiology. J Trauma6; 1966
Chiroff & Cooke. OCD: microradiographic analysis. J Trauma 15; 1975
Ribbing S. Hereditary ME disturbances. Actav Orth Scan 24;1955
Stougard J. Familial occurrence of OCD. JBJS 46-B; 1961
Mubarak & Carroll. Juvenile OCD of the knee: etiology. Clin Orthop 157; 1981
Wilson JN. A diagnostic sign in OCD of the knee. JBJS 49-A; 1967
Cahill & Berg. Tc-99m scintigraphy in the management of OCD. AmJ SportMed 11; 1983
Dipaloa JD et al. Characterising OCD lesions by MRI. Arthroscopy 7;1991
Kramer J et al. MR contrast arthrog in OCD. J Comput Assis Tomog 16;1992
Clanton & DeLee. OCD. History, pathophys & current treatment concepts. Clin Orthop 167; 1982.
Aglietti P et al. Arthroscopic drilling in juvenile OCD. Arthroscopy 10;1994.
Smillie IS. The treatment of OCD. JBJS 39-B; 1957
Cahill B. Treatment of juvenile OCD & OCD of the knee. Clin Sports Med 4;1985
Mackie IG et al. Arthroscopic use of the Herbert screw in OCD. JBJS 72-B;1990
Dervin GF et al. Biodegradable rods in adult OCD of knee. Clin Orthop 356; 1998
Victoroff BN et al. Arthroscopic bone peg fixation in the treatment of OCD in the knee. Arthroscopy 12;1996
Landells JW. The reaction of injured human cartilage. JBJS 39-B; 1957
McDermott GB et al. Fresh small fragment osteochondral allo-grafts. Long term follow up on 1oo cases.
Clin Orthop 197; 1985
Outerbridge HK et al. OCD defects in the knee. Clin Orthop 377; 2000
Berlet, Mascia, Miniaci. Treatment of unstable OCD of the knee using autogenous OC grafts. Arthroscopy
15;1999
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ICL #18
HIP ARTHROSCOPY
Friday, March 14, 2003 • Carlton Hotel, Carlton I
Chairman: J.W. Byrd, MD, USA
Faculty: James Glick, MD, USA, Michael Dienst, MD, Germany and Romain Seil, MD, Germany
J.W. Byrd, MD
I.
Merits of the Supine Position
A. Effective and reproducible
B. Utilizes existing OR equipment (standard fracture table)
C. Positioning simple and time efficient
D. Orientation familiar for orthopaedic surgeons
E. Operating room layout user friendly for the surgeon and support staff
II.
Equipment
A. Fracture table
Tensiometer for monitoring traction forces intraoperatively is the most
important modification
B. C-arm image intensifier
C. 70° and 30° video-articulated arthroscopes
D. Fluid management system
E. Specialized hip arthroscopy cannula system
1.
Extra length cannulas
2.
Shortened bridge accommodates extra length cannulas with standard
arthroscope
3.
Cannulated obturators
Allows prepositioning with spinal needle. Cannula/obturator
assembly can be passed over a guide wire initially placed through
the needle
F. Extra length flexible cannulas allow passage of curved shaver blades
G. Extra length sturdy hand instruments
Avoid instruments designed for other endoscopic purposes that might be
less sturdy and at greater risk of breakage
H. Laser exhibits distinct advantages in the hip
1.
Maneuverability
2.
Ability to effectively ablate tissue despite limits of maneuverability
III.
Anesthesia
Typically performed under general anesthetic. Epidural anesthesia is an
appropriate alternative but requires adequate block for assuring muscle
relaxation.
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y
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Hip Arthroscopy: The Supine Approach
J. W. Thomas Byrd, M.D.
IV.
A.
Patient Positioning
Placed supine on the fracture table (Figure 1)
B. Heavily padded perineal post, lateralized against the medial thigh of the
operative leg (Figure 2)
1.
Lateralizing the post adds a slight transverse component to the traction
vector (Figure 3).
2.
Also lessens the likelihood of compression and possible neuropraxia of
the pudendal nerve
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Fig. 1
Fig. 2
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Fig. 3
C.
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Operative hip positioned in extension, approximately 25° of abduction, and
neutral rotation
1.
Slight flexion might relax the capsule and facilitate distraction, but can
place more traction on the
sciatic nerve and draw it
closer to the joint, making it
more vulnerable to injury.
Thus, significant flexion is
avoided during arthroscopy.
2.
Neutral rotation is important
during portal placement
(Figure 4) although freedom
of rotation during
Fig. 4
arthroscopy can facilitate
visualization.
D. The contralateral extremity is abducted as necessary to accommodate
positioning of the image intensifier between the legs.
Prior to applying traction to the operative leg, counter force is created by
placing the contralateral extremity under light traction. This stabilizes
the pelvis so that it does not shift as traction is gradually applied to the
operative extremity.
E. Traction is applied to the operative extremity and distraction of the joint
confirmed by fluoroscopy.
1.
Typically about 50 pounds is applied. More force may be necessary for
a tight joint, but should be undertaken with caution.
2.
Initially, adequate distraction (8-10 mm) may not be readily achieved.
a.
Allowing a few minutes for the capsule to accommodate to the
tensile forces often results in relaxation of the capsule (physiologic
creep) and adequate distraction without excessive force.
b.
Also, a vacuum phenomenon created by the capsular seal will later
be released when the spinal needle is introduced and the joint is
distended with fluid, which may further facilitate distraction.
F. After confirming the ability to distract the joint, the traction is released until
ready to begin the surgical procedure.
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V.
Portals
The three standard portals are: Anterior, Anterolateral, and Posterolateral
(Figures 5 and 6).
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Fig. 5
Fig. 6
Table 1
DISTANCE FROM PORTAL TO ANATOMIC STRUCTURES
(Based on Anatomic Dissection of Portal Placements in Eight Fresh Cadaver Specimens)
Portals
Anatomic Structure
Average
(cm)
Range
(cm)
Anterior
Anterior Superior Iliac Spine
Lateral Femoral Cutaneous Nerve
b
Femoral Nerve (level of Sartorius)
(level of Rectus Femoris)
(level of Capsule)
Ascending Branch of Lateral Circumflex Femoral
Artery
c
Terminal Branch
6.3
0.3
4.3
3.8
3.7
3.7
0.3
6.0-7.0
0.2-1.0
3.8-5.0
2.7-5.0
2.9-5.0
1.0-6.0
0.2-0.4
Anterolatera
l
Superior Gluteal Nerve
4.4
3.2-5.5
Posterolatera
l
Sciatic Nerve
2.9
2.0-4.3
a
a
Nerve had divided into three or more branches and measurement was made to the closest branch.
Measurement made at superficial surface of sartorius, rectus femoris, and capsule.
c
Small terminal branch of ascending branch of lateral circumflex femoral artery identified in three
specimens.
b
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A.
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Anterior portal (Figure 7)
1.
Positioning
a.
Entry site is at the
intersection of a sagittal
line drawn distally from
the ASIS and a
transverse line across
the superior margin of
the greater trochanter
b. Directed approximately
45° cephalad and 30°
Fig. 7
towards the midline
c.
Enters the joint under the anterior margin of the acetabular labrum
(Position is facilitated by direct arthroscopic visualization)
2.
Relationship to extraarticular anatomic structures
a.
Penetrates the sartorius and rectus femoris before entering the
anterior capsule
b. At the level of this portal, the lateral femoral cutaneous nerve has
trifurcated
i.
One of these branches will usually lie close to the portal
ii.
Most branches lie lateral to the portal
Moving portal more laterally does not reliably avoid
these branches
Moving portal medially is ill-advised because of closer
proximity to femoral nerve
iii. Laceration of the LFCN is avoided by utilizing careful
technique, not incising too deeply with the skin incision
iv. Although laceration can be avoided, neuropraxia of one of
these branches may occur due to manipulation of the cannula
and instrumentation from the anterior position (<1%
incidence)
Neuropraxia of one of these branches may result in a
small area of reduced sensation of the lateral thigh which
is usually permanent
Accompanying morbidity is minimal, but should be
mentioned as part of the pre-operative discussion
c.
The portal runs roughly tangential to the axis of the femoral nerve.
It lies only slightly closer to the nerve at the level of the capsule
with an average minimum distance of 3.2 cm.
d.
The relationship of the ascending branch of the lateral circumflex
femoral artery is variable with an average distance of 3.7 cm
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B.
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Anterolateral Portal (Figure 8)
1. Positioning
a.
Entry site is over the superior margin of the
greater trochanter at its anterior border
b.
Direction
i.
In the AP fluoroscopic view, the
portal passes immediately above the
greater trochanter and then close to the
superior surface of the
femoral head to stay
underneath the lateral
acetabular labrum.
ii.
Accounting for normal
femoral neck
anteversion, with the hip
in neutral rotation, the
portal courses parallel to
the floor, thus entering
the hip joint just anterior
to its mid-coronal plane.
Fig. 8
2.
Relationship to the extraarticular
structures
a.
The anterolateral portal lies most centrally in the "Safe Zone" for
arthroscopy (Consequently it is the first portal established )
b. The portal penetrates the gluteus medius before entering the lateral
capsule
c.
The superior gluteal nerve runs transversely an average of 4.4 cm
cephalad to the portal
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C. Posterolateral Portal (Figure 9)
1.
Positioning
a.
Entry site is over the
superior margin of the
greater trochanter at its
posterior border
b.
Directed slightly
cephalad and anterior
(converges toward
anterolateral portal)
c.
Enters the joint
underneath the
Fig.9
posterolateral margin
of the labrum (Entry location is performed under direct
arthroscopic visualization)
2.
Relationship to the extraarticular structures
a.
The portal pierces the gluteus medius and minimus before entering
the lateral aspect of the capsule posteriorly.
b.
Like the anterolateral portal, the superior gluteal nerve averages a
distance of 4.4 cm.
c.
It enters the capsule superior and anterior to the piriformis tendon.
d.
It lies closest to the sciatic nerve at the level of the capsule with an
average distance of 2.9 cm.
i.
Inadvertent external rotation of the hip during portal
placement will move the greater trochanter more posterior
relative to the hip joint. This will unnecessarily cause the
posterolateral portal to pass closer to the sciatic nerve.
Consequently, external rotation is avoided during initial portal
placement.
ii.
Hip flexion might partially relax the capsule and improve
distraction. However this will place more traction on the
sciatic nerve and may draw it closer to the joint, again placing
it at more risk for inadvertent damage. Thus, inordinate hip
flexion during hip arthroscopy should be avoided.
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VI.
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Portal Placement and Normal Arthroscopic Exam
A. Traction is applied to the hip
B. Anterolateral Portal
1.
Placed first because it lies most centrally in the “safe zone” for
arthroscopy
2.
Prepositioning performed with a custom spinal needle (6", 17 gauge)
under fluoroscopic guidance
3.
Joint is then distended with saline
4.
Important to avoid penetrating the lateral labrum with the needle
a.
The needle meets greater resistance penetrating the labrum and can
be felt during placement.
b.
After distending the joint, if necessary, the needle can be
repositioned closer to the femoral head, further lessening the
likelihood of piercing the labrum.
5.
A guide wire is passed through the needle and the needle is withdrawn.
6.
The cannula/obturator assembly is then passed over the guide wire into
the joint. (Figures 10 and 11)
As the assembly pierces the capsule, it is
lifted up to avoid grazing the articular surface
of the femoral head.
7.
The 70° arthroscope is then introduced in the
anterolateral cannula.
Fig.
a.
Use of the 70° scope allows a direct view of
where the anterior and posterolateral portals
enter the joint simply by rotating the lens
anteriorly and posteriorly.
b.
If there is a chance that the cannula may still
have pierced the labrum, at this point
excessive maneuvering of the cannula should
be minimized.
Fig. 11
C. Anterior Portal
1.
Prepositioned with spinal needle
a.
Facilitated by fluoroscopy
b.
Precise intracapsular positioning confirmed by direct arthroscopic
view
2.
As the cannula/obturator assembly enters the joint, again by utilizing
arthroscopic visualization, the labrum is avoided and the assembly is
lifted off the articular surface of the femoral head.
D. Posterolateral Portal
1.
Rotating the arthroscope posteriorly in the anterolateral portal allows
viewing of the entry site for the posterolateral position.
2.
Needle placement and introduction of the cannula are then carried out in
the standard fashion.
SURGICAL DEMONSTRATION
HIP ARTHROSCOPY BY THE LATERAL APPROACH
James M. Glick, M.D.
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INSTRUMENTS
A. Traction device.
1. Fracture table set for lateral dicubitus position
2. Specially made traction device with tensiometer
B. Image intensifier
C. Hip surgical instruments
1. 14 or 15 gauge extra long spinal needles
2. Nitanol guide wires to fit through the needles
3. Cannulated trochars that fit over nitanol guide wires
4. Long 30 and 70 degree fore-oblique arthroscopes
5. Long shaver sheaths. Diameters should be wide enough to accommodate an arthroscopic knife.
6. Slotted cannulas
7. Long switching sticks
8. Arthroscopic knife (Beaver)
9. Long motorized cutters-straight and curved with cutter on concave side.
10. Radio frequency or laser ablative instruments
11. Graspers
12. Probe
II. ROOM SET-UP
A. Image Intensifier either above or below table
B. Surgeon stands In front of patient
C. Monitors on opposite side of table from surgeon
Ill. TECHNIQUE
A. Place patient on his/her side with involved leg upward
B. Place involved leg in traction device and insert a well-padded perineal post into the crotch.
1. Hip should be placed in slight flexion, abduction and external rotation to relax the capsule.
2. If the diameter of the perineal post is less than 9 cm add extra padding to increase its size. A
large diameter post will distribute the force of the traction, so it is not concentrated as much on
the pudendal nerve.
