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Chapter | 14 |
Acromio-clavicular jointJanette W Powell, Ian Shrier, Peter A Huijbregts
CHAPTER CONTENTS
Introduction 201
Anatomy of acromio-clavicular joint 201
Biomechanics of acromio-clavicular joint 202
Pathology of acromio-clavicular joint 202
Diagnosis of acromio-clavicular joint 203
Management of acromio-clavicular joint 207
Conclusion 209
INTRODUCTION
Shoulder pain is the third most common cause for muscu-loskeletal consultation in primary care (Docimo et al2008). Acromio-clavicular joint (ACJ) pathology anddysfunction is a common component of shoulder pain(Hutchinson & Ahuja 1996, Magee & Reid 1996, Auge &Fischer 1998, Shaffer 1999, Debski et al 2001, Garretson& Williams 2003, Renfree & Wright 2003, Kiner 2004,Walton et al 2004, Powell & Huijbregts 2006, Codsi2007, Docimo et al 2008, Simovitch et al 2009). TheACJ accounts for approximately 9–12% of shoulder inju-ries presenting for general medical care (Rudzki et al2003, Docimo et al 2008, Fraser-Moodie et al 2008,Macdonald & Lapointe 2008, White et al 2008) and isone of the most frequently injured joints in certain sports,e.g. football, ice hockey, skiing, snowboarding, skating,and rugby (Magee & Reid 1996, Renfree & Wright2003, Powell & Huijbregts 2006, Petron & Hanson2007, Fraser-Moodie et al 2008, White et al 2008). Over-all, ACJ sprains/separations have been described as
accounting for 40–50% of all athletic shoulder injuries(Debski et al 2001, Petron & Hanson 2007, Simovitchet al 2009) and are noted to be twice as common as com-plete ACJ disruptions (Fraser-Moodie et al 2008, Petron &Hanson 2007), which account for 12% of all dislocationsaffecting the shoulder girdle (Magee & Reid 1996). Inaddition to the ACJ, the clavicle is frequently injured withan incidence of 23 per 1000 athletic exposures for icehockey and 17 per 1000 athletic exposures for lacrosse(Hutchinson & Ahuja 1996). The prevalence of atraumaticosteolysis of the distal