3. Support the lower torso. This will decrease the vertical forces on the post.
C. Image hip joint
D. Draw landmarks with marking pen with aid of the image intensifier
1. Anterior superior iliac spine
2. Greater trochanter
E. Scrub and drape with sterile sheets and a sticky drape
F. Find portals with long spinal needles and the aid of the image intensifier
I. Portals
a. Anterior paratrochanteric
b. Posterior paratrochanteric
c. Direct anterior
2. First, apply 50 lbs of traction—distract at least 12mm
3. Second, direct an extra long spinal needle into the hip joint at the proposed anterior para
trochanteric portal, over the anterior edge of the greater trochanter with the aid of the image
intensifier.
a. Aspirate
b. Inject 10cc of air to help break the suction seal which provides more distraction.
c. Insert a nitanol guide wire into the needle and remove the needle leaving the guide wire in
the hip joint.
d. Make a stab incision around the guide wire.
e. Place the arthroscope sheath with a cannulated trochar over the guide wire and direct it into
the hip joint. Next, couple the arthroscope into the sheath.
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4. The next two portals are made under direct vision, viewing needle entrance through the
arthroscope. Most of the time this can be accomplished without introducing fluid into the
joint. Occasionally a small amount of fluid might be required. These needles should be placed
away from the labrum, to keep from damaging it.
a. Place one needle into the proposed posterior paratrochanteric portal at the level of
posterior edge of the greater trochanter and another needle in the direct anterior portal sight
and watch them enter the joint.
b. Once both needles are correctly placed in the joint the image intensifier may be removed.
5. Prepare for arthroscopy
a. Place inflow tubing on scope stopcock
b. Place outflow tubing on one or the other two needles
6. The next portals are made in a similar manner as the first: One portal for instrumentation and
the other for outflow.
7. Accessory portals
a. In-between regular portal sights
b. Outside portal sights--No further anterior than the level of the anterior superior iliac spine
and always aim for joint when posterior. Use needles to identify the portals.
c. Distal portals to reach the intra-capsular portion of the femoral neck.
G. Capsulotomy--Important step In order to increase mobility of the instruments and to simplify
instrument Insertion.
1. Place 5.6mm cannula with cannulated trochar over nitanol wire in posterior paratrochanteric
portal and insert into joint under direct vision. Then insert straight shaver into the cannula to
clean the area.
2. Next, remove the shaver and insert the arthroscopic knife through the cannula and remove the
cannula leaving the knife in the joint.
3. Cut the capsule as widely as possible in all directions under direct vision.
4. After cutting the capsule, a curved shaver and other instruments should be easy to insert
without necessitating switching sticks.
5. If difficulty entering the joint with curved instruments is encountered, a slotted cannula may be
inserted over a switching stick for directing these instruments into the joint.
H. Observe hip joint and perform surgery
1. Complete visualization by switching portals
2. Might have to temporarily increase traction to visualize and reach depths of the joint.
IV. TRICKS, OBSERVATIONS AND PREVENTATIVE MEASURES
A. Relationship of portals to vital structures
1. None near portal sights
2. Lateral femoral cutaneous nerve is closest.
a. Make direct anterior portal incision along the line of the nerve.
b. Make incision just through the skin
B. Traction device
1. Minimize traction force to take pressure off of the pudendal and sciatic nerves
a. Decrease traction during prep and drape
b. Minimize hip adduction
c. Reduce traction whenever possible--ideal amount of traction is less than 75# and like a
tourniquet, stop after two hours.
d. To protect the pudendal nerve, the perineal post should be at least 9 cm in diameter. Build it
up with padding if it is not. Also make sure the pelvis is supported.
2. Ways of keeping the traction forces at a minimum
a. Placing hip in slight flexion, abduction and external rotation to relax the capsule.
b. Breaking the suction seal before traction is applied
c. Do not flex hip around a perineal post as it places a stretch on the sciatic nerve
C. Portals to reach extra-capsular pathology or structures around the neck (tumors, pvns, synovial
chondromatosis or loose bodies and release of the iliopsoas tendon)
1. Patient in the lateral position. Externally rotate the hip to bring into view the lesser trochanter
on the image intensifier
2. Release the traction
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3. Mark level of lesser trochanter or the area of pathology
4. Portal for the scope is at the level of the marker and in line with the anterior para-trochanteric
portal
5. Portal for operating instruments below the scope portal and in line with the anterior superior
iliac spine
6. Line up the tips of the scope and a motorized instrument at the surgical sight on the image
intensifier
7. Keep the tip of the motorized instrument close to the bone and start shaving. When the
pathology or the indicated structure comes into view appropriate surgery can be commenced.
8. Once the space is made at the surgical sight it will become easy to exchange instruments
9. Out flow is accomplished with the suction of the operating instruments or an accessory portal
made distal or proximal and in between the first two portals
D. Prevention of fluid extravasations into the retro-peritoneal space and subcutaneous tissues
1. If possible use a pressure gauge that measures the pressure outside the joint
2. Make sure that inflow and outflow portals do not wander outside the joint
3. Make sure the outflow stays open and the fluid is flowing out.
E. Prevent scuffing and labral damage
1. Adjust the needles before making Incisions, so they are not against the femoral head
2. Twist the scope cannula and trochar in slowly under image Intensification. If the sharp trochar
is used, exchange it for the blunt trochar after the sharp pierces the capsule. Once the cannula
is well into the joint, if possible, stop before it strikes the acetabular floor and insert the scope.
3. The rest of the instruments should be inserted under direct vision.
4. Change the needle placement if it is through the labrum before developing the portal.
F. Reaching the deep and medial aspects of the joint
1. Wide capsulotomy
2. Accessory portals
3. Curved instruments
4. May have to increase traction
V. REFERENCES
A. Glick JM, Sampson TG, Hip Arthroscopy by the Lateral Approach. In: McGinty JB, ed. Operative
Arthroscopy. 2nd ed. New York: Raven Press; 1996: 1079-1089.
B. Glick JM, Hip Arthroscopy Using the Lateral Approach. American Academy of Orthopaedic Surgery,
Instructional Course Lectures. 1988, 37: 223-231.
C. Sampson TG, Glick JM, Indications and Surgical Treatment of Hip Pathology. In: McGinty JB, ed.
Operative Arthroscopy. 2nd ed. New York: Raven Press; 1996: 1067-1078.
D. Glick JM, Hip Arthroscopy, the Lateral Approach. In: Clinics in Sports Medicine; Ed. J. W. Thomas Byrd.
Vol. 20, No. 4, Oct. 2001. PP 733-747.
E. Sampson TG, Complications of Hip Arthroscopy. In: Clinics in Sports Medicine; Ed. J. W. Thomas Byrd.
Vol. 20, No. 4, Oct. 2001. PP 831-835.
F. Byrd JWT, Avoiding the Labrum in Hip Arthroscopy. "Arthroscopy" 16; 7: 770-773, 2000.
G. Khapchik.V, O’Donnell, R.J. and Glick, J.M. Arthroscopically Assisted Excision of Osteoid Osteoma
Involving the Hip. "Arthroscopy" 17; 1: 56-61, 2001.
HIP ARTHROSCOPY WITHOUT TRACTION
Michael Dienst, M.D.
Department of Orthopedic Surgery
University Hospital
66 421 Homburg/Saar, Germany
Email: [email protected]
Over the past two decades, different hip arthroscopists around the world have been contributing to the
development of techniques for arthroscopy of the hip joint, with most authors advocating the use of trac3.151
tion. The technique of hip arthroscopy (HA) without traction, however, has been disregarded. Recent
reports have proposed different advantages of the non-traction technique. The low complication rate of this
procedure has been emphasized. Whereas traction is required for inspection of the direct weight-bearing
cartilage, the acetabular fossa and the ligamentum teres, arthroscopy without traction is ideally situated
for evaluation of the hip joint periphery.
This instructional course lecture presents detailed steps how to perform the non-traction technique. A systematic mapping of that part of the joint that can be inspected without traction is included. Indications are
specified and illustrated with selected case examples.
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Peripheral Compartment of the Hip Joint
Understanding of the anatomy and function of the acetabular labrum is important not only for assessment
of integrity of the labrum but also for access to the hip joint. The labrum seals the joint space between the
lunate cartilage and the femoral head. To overcome the vacuum force and passive resistance of the soft tissues, traction is needed to separate the head from the socket, to elevate the labrum from the head and to
allow the arthroscope and other instruments access to the narrow space between the weightbearing cartilage of the femoral head and acetabulum. However, if traction is applied, the joint capsule with its intrinsic
ligaments is tensioned and the joint space peripheral to the acetabular labrum decreases. Thus, in order to
maintain the space of the peripheral hip joint cavity for better visibility and manoeverability during
arthroscopy, traction should be avoided.
In consequence, Dorfmann and Boyer divided the hip arthroscopically into 2 compartments separated by
the labrum. The first is the central compartment comprising the lunate cartilage, the acetabular fossa, the
ligamentum teres and the loaded articular surface of the femoral head. This part of the joint can be visualized almost exclusively with traction. The second is the peripheral compartment consisting of the unloaded
cartilage of the femoral head, the femoral neck with the medial, anterior and lateral synovial folds
(Weitbrecht’s ligaments) and the articular capsule with its intrinsic ligaments including the zona orbicularis. This area can be seen without traction and will be described subsequently.
Positioning, Distension and Portals for Arthroscopy of the Hip Periphery
Hip arthroscopy with and without traction can be performed in the lateral or supine position. However, the
almost exclusive use of the anterolateral portal during HA without traction makes the supine position
preferable.
Free draping and a good range of movement are important to relax parts of the capsule and increase the
intraarticular volume of the area that is inspected. This is important for safe movement of the scope in
order to avoid damage to the cartilage of the femoral head and synovial folds and unwanted sliding of the
scope out of the joint. The distending effect of irrigation fluid pressure is of minor importance because the
pressure should not be increased over 70 mm Hg in order to reduce the risk of development of a severe
soft tissue edema.
In general, the combination of HA without traction and HA with traction is recommended. The combination
of both techniques is important to allow a complete diagnostic arthroscopic examination of the hip. From
my experience, the traction part should be done prior to the non-traction scope since positioning for traction is more demanding. In particular, exact placement of the counterpost is crucial to avoid complications.
This can be done only under non-sterile conditions.
For HA without traction, the patient is placed supine on a standard traction table or a standard operating
table with an additional traction frame or robotic limb positioning device. A comprehensive overview can
be obtained from the anterolateral portal only. Because the soft tissue mantle is relatively thin and the
position of the portal is near the lateral cortex of the femoral neck, maneuverability of the arthroscope is
sufficient for moving the arthroscope into the medial recess, gliding over the anterior surface of the femoral
head to the lateral recess, and frequently passing the lateral cortex of the femoral neck for inspection of the
posterior recess.
First access to the hip joint periphery can be achieved with or without traction. A long needle (∆ 1-2 mm) is
introduced via the anterolateral portal and directed to the transition between the anterior aspect of the
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femoral head and neck. Here, the capsule is elevated from the neck which allows easier access of the needle into the joint. Entry to the joint is then confirmed by distension of the joint with up to 40 ml of saline,
which leads to a visible lateral and caudal displacement of the femoral head under fluoroscopy. This is better seen if the hip is under moderate traction. The standard reflux test is more inconstant because of occlusion of the cannula by hypertrophic synovium.
A guide wire is then inserted through the needle. The blunt guide wire can be advanced medially until it
bounces against the medial capsule. The capsular penetration is then dilated (dilating trocars, cannulated
trocar) and the arthroscope is introduced in the peripheral compartment under fluoroscopy. Traction (if
applied for access) is then released and the counterpost removed.
Fig. 1: Positioning for arthroscopy of the hip joint periphery
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The knee is flexed to about 45° and held by either a specially designed long bar at the end of the table or
an assistant – the degree of flexion, rotation and abduction of the hip joint are controlled (Fig. 1). A second portal is placed under arthroscopic control in the anterolateral zone. Irrigation is used to clear the view
via the scope sheath and outflow via the additional portal. Standard and extra-long 25° and 70° lenses are
used for the diagnostic round.
Diagnostic Round and Anatomy of the Peripheral Hip Joint Cavity
Similar to the knee joint, the key to an accurate and complete
diagnosis of lesions within the hip joint is a systematic approach
to viewing. A methodical sequence of examination should be
developed, progressing from one part of the joint cavity to another
and systematically carrying out this sequence in every hip (Fig. 2).
Fig. 2: Diagnostic round through the hip joint periphery
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For arthroscopic examination, the peripheral compartment of the hip can be divided routinely into the following areas: anterior neck area (Fig. 2B-C), medial neck area (Fig. 2A), medial head area (Fig. 2D), anterior
head area (Fig. 2E), lateral head area (Fig. 2F), lateral neck area (Fig. 2G) and posterior area (Fig. 2H). From
my experience, the peripheral compartment can be best viewed during a diagnostic round trip starting from
the anterior/medial surface of the femoral neck. Under slow rotation and sliding of the arthroscope over the
femoral neck and head, the arthroscope is brought into the different areas of the peripheral compartment
of the hip.
Indications:
Indications, contraindications and complications have been described in detail by Dr. Seil. I would like to
emphasize that the indications for HA without traction do not differ from those published for the traction
technique. In my opinion, the traction and non-traction technique should be combined to allow a complete
diagnostic inspection of the hip joint. Particularly in synovial diseases such as chondromatosis and patients
with unclear hip pain the combination of both techniques appear mandatory. The hip joint periphery contains most of the synovium of the hip joint. I have seen cases with manifestation of synovial chondromatosis in the peripheral compartment only. In addition, loose bodies of different origin tend to accumulated
not only in the acetabular fossa and perilabral sulcus but also in the pouches around the femoral neck.
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Suggested Readings (Hip arthroscopy without traction):
• Dienst M, Goedde S, Seil R, Hammer D, Kohn D. Hip Arthroscopy without Traction: In Vivo Anatomy of
the Peripheral Hip Joint Cavity. Arthroscopy 2001; 17: 924-931.
• Dienst M, Goedde S, Seil R, Kohn D. Diagnostic arthroscopy of the hip joint. Orthop Traumatol 2002;
10:1-14.
• Dorfmann H, Boyer Th, Henry P, DeBie B. A simple approach to hip arthroscopy. Arthroscopy 1988;
4:141-142.
• Dorfmann H, Boyer T. Arthroscopy of the hip: 12 years of experience. Arthroscopy 1999; 15:67-72.
• Gondolph-Zink B, Puhl W, Noack W. Semiarthroscopic synovectomy of the hip. Int Orthop 1988; 12:3135. Stuttgart: G. Fischer, 1995:511-571.
• Klapper R, Dorfmann H, Boyer T. Hip arthroscopy without traction. In: Byrd JWT, editor. Operative hip
arthroscopy. New York: Thieme, 1998:139-152.
• Klapper RC, Silver DM. Hip arthroscopy without traction. Contemp Orthop 1989; 18:687-693.
HIP ARTHROSCOPY
INDICATIONS, CONTRAINDICATIONS AND COMPLICATIONS
Romain Seil, M.D.
Saarland University Medical Center
Homburg / Saar, Germany
INDICATIONS
The indications of arthroscopy of the hip are evolving with the development of our technical skills and the
understanding of the normal and the pathologic anatomy of this joint. Recently Byrd et al. presented an
exhaustive table of diagnoses representing potential indications for hip arthroscopy (see below). Despite
this large number of diagnoses most hip arthroscopies are performed for intraarticular loose bodies and
synovial pathologies (Kelbérine & Boyer). Other diagnoses like acetabular labral tears are increasingly recognized and arthroscopic management of such tears has been reported to be successful (Santori & Villar;
Mason). Currently one of the most challenging aspects of hip arthroscopy might be the understanding and
treatment of early osteoarthritis (OA) of the hip (McCarthy J et al.; Dienst et al.), even if the therapeutic
approach of OA must still be considered as experimental.
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Diagnoses for Hip Arthroscopy (from: Byrd JWT, 2000)
Rheumatoid arthritis, Inflammatory arthritis, Osteoarthritis (primary, secondary to inverted
labrum, posttraumatic, secondary to synovial chondromatosis, secondary to Perthes
disease, secondary to dysplasia, secondary to slipped capital femoral epiphysis), Gout,
Calcium pyrophosphate disease, Other
Dysplastic disease of the hip (CE angle ,20°)
Borderline dysplastic disease of the hip (CE angle 20°-25°)
Perthes disease
Avascular necrosis of the femoral head:
Stage: I, II, III, IV, V, VI
Articular surface: intact, fragmented
Synovial chondromatosis
Sepsis
Total hip replacement:
Free fragments, Inflammatory process, Fibrosis, Soft tissue impingement, Infection
Loosening: acetabular component, femoral component, both components
Loose bodies:
Post-traumatic, Avascular necrosis, Synovial chondromatosis, Foreign body
Osteochondritis dissecans
Synovitis
Etiology: rheumatoid arthritis, synovial chondromatosis, gout; calcium pyrophosphate disease
(inflammatory), chemical induced, idiopathic, traumatic, pigmented villonodular synovitis, other
Pattern: focal (pulvinar), diffuse
Ligamentum teres damage
Complete rupture, Partial rupture, Degenerate ligament
Chondral damage
Acute traumatic, Chronic traumatic
Arthritic (Grade: I, II, III, IV)
Location: femoral head, acetabulum, femoral head and acetabulum
Labral pathology
Etiology: traumatic, degenerative, idiopathic, congenital, acetabular dysplasia
Morphology: radial flap, radial fibrillated, peripheral longitudinal, inverted, unstable
Location: anterior, posterior, lateral, anterolateral
Osteochondritis dissecans
Grade: stable—intact articular surface, fragmented articular surface; unstable
Post-traumatic
Perthes disease
Idiopathic
Fibrosis
With limited range of motion
Without limited range of motion
Osteophyte
Impinging
Not impinging
Other
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Arthritic disorders
CONTRAINDICATIONS
Recent acetabular fractures (risk of retroperitoneal and/or intraabdominal fluid extravasation).
Severe osteoarthritis, arthrofibrosis, capsular constriction, joint ankylosis (difficult or impossible distraction of the joint).
Severe obesity (difficult access to the joint, even with extra-length instruments).
Contraindications of traction: potential stress risers in the bone from previous trauma, disease or surgery;
soft-tissue problems (skin, vascularisation).
COMPLICATIONS
Complications associated with hip arthroscopy are rare (between 1.6% and 5%). Their incidence seems to
be related to the surgeons’ experience. Most of them are related to arthroscopies of the central compartment of the hip which are performed with traction and mostly cause neurapraxias (Sampson). In a large
series of 413 arthroscopies of the peripheral compartment which have been performed without traction, no
complications have been reported (Dorfmann & Boyer).
Complications in Hip Arthroscopy (from: Dienst M, 2002)
Intraarticular:
Instrument breakage
Iatrogenic articular cartilage / labral lesions
Extraarticular:
Inguinal / genital soft tissue injuries due to pressure by the traction post
(i.e. scrotal necrosis; labia majora hematoma; vaginal lesion).
Neurological:
Sensory:
A) anterior aspect of the proximal thigh due to a lesion of the femorocutaneous
nerve during placement of the anterior portal
B) forefoot caused by a compression of the deep peroneal nerve in the foot holder
C) medial aspect of the proximal thigh due to pressure on the pudendal nerve by the
post
Motor:
Sciatic / femoral nerve due to prolonged and too strong traction
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Other
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Fluid extravasations (intraabdominal / thigh)
Heterotopic ossifications
SELECTED REFERENCES:
• Byrd JWT. Arthroscopy of select hip lesions. In: Byrd J (ed): Operative Hip Arthroscopy. New York,
Thieme, 1998: 153-171
• Byrd JWT. Complications associated with hip arthroscopy. In: Byrd J (ed): Operative Hip Arthroscopy.
New York, Thieme, 1998: 171-176
• Byrd JWT, Jones KS. Prospective analysis of hip arthroscopy with 2-year follow-up. Arthroscopy 16 (6),
2000: 578-587
• Dienst M, Gödde S, Seil R, Kohn D. Diagnostic arthroscopy of the hip joint. Orthop Traumatol 2002; 10:
1-14
• Dienst M, Seil R, Gödde S, Georg T, Kohn D. Arthroscopy for diagnosis and therapy of early osteoarthritis of the hip. Orthopade 1999; 28: 812-818
• Dorfmann H, Boyer T. Arthroscopy of the hip: 12 years of experience. Arthroscopy 15 (1): 67-72, 1999
• Funke EL, Munzinger U. Complications in hip arthroscopy. Arthroscopy 12 (2): 156-159, 1996
• Griffin DR, Villar RN. Complications of arthroscopy of the hip. J Bone Joint Surg Br 1999; 81 : 604-6
• Kelbérine F, Boyer T. L’arthroscopie de la hanche. In : Société Francaise d’Arthroscopie. Perspectives en
arthroscopie. Vol. 2 : 39-45, 2003
• Mason JB. Acetabular tears in the athlete. Clin Sports Med, 20 (4): 779-790, 2001
• McCarthy JC, Noble PC, Schuck MR, Wright J, Lee JA. The role of labral lesions to development of early
degenerative hip disease. Clin Orthop, 393: 25-37, 2001
• McCarthy JC, Lee JA. Acetabular dysplasia: a paradigm of arthroscopic examination of chondral injuries.
Clin Orthop, 405: 122-128, 2002
• Sampson TG. Complications of hip arthroscopy. Clin Sports Med 20 (4): 831-835, 2001
• Santori N, Villar RN. Acetabular labral tears: result of arthroscopic partial limbectomy. Arthroscopy 16:
11-15, 2000
• Villar RN. Hip arthroscopy. J Bone Joint Surg 77 B: 517-518, 1995
ICL #19
STRESS FRACTURES
Friday, March 14, 2003 • Carlton Hotel, Carlton II
Chairman: Gideon Mann, MD, Israel
Faculty: Sakari Orava, MD, PhD, Finland, Ingrid Ekenman, Sweden, Peter Brukner, MD, Australia
and Charles Milgrom, MD, PhD, Israel
Peter Brukner, Australia - Epidemiology of Stress Fractures
Charles Milgrom, Israel - Preventable and Inborn Causes of Stress Fracture
Ingrid Ekenman, Sweden - How Important is Accurate Diagnosis for Stress Fractures?
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Sakari Orava, Finland - Uncommon Stress Fractures and their Treatment Principles
Gideon Mann, Israel – Career Ending Stress Fractures of the Foot
Charles Milgrom, Israel - Does the Asymptomatic Stress Fracture Exist?
CAREER ENDING STRESS FRACTURES OF THE FOOT
Gideon Mann, MD
Meir Hospital, Kfar Saba, Israel and
The Ribstein Center for Sport Medicine Sciences & Research, Wingate Institute, Israel
Co-authors: S Shabat, D Morgenstern, Y Hezroni, A Finsterbush, M Nyska, N Constantini
Introduction:
Most stress fractures of the foot would not put in risk the sportsman's career. The few fractures that on the
one hand occur relatively often and do tend to non-union and to long standing symptomatology are fractures of the Hallux Sesamoid, the Jones Fracture of the fifth metatarsal bone and fractures of the Tarsal
Navicular.
Sesamoid Stress Fractures
The term "sesamoid" is derived from the Greek word "sesamum" due to the resemblance of the bone to the
seeds of the plant Sesamum Indicum used as a purgative by the ancient Greeks (14,21).
Sesamoid stress fractures occur in a wide variety of sports such as football, long distance running, sprinting, dancing, basketball, tennis and figure skating (4,5,6,7,8).
Pathophysiology:
Stress fractures of the sesamoid comprise approximately 5% of foot stress fractures (11). They usually
evolve following repeated traction (2) while acute fractures could occur following both direct compression
injuries such as a fall and traction injuries (1, 14). The stress fracture involves mostly the medial sesamoid
(2,9,10).
Sesamoid stress fractures have a strong tendency to non-union, probably more than any other bone (12).
Orava and Hulkko have shown non-union in 15 of 37 cases and only 10 of 15 showed union after using
modified foot wear and relative rest (12).
Clinical Presentations:
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Pain is of insidious onset and unusually long standing. It is poorly localized, occurring during or after
activity and relieved by rest (1,2). Pain is increased by hypertension and by local pressure.
Diagnosis:
Diagnosis is confirmed by x-rays inclusive of an anterior-posterior projection, a lateral projection and an
axial projection, and by a bone scan which would differentiate a fracture from a bipartite sesamoid. Serial
x-rays in intervals of 3 weeks (1) and up to 3 or 6 months (3) would be helpful if a pre-injury x-ray showing
no partition is unavailable, which is usually the case.
A fractured sesamoid would usually show equal sized fragments, ragged in texture, while a bipartite
sesamoid would have smooth and unequal fragments (1).
75% of bipartite sesamoids are bilateral (16,17,18).
The fracture line would usually be transverse, with osteoporotic edges which would become smoother in
time (14). Further fragmentation could be seen (14). Both computerized tomograms (CT) (19) and magnetic resonance (MRI) (20) have been suggested for accurate diagnosis.
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Treatment:
Treatment would therefore be relatively aggressive with orthoses preventing Hallux dorsiflexion, and
padding along side with relative rest (2). If symptoms are severe a platform cast for 6 weeks with protection from toe dorsiflexion may be used (1,8,11), controlled by repeated x-ray (1). Others recommend a cast,
possibly non weight bearing, for 6 weeks as the initial treatment (14, 19), with appropriate padding to
reduce pressure on the injured bone.
If symptoms persist bone grafting may be attempted (13). Though excision of the fractured sesamoid is
probably more often practical (1,2,4,11) a procedure allowing return to full activity often an initial 3 week
period of immobilization (4). Excision could be total or partial (14,15).
Summary:
Stress fractures of the sesamoids occur following repeated traction and usually involve the medial
sesamoid. Acute injury caused either by crush or by traction ("Turf Toe") would involve either sesamoids.
Pain is insidious and long standing. Diagnosis is clinical, as pain is caused by both toe dorsiflexion as by
local pressure. Diagnosis is assisted by x-rays and bone scan and occasional CT or MRI. Radiological
Differential Diagnosis includes bipartite or multipartite sesamoid. Clinical differential diagnosis includes
mainly sesamoid chondromalacia. The sesamoid stress fracture has a strong tendency to non-union.
Treatment should be initiated immediately after diagnosis and includes orthoses or cast for 6 weeks with a
platform to prevent toe extension.
If clinical and radiological healing fails to occur, surgical treatment by partial or total excision of the
sesamoid should be initiated followed by 3 weeks of immobilization before gradually returning to sports.
In selected cases, bone graft to the fracture could be considered.
REFERENCES
1. Linz J, Conti S, Stone D. Foot and Ankle Injuries in Sports Injuries, Fu F and Stone D, Eds. Lippincott,
Williams & Wilkens, Philadelphia: 2001;1152-1153.
2. Puddu G, Cerulli G, Selvanetti A, De-Paulis F. Stress Fractures in Oxford Textbook of Sports Medicine,
Harries M, Williams C, Stanish WD, Micheli LJ, Eds. Oxford: 1998;663.
3. Scranton P. Pathologic and anatomic variations in the sesamoids. Foot Ankle 1981;1:321-6.
4. Hulkko A, Orava S, Pellinen P, et al. Stress fractures of the sesamoid bones of the first metatarsophalangeal joint in athletes. Arch Orthop Trauma Surg 1985;104:113-7.
5. Val Hal ME, Keene JS, Lange TA and Clancy WG. Stress fractures of the great toe sesamoids. Am J Sports
Med 1982;10:122-8.
6. Davis AW, Alexander IJ. Problematic fractures and dislocations in the foot and ankle of athletes. Clinics in
Sports Medicine 1990;9:163-81.
7. Hamilton WG. Foot and ankle injuries in dancers. Clinics in Sports Medicine 1988;7:143-73.
8. McBryde AM, Anderson RB. Sesamoid foot problems in the athlete. Clinics in Sports Medicine 1988;7:51-60.
3.158
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9. McBryde AM, Anderson RB. Stress fractures in runners. in Prevention and Treatment of Running Injuries
(2nd ed.), D'Amrosia R and Drez D, Eds. Slack, Thoroughfare, NJ: 1989.
10. Zinman H, Keret I, Reis NI. Fractures of the medial sesamoid bone of the hallux. J Trauma 1981;21:581-2.
11. McBryde AM. Stress fractures of the foot and ankle in Orthopaedic Sports Medicine, DeLee JC and Drez
D, Eds. Saunders, Philadelphia: 1996;1970-7.
12. Orava S, Hulkko A. Delayed unions and nonunions of stress fractures in athletes. Am J Sports Med
1988;16:378-82.
13. Anderson RB, McBryde AM. Autogenous bone grafting of hallux sesamoid nonunions. Foot Ankle
1997;18:293-6.
14. Brukner P, Bennel K, Matheson G. Stress Fractures, Blackwell, 1999:178-83.
15. Peterson L, Renstrom P. Sports Injuries, Martin Dunitz, 2001:421.
16. Inge GAL, Ferguson AB. Surgery of the sesamoid bones of the great toe. Archives of Surgery
1933;27:466-89.
17. Golding C. Museum pages V: the sesamoids of the hallux. J Bone and Joint Surg 1960;42B:840-3.
18. Mann R. Surgery of the foot (4th ed), CV Mosby CO, St. Louis: 1978:122-5.
19. Biedert R. Which investigations are required in stress fracture of the great toe sesamoids? J of Ortho
and Trauma Surg, 1993;94-5.
20. Burton EM, Amaker BH. Stress fracture of the great toe sesamoid in a ballerina: MRI appearance. Ped
Radiol 1994;24:37-8.
21. Helal B. The great toe sesamoid bones: the lus or lost souls of Ushaia. Clin Ortho 1981;157:82-7.
Jones Fracture
Introduction
The Jones fracture was originally described by Sir Robert Jones in 1902 (1). He described a fracture that he
sustained himself while dancing around a tent pole. Though originally described as an acute fracture
(2,13,14) the term is more often used inclusive of stress fractures (12,15).
The fracture occurs at the junction of the diaphysis and the metaphysis of the fifth metatarsal often involving the articular facet between the fourth and fifth metatarsals but not extending distal to the facet (2). It
is a transverse fracture best known for its nasty tendency to non-union (3-10).
Pathophysiology and Differential Diagnosis
The acute Jones fracture may be caused by a strong adduction force applied to the plantar flexed forefoot
(2). Weight bearing accompanied by a pivoting force may cause an acute fracture when force is excessive,
or a stress fracture when the force is repeated (11). It has been claimed to possibly occur more often in a
supinated foot (3) or possibly both in the cavus foot which is more rigid and in the planovalgus foot
because of increased stresses exerted along the lateral foot border (11,44). The fracture should be differentiated from a diaphyseal stress fracture which behaves similar to other metatarsal stress fractures (31) and
from the avulsion fracture of the base of the fifth metatarsal which need virtually no treatment at all (16)
though some would provide a walking cast for 4 weeks (17).
Occurrence
Metatarsal fractures are dominant in civilian sports, comprising 16% to 23% of the total number of fractures
(18-24, 30). Figure skating has shown an incidence of 22% (32). The figures reported in the military are in
the range of 8 to 24%, generally lower than the incidence in athletes (25-31) with some reporting only 2-8%
(24,28-31). The exact occurrence of the true Jones fracture is not known especially as they are often reported alongside base or diaphyseal fractures. The acute fracture is probably more prevalent in non-athletes
over age 21 and is equally distributed between both sexes (11). The stress variety occurs more in athletes
aged 15 to 21 and is seen more frequently in males (11). Stress fracture of the fifth metatarsal comprises
approximately 5% of stress fractures of the foot (46).
Types of Fractures
Torg in 1984 (33), following a previous publication on stress fractures of the navicular in 1982 (34), divided
the Jones Fracture into three types:
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I. An acute fracture, with no pre-existing pain
II. A sub-acute fracture, when the patient complains of some degree of pre-existing pain. Cortical thickening and medollary sclerosis may be evident.
III. A chronic fracture, with established non-union.
Treatment
The acute Jones fracture and possibly also the sub-acute (Torg type II) may be treated conservatively with a
non weight-bearing cast for 6 week to 12 weeks (2,11,13,16,35,45,47). While some demand a full three
months non weight bearing cast (11), others are content with a non weight bearing cast for 4 weeks followed by a weight bearing cast for 3 weeks (17) or possibly no cast at all if the patient is reasonably cooperative (31). As about one quarter of the conservatively treated fractures tend towards delayed union or
non-union (15), surgical treatment would be preferred on occasion even for the acute stage (2). In 1994,
Josefsson (15) pointed out that though one quarter of the conservatively treated fractures will eventually be
treated surgically, only 12% of the acute fractures will be operated as opposed to 50% of the stress fractures.
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When displacement has occurred (35), delayed union is apparent (Torg III) (2,11,15,16,35) or the athlete
cannot afford the lengthy conservative treatment (2) which may continue up to 5 months (16), surgical
treatment should be considered using a large canulated 4.5 mm intramedullary screw or a large inlay bone
graft (11,36,37,38,47). A large intramedullary screw will give a fixation strength higher than forces exerted
at walking (39). It will hasten healing to half the time (16). A medullary screw could be inserted as an outpatient clinic procedure and will allow walking within 10 days, running within 6 weeks, and competing within 9 weeks (40,47). Surgical failures would usually be accounted when using a screw that is too small or
bone graft which is too small or failing to rim the medullary canal as required (41). Capactive coupled
electric fields (42) and pulsed low intensity ultrasound [LUS] (43) may have a place in treating persistent
cases and thus achieving healing of the fracture.
Summary
The Jones fracture was originally described in 1902 as an acute transverse fracture just distal to the base of
the fifth metatarsal bone. The fracture could occur following an acute injury, following an acute injury
super imposed on a partial stress fracture or as a classic stress fracture with no apparent acute trauma.
Conservative treatment with non weight bearing with or without a cast for 6 to 12 weeks will usually suffice
for the first two fracture types. Surgical treatment with a large intramedullary screw or inlay bone graft will
be performed in cases of delayed union, displacement or lack of willingness of the athlete to cooperate
with a 3 to 6 month program of conservative treatment. Surgical treatment will allow resumption of walking within 10 days, running within 6 weeks and competition within 9 weeks of the injury.
REFERENCES
1. Jones R. Fractures for the base of the fifth metatarsal bone by indirect violence. Annals of Surg
1902;34:697-700.
2. Brukner P, Bennell K, Matheson G. Stress Fractures, Blackwell Science:1999;178-181.
3. Anderon EG. Fatigue fractures of the foot. Injury 1990; 21:275-9.
4. Hulkko A, Orava S, Nikula P. Stress fracture of the fifth metatarsal in athletes. Annal Chirurg Et Gyn 1985;
74:233-238.
5. Dameron TB. Fractures and anatomical variations of the proximal portion of the fifth metatarsal. J Bone
Joint Surg 1975; 57(A):788.
6. Kavanaugh JH, Brower TD, Mann RV. The Jones fracture revisited. J Bone Joint Surg 1978; 60(A):776.
7. Laurich LJ, Witt CS, Zielsdorf LM. Treatment of fractures of the fifth metatarsal bone. J Foot Surg 1983;
22:207.
8. Torg JS, Baluini FC, Zelko RR, et al. Fractures of the base of the fifth metatarsal distal to tuberosity.
Classification and guidelines for non-surgical and surgical treatment. J Bone Joint Surg 1984; 66(A):209.
9. Orava S, Hulkko A. treatment of delayed and non-unions of stress fractures in athletes. Sports Injuries:
Proceedings of the third Jerusalem Symposium, edited by G. Mann, Freund Publishing House Ltd. London,
England1987.
3.160
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10. Orava A, Hulkko A. Delayed unions and non-unions of stress fractures in athletes. Am J Sports Med
1988; 16(4):378
11. Sammarco GJ. The Jones Fracture. Instr course lect, 1993;42:201-5.
12. Landorf KB. Clarifying proximal diaphyseal fifth metatarsal fractures. The acute fracture versus the
stress fracture. J Am Podiatr Med Assoc 1999;89(8):398-404.
13. Lawrence SJ, Botte MJ. Jones fractures and related fractures of the proximal fifth metatarsal. Foot Ankle
1993;14(6): 358-65.
14. Byrd T. Jones fracture: relearning an old injury. South Med J 1992; 85(7):748-50.
15. Josefsson PO, Karlsson M, Redlund-Johnell I, et al. Jones fracture. Surgical versus non-surgical treatment. Clin Orthop 1994; (299):252-5.
16. Clapper MF, O’Brien TJ, Lyons PM. Fractures of the fifth metatarsal. Analysis of a fracture registry. Clin
Orthop 1995; (315):238-41.
17. Holubec KD, Karlin JM, Scurran BL. Retrospective study of fifth metatarsal fractures. J Am Podiatr Med
Assoc 1993; 83(4):215-22.
18. McKeag DB, Dolan C. Overuse syndromes of the lower extremity. Phys Sportsmed 1989; 17:108-23.
19. Warren RH, Sullivan D. Stress fractures in athletes: recognizing the subtle signs. J Musculoskel Med
1984; 1(4):33-36.
20. McBryde AM, Stress fractures in runners. Clin Sports Med 1985; 4(4):737-51.
21. Matheson GO, Clement DB, McKenzie DC et al. Stress fractures in athletes. A study of 320 cases. Am J
Sp Med 1987; 15(1):46-57.
22. Hulkko A, Orava S. Stress fractures in athletes. Int J Sp Med 1987; 8:221-6.
23. Brukner P, Bradshaw C, Khan K, et al. Stress Fractures: a review of 180 cases. Clin J of Sp Med 1996;
6(2):85-9.
24. Orava S, Hulkko A. A survey of stress fractures in Finnish athletes. Sports Injuries: Proceedings of the
third Jerusalem Symposium, edited by G. Mann, Freund Publishing House Ltd. London, England 1987.
25. Sahi T et al. Epidemiology, etiology and prevention of stress fractures in the Finnish defense forces and
the frontier guard. Sports Injuries: Proceedings of the third Jerusalem Symposium, edited by G. Mann,
Freund Publishing House Ltd. London, England 1987.
26. Hallel T, Amit S, Segal D. Fatigue fractures of the tibial and femoral shaft in soldiers. Clinic Orthop
1976; 118:35.
27. Dudelzak Z, Stress fractures in military activity. The IDF army centre of physical fitness, 1991.
28. Giladi M, et al. Publication of the Israel Defense Force Medical Corps, 1984.
29. Giladi M, Ahronson Z, Stein M et al. Unusual distribution and onset of stress fractures in soliders. Clin
Orthop 1985;192:142-6.
30. Friberg O, Sahi T. Clinical biomechanics, diagnosis and treatment of stress fractures in 146 Finnish conscripts. Sports Injuries: Proceedings of the third Jerusalem Symposium, edited by G. Mann, Freund
Publishing House Ltd. London, England 1987
31. Mann G. Stress fractures in Sports Injuries. Arthroscopy and Joint Surgery, Current Trends and
Concepts. Doral MN, Ed. Ankara:2000:307.
32. Pecina M, Bojanic I, Dubravcic S. Stress fractures in figure skaters. Am J Sp Med 1990;18(3):277-9.
33. Torg JS, Balduini FC, Zelko RR, et al. Fractures of the base of the fifth metatarsal distal to the tuberosity:
classification and guidelines for non-surgical and surgical management. J Bone Joint Surg 1984;66A:209-214.
34. Torg JS, Pavlov H, Cooley LH, et al. Stress fracture of the tarsal navicular. A retrospective review of twenty-one cases. J Bone Joint Surg 1982;64(A):700.
35. Strayer SM, Reece SG, Petrizzi MJ. Fractures of the proximal fifth metatarsal. Am Fam Physician
1999;59(9):2516-22.
36. O’Shea MK, Spak W, Sant’Anna S, et al. Clinical perspective of the treatment of fifth metatarsal fractures. J AM Podiatr Med Assoc 1995; 85(9);473-80.
37. Traina SM, McElhinney JP. Tips of the trade #38. The Herbert screw in closed reduction and internal fixation of the Jones fracture. Orthop Rev 1991;20(8):713, 716-7.
38. Hens J, Martens M. Surgical treatment of Jones fractures. Arch Orthop Trauma Surg 1990; 109(5):277-9.
39. Pietropaoli Mp, Wnorowski DC, Werner FW, et al. Intramedullary, screw fixation of Jones Fracture: a biomechanical study, Foot Ankle Int 1999;20(9):560-3
40. Mindrebo N, Shelbourne KD, Van Meter CD, et al. Outpatient percutaneous screw fixation of the acute
Jones fracture. Am J Sp Med 1993;21(5):720-3.
41. Glasgow MT, Naranja RJ, Glasgow SG, et al. Analysis of failed surgical management of fractures of the
base of the fifth metatarsal distal to the tuberosity: the Jones fracture. Foot Ankle Int 1996;17(8):449-57.
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42. Benazzo F, Mosconi M, Beccarisi G, et al. Use of capacitive coupled electric fields in stress fractures in
athletes. Clin Orthop 1995;310:145-9.
43. Brand JC, Brindle T, Nyland J, et al. Does pulsed low intensity ultrasound allow early return to normal
activiites when treating stress fractures? A review of one tarsal navicular and eight tibial stress fractures.
Iowa Orthop J 1999;19:26-30.
44. Egol KA, Frankel VH. Problematic stress fractures in Musculoskeletal fatigue and stress fractures, Burr
DB and Milgrom C, Eds. CRS Press, London:2001;317.
45. Acker JH, Drez D. Non-operative treatment of stress fracture of the proximal shaft for the fifth metatarsal
(Jones fracture), Foot Ankle 1986, 7(3):152.
Tarsal Navicular Stress Fractures
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Introduction
Stress Fractures of the tarsal navicular have been considered relatively unusual (37). The tendency for nonunion with or without avascular necrosis (1) has made this fracture unwelcome in sports medicine clinics
(2-9).
In 1982, Torg reviewed 21 cases of navicular stress fracture (6). Further publications by Khan (9), Kiss (10),
Matheson (16), Benazzo (8) and Brukner (17) brought to our attention that these fractures may not be as
rare as previously believed.
Pathophysiology
The Navicular bone may be repeatedly compressed between the talus and the cuneiforms during repeated
stress (11,12). Reduced dorsiflexion of the ankle may be a contributing factor as demonstrated by Agosta
and Morarty (11), a short first metatarsal and a long second metatarsal have also been mentioned as possible causes (6) but not the shape of the arch (21). Excessive sub-talar pronation has also been suggested as
a possible contributing factor (11). The bone in this location has a sparse blood supply, which would contribute to its disability to withstand repeated stress (11, 13, 14). The fracture involves the dorsal middle
third of the bone (9,10), in 96% is partial (10), 10% of the fractures involve 10% or less of the height of the
bone (10).
Navicular stress fractures are seen in athletes using explosive sports as jumping or sprinting, inclusive of
figure skating, ball games and dance (33,38,39). These fractures are also seen in long distance runners if
they use the forefoot in the footstrike (5,7,12,34,35,36).
Epidemiology
Previous work in the Finnish and Israeli military as summarized by Mann in 2000 (15), and in the Israel
Border Police (18) disclosed only few navicular stress fractures. Research with figure ice-skating reported
22% of the total stress fractures in ice-skating to be navicular stress fractures (2 of 9 cases) (20). Within the
athletic population (8,9,10,16,17,19), navicular stress fractures comprised 3% of the total stress fractures in
Korean athletes (19), 14.5% of stress fractures in the Australian athletes (9) and 35% of the stress fractures
of the Australian track & field team (9). These fractures comprise approximately 3% of stress fractures of
the foot (32).
Diagnosis
Deep located pain, insidious in onset, occurring after sprinting, running or jumping should raise the suspicion of a navicular stress fracture (7,9,11,22). The pain may radiate to the distal forefoot medially or dorsally (6,11,21) and a limp may be apparent (7,21,24). Physical examination will disclose local tenderness of
the navicular on the dorsal aspect of the foot (9,11,13) and often reduced dorsal flexion and subtalar
motion (6,33,39). Pain may be reproduced by hopping (7). Imaging will include x-rays which are often of
low sensitivity (9,11), inclusive of a lateral stress view if a dorsal "avulsion stress fracture" is suspected (12)
and a planter view (25). X-rays will often show changes in the surrounding joints already on the original
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views (11). X-rays have been shown by Khan to be originally positive for a fracture only in 14% of cases
(13). The bone scan will show high sensitivity usually showing a strong reaction of the whole navicular
bone (9,11). A computerized tomogram will disclose the fracture when the appropriate protocol is used (9,
10, 11, 22). 1.5 mm slices are used on the axial view and 3 mm slices on the coronal view (10). The CT is
the most accurate of the imaging method for the navicular stress fracture. The CT will also differ a stress
reaction picked up by the bone scan from a true stress fracture (11), though 11% of these fractures will not
be located on the original CT examination (10). Magnetic Resonance (MRI) is not often used in the diagnosis of navicular stress fracture though it has been used for serial follow-up of healing (23) along side local
sensitivity (11, 23) and pain during activity (11). Diagnosis is frequently delayed 4-7 months because of the
vague symptoms and frequently normal initial x-rays (6,42,44).
Differential Diagnosis
A bipartite navicular should be suspected according to its appearance on x-ray and CT (26). This could be
a painful condition and a bone scan could be mildly positive. An accessory navicular would show only
medial uptake on the bone scan, the bone would be sensitive not dorsally but rather medially and an x-ray
would disclose the accessory bone (11). Bone reaction to stress will show uptake on the bone scan but the
CT will be normal (11).
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Types of navicular stress fracture:
Kiss evaluated CT findings in 55 stress fractures of the navicular (10). 78% were linear, 9% were linear with
a fragment and 11% were rim fractures with an ossicle. The last type was further defined by Orava (12) who
described a dorsal triangular fracture (stress avulsion fracture) which would benefit from surgical excision.
In all cases, especially those with a complete fracture, avascular necrosis or Kienbuck’s Disease should be
kept in mind, especially in youth and childhood (15). This disease involves the whole bone and is treated
conservatively in the great majority of cases. Tarsal coalition of various types should always searched for
clinically and radiologically (15) as they may cause excessive force on the navicular and on other tarsal
bones.
Treatment
Khan in 1994 (9), summarized the treatment previously given for navicular stress fractures. The method of
"weight-bearing rest", or stopping physical activity with or without a Weight Bearing Cast, met with a high
rate of failure (4,6,7,13). Only 24% of 45 cases healed while weight bearing, though symptoms were largely
alleviated (9,11). Apparently, the weight bearing did not allow osteoblastic activity to bridge the fracture
(27,28). Treatment by "non weight bearing-cast immobilization" achieved union in 89% of 36 cases (9,11).
Accordingly, Khan recommended treatment by non weight bearing with immobilization for 6 weeks, followed by 6 weeks of rehabilitation program (9,11) and followed-up on a clinical basis based on pain on
activity and dorsal sensitivity on examination (9,11, 23). Other publications recommend similar treatment
(5, 8). To follow up union, MRI may be used (23) or CT may be used which might show union beginning at 6
weeks and complete union at 4 months (10). All types of treatment may be assisted by a well-fitted orthotic device (11).
Surgical treatment is usually not necessary and not recommended (5,9,15). As these fractures are often
diagnosed late, patients may often decide to reduce their physical activity and not proceed with surgical or
other treatment (15). Patients undertaking conservative treatment should be cautioned that healing may
take 4 (10) to 6 (9) months. Healing may possibly be assisted by pulsed low intensity ultrasound (30) or
capactive coupled electric fields (31).
Surgical treatment for painful persistent non-union remains an option in selected cases (5,7,43). Ha in
1991 presented within a series of 169 fractures, 5 navicular fractures who were all treated surgically. Hulkko
and Orava presented similar experience in their series of Finnish athletes (29) and Orava in 1993 presented
similar experience with the dorsal-avulsion stress fracture (12). Surgical treatment will be assisted by
opening the talo-navicular joint to locate the fracture (7,11) and marking the site with a Kirshner wire (11).
Surgery may include internal fixation with a screw or curettage and bone graft (11).
Overall, there seems to be a growing tendency to refer to surgical treatment in selected cases (3). Puddu et
al, following Torg (41) and Mann (13) suggested the following outline for treatment (33):
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1. Non-complicated partial fracture and undisplaced complete fracture: non-weight bearing plaster for 6 to
8 weeks
2. Displaced complete fracture: treatment as above or alternatively, surgical reduction and fixation followed
by non-weight bearing immobilization in plaster for 6 weeks.
3. Fracture complicated by delayed union or non-union: curettage and inlaid bone grafting with internal fixation of unstable fragments (without attempting reduction because in general there is already a fibrous
union). Any sclerotic fragments found must not be removed but must be fixed. After the operation, a nonweight bearing cast must be applied for 6 to 8 weeks. Recovery is monitored by radiographs (sometimes 3
to 6 months are necessary).
4. Partial fracture complicated by a small transverse dorsal fracture: the dorsal fragment may have to be
removed.
5. Complete fracture complicated by a widespread transverse dorsal fracture: recovery takes place by immobilization.
Dorsal talar beaks must be removed during surgery.
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Peterson and Renstrom (44) pointed out the high rate of re-fracture, delayed union and non-union after
surgery, which may necessitate repeated surgical procedures. The injury, the pre-existing foot anomaly (as
sub-talar condition and reduced dorsiflexion), the surgical procedure and immobilization may all contribute to arthritic changes around the injured bone and enhance a disappointing and less than optimal
final result.
Summary
Navicular stress fractures are apparently not unusual in athletics though they seem to be scarcely reported
in the military. They present as vague insidious onsetting pain on activity, alleviated by rest often radiating
distally to the forefoot. Bone scan will show strong uptake, and a CT will define the diagnosis. The great
majority of the fractures are partial always including the dorsal middle third of the bone. Avascular necrosis, Kienbuck’s disease and tarsal coalition, especially subtalar coalition, should always be excluded as
should bipartite navicular, an accessory navicular or a stress reaction.
Athletes may decide to retire and not proceed with treatment. "Weight bearing rest" does not seem to allow
reasonable healing and treatment should comprise of "non-weight bearing cast immobilization" for 6 weeks
followed by 6 weeks of rehabilitation. The healing process is followed by estimating pain and local sensitivity and possibly repeated CT or MRI. Healing may be expected at 3 to 6 months. Occasionally, surgical
means would be required, including internal fixation with a screw or curettage and bone grafting.
Conservative or surgical treatment may be aided by a well-fitted orthotic.
Surgical intervention has a relatively high occurrence of failure and complication and the patient should be
informed of possibly less than optimal results before surgical treatment is initiated.
REFERENCES
1. Helstad PE, Ringstrom JB, Erdmann BB, Bilateral stress fractures of the tarsal navicular with associated
avascular necrosis in a pole vault. J Am Pod Med Assoc 1996;86(11):551-4.
2. Anderson EG. Fatigue fractures of the foot. Injury 1990;21:275-9.
3. Orava S, Hulkko A. Treatment of delayed and non unions of stress fractures in athletes. Sports Injuries:
Proceedings of the third Jerusalem Symposium, Edited by G Mann, Freund Publishing House Ltd. London,
England 1987.
4. Orava S, Hulkko A. Delayed unions and non unions of stress fractures in athletes. Am J Sp Med
1988;16(4):378.
5. Hulkko A, Orava S, Peltokallio P, et al. Stress fracture of the navicular bone. Nine cases in athletes. Acta
Orthop Scand 1985;56:503-5.
6. Torg JS, Pavlov H, Cooley LH, et al. Stress fracture of the tarsal navicular. A retrospective review of twenty-one cases. J Bone Joint Surg 1982;64(A):700-12.
7. Fitch KD, Blackwell JB, Gilmour WN. Operation for non union of stress fracture of the tarsal navicular. J
Bone Joint Surg 1989;71(B):105-10.
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8. Benazzo F, Barnabei G, Ferrario A, et al. Le Fratture da durata in atletica leggera. It J Sports Med
1992;14(1):51-65.
9. Khan KM, Brukner PD, Kearney C, et al. Tarsal navicular stress fractures in athletes. Sports Med
1994;17(1):65-76.
10. Kiss ZA, Khan KM, Fuller PJ. Stress fractures of the tarsal navicular bone: CT findings in 55 cases. Am J
of Roentgenology 1993;160:111-15.
11. Brukner P, Bennel K, Matheson G. Stress Fractures, Blackwell Science:1999:167-73.
12. Orava S, Karpakka J, Hulkko A, et al. Stress avulsion fracture of the tarsal navicular. An uncommon
sport related overuse injury. Am J Sp Med 1991;19(4):392-5.
13. Khan KM, Fuller PJ, Brukner PD, et al. Outcome of conservative and surgical management of navicular
stress fracture in athletes. Am J of Sp Med 1992;20:657-666.
14. Waugh W. The ossification and vascularization of the tarsal navicular and the relation to Kohler’s disease. J Bone Joint Surg 1958;40B:765-77.
15. Mann G. Stress Fractures in Sports Injuries. Arthroscopy and Joint Surgery, Current Trends and
Concepts. Doral MN, Ed. Ankara:2000:307.
16. Matheson GO, Clement DB, McKenzie DC, et al. Stress fractures in athletes: a study of 320 cases. Am J
of Sp Med 1987;15:46-58.
17. Brukner P, Bradshaw C, Khan K, et al. Stress Fractures: a review of 180 cases. Clin J of Sp Med 1996;
6(2):85-9.
18. Mann G, Lowe J, Matan Y, et al. Shoe and insole effect on medical complaints, overuse injuries and
stress fractures in infantry recruits – a prospective, randomized study-preliminary results. Proceedings of
the combined congress of the international arthroscopy association and the international society of the
knee, Hong Kong, May 1995.
19. Ha KI, Hahn SH, Chung M, et al. A clinical study of stress fractures in sports activities. Orthop
1991;14(10)1089-95.
20. Pecina M, Bojanic I, Dubravcic S. Stress fractures in figure skaters. Am J Sp Med 1990;18(3):277-9.
21. Ting A, king W, Yocum L, et al. Stress fractures of the tarsal navicular in long distance runners. Clinics in
Sp Med 1988; 7(1):89-101.
22. Alfred Rh, Belhobek G, Bergfeld JA. Stress fractures of the tarsal navicular. A case report. Am J Sp Med
1992;20(6):766-8.
23. Ariyoshi M, Nagata K, Kubo M, et al. MRI monitoring of tarsal navicular stress fracture healing – a case
report. Kurume Med J 1998;45(2):223-5.
24. Hunter LY. Stress fracture of the tarsal navicular: more frequent than we realize? Am J Sp Med
1981:9:217-18.
25. Pavlov H, Torg JS, Freiberger RH. Tarsal navicular stress fractures: radiographic evaluation. Radiology
1983;148:641-5.
26. Shawdon A, Kiss ZS, Fuller P. The bipartite tarsal navicular bone: radiographic and computed tomography findings. Australian Radiol. 1995;39(2):192-4.
27. Gordon TG, Solar J. Tarsal navicular stress fractures. J Am Podiatric Med Assoc 1985;75:363-6.
28. O’Connor K, Quirk R, Fricker P, et al. Stress fracture of the tarsal navicular bone treated by bone grafting
and internal fixation: three cases studies and a literature review. Excel 1990;6:16-22.
29. Hulkko A, Orava S. Diagnosis and treatment of delayed and non-union stress fractures in athletes. AnnChir-Gynaecol 1991;80(2):177-84.
30. Brand JC, Brindle T, Nyland J, et al. Does pulsed low intensity ultrasound allow early return to normal
activiites when treating stress fractures? A review of one tarsal navicular and eight tibial stress fractures.
Iowa Orthop J 1999;19:26-30.
31. Benazzo F, Mosconi M, Beccarisi G, et al. Use of capacitive coupled electric fields in stress fractures in
athletes. Clin Orthop 1995;310:145-9.
33. Puddu G, Cerulli G, Selvanetti A, De-Paulis F. Stress Fractures in Oxford Textbook of Sports Medicine,
Harries M, Williams C, Stanish WD, Micheli LJ, Eds. Oxford: 1998;663.
34. Davis AW, Alexander IJ. Problematic fractures and dislocations in the foot and ankle of athletes. Clinics
in Sports Medicine 9:163-81, 1990.
35. Campbell G, Warnekros W. Tarsal stress fracture in a long distance runner. A case report. J of Am Ped
Assoc 1983;72-532-5.
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36. Towne LC, Blazina ME, Cazen LN. Fatigue fracture of the tarsal navicular. J Bone Joint Surg
1970;52A:376-8.
37. Eichenholtz SN, Levine DB. Fractures of the tarsal navicular bone. Clin Orthop 1964;34:142-157.
38. Kroening PM, Shelton ML. Stress fractures. Am J Roentgenology 1963;89:1281-6.
39. Linz J, Conti S, Stone D. Foot and Ankle Injuries in Sports Injuries, Fu F and Stone D, Eds. Lippincott,
Williams & Wilkens, Philadelphia: 2001;1152-1153.
40. Pavlov H, Torg JS, Freiberger RH. Tarsal navicular stress fractures: radiographic evaluation. Radiology
1983;148:641-5.
41. Torg JS, Pavlov H, Torg E. Overuse injuries in sport: the foot. Clinics in in Sports Medicine 1987;6:291320.
42. Ekenman I. Physical diagnosis of stress fractures in Musculoskeletal fatigue and stress fractures, Burr
DB and Milgrom C, Eds. CRS Press, London:2001;276.
43. Egol KA, Frankel VH. Problematic stress fractures in Musculoskeletal fatigue and stress fractures, Burr
DB and Milgrom C, Eds. CRS Press, London:2001;314-16.
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EPIDEMIOLOGY OF STRESS FRACTURES
Peter Brukner, MD
Stress fractures occur in association with a variety of sports and physical activities. Clinical impression
suggests that stress fractures are more common in weight-bearing activities particularly those with a running or jumping component. However, it is difficult to compare the incidence of stress fractures in different
sports or to identify the sport or activity with the greatest risk due to a lack of sound epidemiological data.
Most of the literature in this area pertains to female runners and to male military populations. There is no
information about stress fracture rates in the general community.
STRESS FRACTURE INJURY RATE
Stress fracture rates in athletes
A number of studies have investigated stress fracture rates in athletes (Warren, Brooks-Gunn et al. 1986;
Barrow and Saha 1988; Brunet, Cook et al. 1990; Frusztajer, Dhuper et al. 1990; Pecina, Bojanic et al. 1990;
Cameron, Telford et al. 1992; Kadel, Teitz et al. 1992; Dixon and Fricker 1993; Goldberg and Pecora 1994;
Johnson, Weiss et al. 1994; Bennell, Malcolm et al. 1995; Bennell, Malcolm et al. 1996). Of these, only two
allow a direct comparison of annual stress fracture rates in different sporting populations (Goldberg and
Pecora 1994; Johnson, Weiss et al. 1994). Johnson et al (Johnson, Weiss et al. 1994) conducted a two year
prospective study to investigate sports related injuries in collegiate male and female athletes. In total, 34
stress fractures were diagnosed over the study period. Track accounted for 64% of stress fractures in
women and 50% of stress fractures in men. The stress fracture incidence rate (expressed as a case rate) in
males was highest for track (9.7%) followed by lacrosse (4.3%), crew (2.4%) and American football (1.1%).
The stress fracture incidence rate in women was highest for track athletes (31.1%), followed by crew (8.2%),
basketball (3.6%), lacrosse (3.1%) and soccer (2.6%). No athlete sustained a stress fracture in fencing,
hockey, golf, softball, swimming or tennis.
Goldberg and Pecora (1994) reviewed medical records of stress fractures occurring in collegiate athletes
over a three year period. Approximate participant numbers were available to allow calculation of estimated
incidence case rates in each sport. The greatest incidence occurred in softball (19%), followed by track
(11%), basketball (9%), lacrosse (8%), baseball (8%), tennis (8%) and gymnastics (8%). However, participant
numbers were small in some of these sports which may have led to a bias in incidence rates.
Both studies suggest that track athletes are at one of the highest risk for stress fracture. However, since
neither expressed incidence in terms of exposure it may not be strictly valid to compare the risk of stress
fracture in such diverse sports. There is only one athlete study which has expressed stress fracture incidence rates in terms of exposure (Bennell, Malcolm et al. 1996). This 12 month prospective study followed
a cohort of 95 track and field athletes. Results showed an overall rate of 0.70 stress fractures per 1000
training hours. Further research is needed to quantify incidence rates in this manner to allow more valid
comparison between studies.
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Stress fracture rates in the military
Reports of the incidence of stress fractures in male recruits undergoing basic training for periods of 8 to 14
weeks are remarkably similar and generally range from 0.9% to 4.7% (Protzman and Griffis 1977; Reinker
and Ozburne 1979; Scully and Besterman 1982; Brudvig, Gudger et al. 1983; Gardner, Dziados et al. 1988;
Pester and Smith 1992; Taimela, Kujala et al. 1992; Jones, Bovee et al. 1993; Beck, Ruff et al. 1996).
However, in two particular studies involving the Israeli army, the reported incidence was 31% (Milgrom,
Giladi et al. 1985) and 24% (Milgrom, Finestone et al. 1994). The authors attributed this much higher incidence to several factors including meticulous follow-up, a high index of suspicion and the use of the
radioisotope bone scan for diagnosis. In addition, asymptomatic areas of uptake on bone scan were also
classified as lesions which would inflate the reported figures. Stress fracture rates in female military
recruits during basic training are generally higher than those in males ranging from 1.1% to 13.9%
(Protzman and Griffis 1977; Reinker and Ozburne 1979; Brudvig, Gudger et al. 1983; Jones, Harris et al. 1989;
Pester and Smith 1992; Jones, Bovee et al. 1993).
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Retrospective studies have measured stress fractures rates in specific sporting populations, mostly runners
and ballet dancers (Warren, Brooks-Gunn et al. 1986; Barrow and Saha 1988; Brunet, Cook et al. 1990;
Frusztajer, Dhuper et al. 1990; Pecina, Bojanic et al. 1990; Cameron, Telford et al. 1992; Kadel, Teitz et al.
1992; Dixon and Fricker 1993; Goldberg and Pecora 1994; Bennell, Malcolm et al. 1995). Variation in reported rates reflect differences in methodology particularly cohort demographics and method of data collection. A history of stress fracture has been reported by 13% to 52% of female runners. The lowest rate was
found in one which included recreational as well as competitive runners. Ballet dancers are another population where stress fracture rates appear high with 22% to 45% of dancers reporting a history of stress fracture. However, most studies failed to confirm the accuracy of subject recall which may introduce bias into
the figures reported. Nevertheless, it is clear that a stress fracture is a relatively common athletic injury.
Comparison of stress fracture rates in men and women
It is often suggested that women sustain a disproportionately higher number of stress fractures than men.
The relative risk of stress fracture for women compared with men from studies where stress fracture rates
can be directly compared is shown in Figure 1. In the military, reported incidence rates over an eight week
training period vary from 1.1% to 13.9% in women and from 0.9% to 3.2% in men. These studies consistently show that female recruits have a greater risk of stress fracture than male recruits with relative risks ranging from 1.2 to 10 (Protzman and Griffis 1977; Reinker and Ozburne 1979; Brudvig, Gudger et al. 1983; Jones,
Harris et al. 1989; Pester and Smith 1992; Jones, Bovee et al. 1993). This increased risk persists even when
training loads are gradually increased to moderate levels and when incidence rates are separated by age
and race. The most likely explanation for these findings in the military is lower initial physical fitness in
the female recruits. Other possible reasons include differences in bone density and geometry, gait, biomechanical features, body composition and endocrine factors, particularly estrogen status.
In contrast, a gender difference in stress fracture rates is not as evident in athletic populations (Brunet,
Cook et al. 1990; Cameron, Telford et al. 1992; Dixon and Fricker 1993; Goldberg and Pecora 1994; Johnson,
Weiss et al. 1994; Bennell, Malcolm et al. 1996). Studies either show no difference between male and
female athletes or a slightly increased risk for women, up to 3.5 times that of men. A possible confounding
variable is that, unlike the military where the amount and intensity of basic training is rigidly controlled, it
is difficult to assume equivalence of training between men and women in most of these studies. However,
Bennell et al (1996) found no significant difference between gender incidence rates even when expressed in
terms of exposure. Women sustained 0.86 stress fractures per 1000 training hours compared with 0.54 in
men. It is feasible that a gender difference in stress fracture risk is reduced in athletes as female athletes
may be more conditioned to exercise than female recruits and hence the fitness levels of male and female
athletes may be closer.
REFERENCES
Barrow, G. W. and S. Saha (1988). "Menstrual irregularity and stress fractures in collegiate female distance
runners." The American Journal of Sports Medicine 16(3): 209-216.
Beck, T. J., C. B. Ruff, et al. (1996). "Dual-energy x-ray absorptiomety derived structural geometry for stress
fracture prediction in male U.S. marine corps recruits." Journal of Bone and Mineral Research 11(5): 645653.
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Bennell, K. L., S. A. Malcolm, et al. (1995). "Risk factors for stress fractures in female track-and-field athletes: a retrospective analysis." Clinical Journal of Sport Medicine 5: 229-235.
Bennell, K. L., S. A. Malcolm, et al. (1996). "The incidence and distribution of stress fractures in competitive
track and field athletes." The American Journal of Sports Medicine 26(2): 211-217.
Brudvig, T. J. S., T. D. Gudger, et al. (1983). "Stress fractures in 295 trainees: a one-year study of incidence
as related to age, sex, and race." Military Medicine 148: 666-667.
Brunet, M. E., S. D. Cook, et al. (1990). "A survey of running injuries in 1505 competitive and recreational
runners." The Journal of Sports Medicine and Physical Fitness 30: 307-315.
Cameron, K. R., R. D. Telford, et al. (1992). Stress fractures in Australian competitive runners. Australian
Sports Medicine Federation Annual Scientific Conference in Sports Medicine, Perth, Australia.
Dixon, M. and P. Fricker (1993). "Injuries to elite gymnasts over 10 yr." Medicine and Science in Sports and
Exercise 25: 1322-1329.
Frusztajer, N. T., S. Dhuper, et al. (1990). "Nutrition and the incidence of stress fractures in ballet dancers."
American Journal of Clinical Nutrition 51: 779-783.
Gardner, L. I., J. E. Dziados, et al. (1988). "Prevention of lower extremity stress fractures: a controlled trial of
a shock absorbent insole." American Journal of Public Health 78(1563-1567).
Goldberg, B. and C. Pecora (1994). "Stress fractures. A risk of increased training in freshman." The
Physician and Sportsmedicine 22: 68-78.
Johnson, A. W., C. B. Weiss, et al. (1994). "Stress fractures of the femoral shaft in athletes-more common
than expected. A new clinical test." The American Journal of Sports Medicine 22: 248-256.
Jones, B. H., M. W. Bovee, et al. (1993). "Intrinsic risk factors for exercise-related injuries among male and
female army trainees." The American Journal of Sports Medicine 21: 705-710.
Jones, H., J. M. Harris, et al. (1989). "Exercise-induced stress fractures and stress reactions of bone: epidemiology, etiology, and classification." Exercise and Sports Sciences Review 17: 379-422.
Kadel, N. J., C. C. Teitz, et al. (1992). "Stress fractures in ballet dancers." The American Journal of Sports
Medicine 20: 445-449.
Milgrom, C., A. Finestone, et al. (1994). "Youth is a risk factor for stress fracture. A study of 783 infantry
recruits." The Journal of Bone and Joint Surgery 76-B(20-22).
Milgrom, C., M. Giladi, et al. (1985). "The long-term followup of soldiers with stress fractures." The
American Journal of Sports Medicine 13(398-400).
Milgrom, C., M. Giladi, et al. (1985). "Stress fractures in military recruits. A prospective study showing an
unusually high incidence." The Journal of Bone and Joint Surgery 67-B: 732-735.
Pecina, M., I. Bojanic, et al. (1990). "Stress fractures in figure skaters." The American Journal of Sports
Medicine 18: 277-279.
Pester, S. and P. C. Smith (1992). "Stress fractures in the lower extremities of soldiers in basic training."
Orthopaedic Review 21: 297-303.
Protzman, R. R. and C. G. Griffis (1977). "Stress fractures in men and women undergoing military training."
The Journal of Bone and Joint Surgery 59-A(825).
Reinker, K. A. and S. Ozburne (1979). "A comparison of male and female orthopaedic pathology in basic
training." Military Medicine Aug: 532-536.
Scully, T. J. and G. Besterman (1982). "Stress fracture - a preventable training injury." Military Medicine
147(285-282).
Taimela, S., U. M. Kujala, et al. (1992). "Risk factors for stress fractures during physical training programs."
Clinical Journal of Sports Medicine 2: 105-108.
Warren, M. P., J. Brooks-Gunn, et al. (1986). "Scoliosis and fractures in young ballet dancers: relation to
delayed menarche and secondary amenorrhea." The New England Journal of Medicine 314: 1348-1353.
PREVENTABLE AND INBORN CAUSES OF STRESS FRACTURE
C. Milgrom, PhD
Why does one person sustain a stress fracture while another person doing exactly the same training
remains injury free? Today there exists solid epidemiological evidence to indicate that intrinsic and extrinsic risk factors for stress fractures exist as they do for many disease entities.
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The principal biological role of bone is skeletal support. Genes regulating bone strength have been identified in lines of mice. Interbreeding of these lines results in intermediate bone strength. A similar genetic
regulatory system may be present in humans resulting in genetic differences in bone strength. The first evidence that there may be a genetic basis for stress fracture was in the 1990 report of Singer et al. They
described multiple stress fractures in monozygotic twins. Both individuals who served in the same unit,
sustained stress fractures in the same anatomical site, with presenting symptoms in both being in the 6th
week of training. Friedman et al have ongoing work to characterize the putative genes conferring in
increased risk for stress fractures.
In the young, bone can be strengthen by vigorous exercise. An Israeli military study showed a mean
increase in tibial bone density of seven per cent after fourteen weeks of vigorous training. A history of regular basketball playing for at least two years prior to induction into the army has been shown to markedly
decrease the risk for stress fracture in infantry training from 20 to less than 3 per cent. Regular running
however has never been shown to decrease the risk for stress fracture in any military study. These observations indicate that strengthening of bone is not an overnight phenomena and may take years to accomplish. It also indicates that running because it is a largely same plane repetitive activity, does not result in
bone strengthening in muliple axes.
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Although medical students are taught to think of bone strength in terms of the easily measurable parameter, bone density, this is not the major determinant of a bone’s strength. The major determinant of a bone’s
strength is its size. If the diameter of mid shaft tibia is increased from 22 to 27 mm, the bone’s strength in
bending and torsion is increased 106% and compression by 50%. Tibial bone width has been found to be a
risk factor for stress fracture. In a prospective Israeli study infantry recruits with wider tibias in the mediallateral plane were found to be at decreased risk for both femoral and tibial stress fractures than those with
narrower tibias. This corresponds to the fact that the major bending moment in the tibial is in the mediallateral plane. The observations of this research were verified in a subsequent American military study.
It is recognized that bone reaches its maximum strength at about the age of twenty-five. The difference
between eighteen year old and 30 year old bone can be easily seen in microscopic examination. The
younger bone still has cartilaginous elements and is not fully mineralized. Israeli army studies have shown
that younger infantry recruits have lower risk for stress fractures than older recruits. With each year of
increase in recruit age between 17 and 25, the risk for stress fractures decreased by 26 per cent. An
American study reported an opposite trend, but lack the controls and surveillance of the Israeli study.
Other identified instrinsic anatomical risk factors for stress fractures are high external rotation of the hip
and foot type. The low, but normal arch foot was reported to be protective for stress fractures, while the
high cavus foot reported to have increased risk for stress fracture. Poor prior physical fitness has been
implicated as a risk factor for stress fracture. For an athlete this factor would usually be important after a
return from an injury or a change of activity. It has become a less important factor in military medicine,
with many armies being volunteer forces and not universal conscripts.
The issue of the importance of shoes and orthotics in stress fracture prevention is clouded with much myth
and salesmanship. The large strains and strain rates that cause stress fractures of the tibia and femur are
more the result of muscle force on the bone than the force of foot impaction. This has been shown by in
the vivo bone strain measurements of Milgrom et al. There however is good scientific data to show that
proper shoe gear and orthotics can lower the incidence of metatarsal stress fractures. Their role in preventing tibial and femoral stress fractures has not been established.
The recent in vivo strain measurement study of Ekenman et al shows that the addition of orthotics to athletic shoes does not decrease and in fact increases some types of strains during running.
From the in vivo strain gage studies of Milgrom, Burr and Ekenman there is evidence that the majority of
tibial and femoral stress fractures are mediated through the bone remodeling response. Metatarsal stress
fractures are more likely to be the result of pure high cyclic loading. The remodeling response occurs when
trainees are exposed to new high strain or strain rate patterns. They attempt to strength bone by initiating
a remodeling response, the first phase of which is bone absorption. If the high strains or strain rates continue during the absorption period, then stress fracture can result. Looking to the future, this seemingly
inappropriate bone response may be possibly altered by agents such as bisphosponates. By their use the
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amount of bone absorption may be reduced and thereby remodeling driven stress fracture incidence
reduced.
UNCOMMON STRESS FRACTURES AND THEIR TREATMENT PRINCIPLES
Sakari Orava, MD, PhD, Professor, Orthopaedic surgeon
Mehilainen Sports Clinic and Private Hospital, and Sports Trauma Research Center
Turku, Finland
Stress fractures usually heal well, if the diagnosis is done early and the causative factor – excessive loading
of the bone – is adequately eliminated. However, some stress fractures in athletes are not diagnosed in
time or in spite of the right diagnosis, exercise is started too early or continued in spite of the symptoms.
In these cases, chronic symptoms develop, and delayed union or non union may follow. The number of
these was estimated to be approximately 10 per cent 15 years ago. To day, due to the grown knowledge of
stress fractures the number probably is smaller. Delayed or non unions require either a long rest from all
physical activity or surgical treatment.
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Some stress fractures are very uncommon. The diagnosis of them may cause problems, because the differential diagnosis is difficult and other injuries are suspected and treated for a long time before the right
diagnosis. These rare stress fractures are reviewed and their treatment principles discussed.
1. Hallux sesamoid bones
The sesamoid bones under the first metatarsophalangeal joint are very hard and tolerable bones. There are
three possible diseases or injuries during physical exercise, that can cause pain of the sesamoid bones:
acute fracture, stress fracture, osteochondritis or osteonecrosis of bone. The traction and compression
stress on the sesamoid bones is high during running and jumping. The bones are not only subject to the
pull of muscles via tendons, but they also directly bear the body weight. Stress fracture may affect the
medial or lateral or both sesamoids.
The diagnosis requires careful clinical examination, anteroposterior and oblique radiographs with tangential views of the sesamoid bones and bone scan. MRI will show bone oedema.
Conservative treatment consists of rest from training, shoes with thick and stiff soles and special orthoses.
Healing may take several months and some cases are painful up to two years from the onset of the symptoms. In cases with symptomatic non union the bone or one of the fragments can be removed. In case of
osteonecrosis the affected bone is excised. Both sesamoids are not advised to excise.
2. Stress fracture of anterior mid-tibia
Slowly healing stress fracture of the anterior cortex of the mid-tibia is seen as an adaptation process of the
cortex to physical exercise. It is seen in dancers, jumpers and runners. Only five per cent of the stress fractures of tibia localize at the middle of it. The fracture is caused by compressive and tensile forces. The
patients often have a along history of mild symptoms. This stress fracture has a tendency for delayed union
or non union and even a complete fracture may occur.
In radiographs, a small fissure (or several) is seen transversally at the mid-tibia. The anterior cortex is usually thickened and hypertrophic. In tomography, CT or MRI there is a "cavity" – like "hole" inside the cortex.
In MRI oedema of the medullary canal of tibia is also seen.
Rest from running or jumping is several months. Supportive special orthosis can be used. Local low intensity ultrasound treatment and magnetic field treatment have been tried. Electrical stimulation for 3-6
months may lead to healing, until surgical procedures are considered. In surgery, biopsy of the fracture line
is done, drill holes with 2 mm diameter drill are made through the lateral and medial cortex. appr. five cm
distally and proximally from the fracture line. Postoperatively lower leg orthosis is used. In chronic non3.170
unions short tension plate is set on the lateral side of the tibia. Intramedullary nailing has also been used.
Postoperatively the above mentioned methods are still available.
Tarsal Navicular
The number of stress fractures of the tarsal navicular has increased during the last decade. Jumpers and
runners, as well as gymnasts, dancers and other athletes are in the risk group to get this stress fracture. In
midfoot pain of young athletes, navicular stress fracture should be suspected as one of the main reasons
for prolonged pain.
Treatment consists of rest from impact training. Magnetic field, electrical stimulation and low intensity
ultrasound can be used. Foot orthosis or solid shoe sole may help, too. Healing time is from 2 to 4
months. Grading with MRI as well as the history of symptoms can make the decision for operative treatment easier, especially, if no healing occurs during the follow-up time. Drilling of the bone across the fracture line and fixation with absorbable pins or screws is recommended. In complete fractures same method
or fixation with metal screws is used. After a short non-weight bearing period full weight can be allowed
with solid footwear. Healing after surgery until full sports capacity may take half a year.
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Radiograps seldom are positive in early phase. Some fractures appear suddenly with a dislocated complete
fracture and a positive history of midfoot pain is usually obtained later from the patient. Isotope scan usually is positive, as well as MRI examination. In MRI intraosseous oedema often is seen also in other bones
around the navicular bone.
3. Stress fracture at the superior proximal corner of the navicular bone may become chronic and annoying.
If the fragment is small, it will become rounded and asymptomatic during one year. If it is bigger or the
avulsion – compression – rotation stress affects also the distal joint surface of talus, symptoms usually
persist for a long time. Then surgical excision of the fragment may become necessary.
Base of fifth metatarsal
The fracture of the metatarsal five basis – Jones's fracture – is known as a risk fracture for delayed or non
union. Stress fracture usually develops somewhat more distally as the original "Jones's fracture", to the
proximal diaphysis. If intramedullary sclerosis occurs, the healing is disturbed. In Radiograps and in MRI
the medullary canal obliteration can be seen. Isotope scan sometimes is only weakly positive or even negative.
The treatment is conservative in the beginning. Non-weight bearing for three weeks is recommended and a
good foot orthosis with whole sole bearing during the gait is recommended. If surgery is indicated, best
results are obtained with tension band method (two 1.8 mm K-wires and a metal cerclage.
Base of second metatarsal
One of the uncommon stress fractures at the foot is that in the base of the 2nd MT. This bone is usually
longer than 1.st (Morton's foot) and the patients need rising up to toes or standing toes extended (ballet
dancers). The stress fracture of the base may become chronic, a non union develops and pain continues.
With rest and shoe correction with elevation under the 1.st and 3.rd MT head may help and the healed
bone itself will be stronger later. However, sometimes drilling of the sclerotic fracture area or shortening
osteotomy in the neck of the 2.nd MT must be considered. In some cases delayed or non union develops
also into the base of the 3rd. metatarsal.
Toe stress fractures
Stress fractures in toe bones are rare, The toe is swollen and gout or other inflammatory diseases are at
first suspected. Later the radiographs show sclerosis and the right diagnosis can be made. In the proximal
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phalanx of the big toe oblique intra-articular medial stress fractures have been described in cross country
skiers. They are painful but heal in a few weeks with conservative treatment.
5. Stress osteopathy of tarsal bones
Uncommon stress oedema or osteopathy in tarsal bones may cause pain and prevent athletic exercises.
This reaction is seen in only in MRI pictures and is located at the cuboid bone, talus, navicular and sometimes in cuneiforms and in the base of the 1.st and 2.nd metatarsals. It is very uncommon in athletes at the
calcaneal bone, but the lateral side articulating with cuboid bone can be affected, too. The etiology is multifactorial and the oedema may last is spite of all conservative treatment methods. In chronic cases drilling
of the affected bone / bones can be done.
Chronic pelvic stress fractures
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In female endurance athletes a pubic stress fracture may heal very slowly. Amenorrhea is usually found in
those athletes. Sometimes wide callus and inside it a pseudoarthrosis can be seen in all radiological examinations. Osteoporosis treatment with calcium and possibly D – vitamin has to be added the treatment
protocol, in addition to the rest from training (running, jumping). If ischial bone is affected at the same
time as pubic bone or alone, it will lead even longer healing time.
Stress fractures of sacrum are uncommon, but can be found in runners and ball players. Sometimes this
fracture can be bilateral. Healing, however, usually is uneventful.
Isthmic stress fractures of lumbar vertebrae
These stress fractures usually develop to athletes, who need repetitive maximal extension - flexion of the
back combined with hard muscular forces or vertical jumping. They are seen in gymnasts, figure skaters,
aerobic athletes, javelin throwers, hurdlers as well as in many other athletes. Isotope scanning in young
athletes does not always tell the right diagnosis. MRI is more specific. examination. Follow-up is needed to
see that spondylolisthesis will not develop. The disc lesions often connected with lumbar stress fractures
require rest to regenerate.
Rib stress fractures
Some stress fractures in the ribs may last long and the diagnosis of them may be difficult. Rowers, golfers
and many other ball or racket sport athletes can be affected. Sometimes two or even several simultaneous
"hot spots" in the ribs can be seen in isotope scanning. Stress fracture of the first rib is an own entity with
"TOS" – symptoms to the arm and long-lasting exertion pain.
Uncommon stress fractures of the upper arm
In the upper arm stress fractures are much more uncommon than in lower extremities. Difficulties with the
diagnosis as well as treatment may come from stress fractures of carpal bones, radial epiphysis, olecranon,
proximal humeral epiphysis and coracoid process. Those in the middle of the upper or lower arm bone diaphyses are easier to detect. If not diagnosed in time total fractures have occurred in some stress fractures
(olecranon, humeral shaft).
General diagnostic recommendations
All of these stress fractures need special attention from physicians treating them. Because of the risk for a
delayed union or non union, radiographs should be taken routinely, if pain suspected to come from bone
lasts 3-4 weeks. After that isotope scanning is recommended, if symptoms do not subside. MRI has to be
considered as the next examination in selected cases. Good examinations for bone pathology are also normal tomography and computerized tomography. 3 – dimensional models or the affected stress fracture site
can also be obtained with modern imaging methods.
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HOW IMPORTANT IS ACCURATE DIAGNOSIS FOR STRESS FRACTURES
Ingrid Ekenman MD, PhD
Karolinska Institute and Sabbatsberg Hospital, Stockholm, Sweden
It has been reported that of all injuries sustained by athlete populations, stress fractures account for
between 0.7% and 15.6%. In studies in which only runners were investigated, the relative frequency is higher: it ranges from 6.0% to 15.6%. In track and field athletes, stress fractures accounted for a large percentage of overuse injuries: 34.2% in women and 24.4% in men, as reported in one study, and 42.0% for men
and women combined, as reported in another.
In elite gymnasts, stress fractures accounted for 18.3% of overuse injuries in women and 9.2% in men.
The difference in results probably reflects differences in the composition of each case series. Composition
is affected by factors such as referral patterns; case loads; area of practise; and demographics and participation patterns of patients in the clinics, including training intensity, type of sport and percentage of elite
versus recreational athletes.
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According to AMA, a stress fracture is a subtotal or total fracture, caused by an imbalance between outer
repetitive and submaximal loading on one side and the remodelling of the bone on the other side.
Although stress fractures are most common in lower-extremity bones, they also occur in non-weightbearing
bones, including the ribs and upper limbs.
Hullko and Orava found in 1988 that tibia was the most affected bone as high as 50%, followed by the
metatarsal bones in about 28%, fibula 12%, femur 8%(including femoral neck), pelvis 1%, spine 1%.
Milgrom et al found 1985 about the same distribution of 184 stress fractures when they examined 295 soldiers during one year of exercise.
Although great variations exists in the absolute percentage of stress fractures reported at each bony site,
the most common sites seem to be the tibia, metatarsals and fibula.
A number of factors may influence reported distributions of stress fractures, including the patient´s gender,
age, and type and level of activity, as well as method of stress-fracture diagnosis.
For example, tarsal navicular stress fractures give rise to subtle clinical findings, are often missed in differential diagnosis of foot and ankle pain, and are rarely evident on radiographs. They will therefore be underreported compared with stress fractures such as ones that occur in metatarsals, for which clinical and radiographic diagnoses are more straightforward.
Devas reported 1975 that when clinical examination and plain radiography are used for diagnosing stress
fractures, the fibula, second metatarsal and calcaneus are commonly affected.
Recent case reports of stress fractures are previously unreported sites such as the ulnar diaphysis, patella
and neck of the seventh and eight ribs may reflect development of more sensitive imaging techniques such
as magnetic resonance imaging (MRI) and the triple-phase isotope bone scan, as well as increased awareness of stress fractures.
The typical stress fracture patient has gradual onset of pain that is activity related. If the patient continues
to exercise, the pain will become more severe or occur at an earlier stage of exercise. If the exercise is continued and severity of symptoms increases, the pain may persist after exercise.
The pain is usually well localized to the site of the fracture, though stress fractures of the neck of the femur
commonly presents with groin pain and pain referred to the knee.
Physical examination gives bony tenderness. This is easier to determine in bones that are relatively superficial.
Range of joint motion is usually unaffected; the exception is when the stress fracture is close to the joint
surface, such as stress fracture of the neck of the femur.
Some authors have suggested that the presence of pain when therapeutic ultrasound is applied over the
stress fracture area can be of use in detection of stress fractures. Boam et al showed that compared with
isotope bone scan, ultrasound sensitivity was only 43% in detection of stress fractures.
Together with the physical examination it is important to take in account the potential intrinsic factors like
for example leg-length discrepancy, malalignment, muscle imbalance, muscle weakness or lack of flexibility.
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In diagnosis of stress fractures, plain radiography has a poor sensitivity and a high specificity. The abnormalities are unlikely to be seen unless symptoms have been present for at least two to three weeks.
When a radiograph is negative and the suspicion is high, a triple-phase bone scan is the next choice for
investigation. It has a high sensitivity but a low specificity. Prather et al stated that the bone scan had a
true positive rate of 100%, and false-negative scans are relatively rare.
CT scan is a useful complement to radiographs or a bone scan for detecting fracture lines as evidence for
stress fractures.
MRI has been the investigation of choice. Its sensitivity is similar to that of isotope bone scan and has the
advantage of anatomic visualization. It also differentiate between a stress fracture and a tumor and it also
localizes the stress fracture.
The question of accuracy when diagnosing stress fractures with the above in mind, tells us about the
importance when differing between tumors and stress fractures and for example when diagnosing a stress
fracture in the collum femoris, as it seems to be the most malignant kind of stress fracture.
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REFERENCES
1.Dixon M, Fricker P. Injuries to elite gymnasts over 10 yr. Med Sci Sports Exercise 1993;25:1322-1329
2.Brubaker CE, James SL. Injuries to runners. J Sports Med 1974;2:189-198
3.James SL, Bates BT, Osternig LR. Injuries to runners. Am J Sports Med 1978;6:40-49
4.Orava S. Stress Fractures.Br J Sports Med 1980;14:40-44
5.Pagliano J, Jackson D. The ultimate study of running injuries. Runners world 1980;Nov:42-50
6.Clement DB, Taunton JE, Smart GW, McNicol KL. A survey of overuse running injuries. Phys Sports Med
1981;9:47-58
7.Milgrom C, Giladi M, Stein M et al.Stress fractures in military recruits:a prospective study showing an
unusually high incidense. J Bone Joint Surg 1985;67-B:732-735
8.Devas. Stress Fractures. Edinburgh:Churchill Livingstone.1975
9.Johansson C, Ekenman I,Tornqvist H, Eriksson E. Stress fractures of the femoral neck in athletes:the consequence of a delay in diagnosis. Am J Sports Med 1990;18:524-528
10.Hulkko A, Orava S.Stress fractures in athletes.Int J Sports Med 1987;8:221-226
11.Boam WD, Miser WF,Yuill Sc et al.Comparison of ultrasound examination with bone scintiscan in the
diagnosis of stress fractures. J Am Board Fam Pract 1996;9(6):414-417
DOES THE ASYMPTOMATIC STRESS FRACTURE EXIST?
C. Milgrom, PhD
The epidemiology and clinical presentation of stress fractures is very variable. It varies according to the
specific bone involved, and the specific anatomic site affected within that bone. It varies according to
whether the stress fracture is secondary to pure cyclic overloading or whether there is an intermediate
bone remodeling response.
There is solid epidemiological evidence available that femoral stress fractures can be asymptomatic.
Milgrom et al, used bone scan as the basis for diagnosis of stress fracture, and found a high incidence of
asymptomatic stress fractures of the femur in Israeli infantry recruits. Their study was prospective and
recruits were questioned and underwent a stress fracture physical examination routinely every two weeks
during the course of 14 weeks of basic training. According to their research protocol x-rays were also taken
of any grade 2, 3 or 4 femoral scintigraphic foci. They found that more than half of the asymptomatic
femoral scintigraphic foci had radiographic evidence of a stress fracture. Therefore one can not say that
these scintigraphic foci did not represent true stress fractures.
Milgrom et al attributed the phenomena of the asymptomatic femoral stress fracture to the low sensitivity
of the femoral periosteum, when compared to that of the tibia or metatarsus. They stated that the tibial
periosteum has to be very sensitive to offer protection for the very superficial anterior and medial aspect of
the tibia. They also stated that femoral stress fracture symptoms may present as a "muscle tightness or
ache" and maybe difficult to differentiate from similar and non-pathological feelings that normally occur
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during vigorous training. Because of this problem the "fist test" was described as an aide in femoral stress
fracture clinical diagnosis.
If these studies and case reports were not enough to convince me fully that an asymptomatic femoral
stress fracture exists, than a personal experience did. I have been running regularly since the age of 16. For
the last 10 years I have been running about 5K three times a week. Last year we got a new dog. The dog is
very large and I started to take her along on a leach for my runs. After about 10 weeks I developed a strange
deep sensation in my upper thigh at night. I continued to run for another 2 weeks, but the sensation
became stronger. During the daytime or during my runs I felt nothing abnormal. At my wife’s urging I took
an x-ray and there it was, a proximal femoral stress fracture. This was enough to make me a believer in the
asymptomatic femoral stress fracture and all of its clinical implications.
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The literature supports the existence of asymptomatic fully displaced femoral stress fractures in runners.
Michaeli et al described a case of two runners in the Boston Marathon who broke their femurs while striding near the end of the run. Both runners denied experiencing femoral pain before their femurs snapped
during the run.
Recently in Israel, we had a case of an infantry recruit who sustained an asymptomatic displaced femoral
stress fracture during a march. He had been checked by his unit doctor, as were all of the recruits just prior
to the march. The doctor accompanied the training unit on the march. While in mid-stride the recruit fell to
the ground. The recruit said he could not get up. The unit doctor ordered the recruit to get up twice but the
recruit could not. X-ray of the recruit in a nearby hospital showed a fully displaced stress fracture.
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ICL #20
ALLOGRAFTS IN KNEE SURGERY
Friday, March 14, 2003 • Aotea Centre, Kaikoura Room
Chairman: Stephen Howell, MD, USA
Faculty: Dieter Kohn, MD, Germany, Konsei Shino, MD, Japan and David Caborn, MD, USA
Technique and Clinical Results of Meniscal Transplantation – Dieter Kohn
Scientific Basis of Meniscal Transplantation – Steve Howell
Technique and Clinical Results of ACL Allografts – Konsei Shino
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Scientific Basis of ACL Allografts – Steve Howell
Technique and Clinical Results of Osteochondral Allografts – David Caborn
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ICL #1 - ISAKOS

Transcription

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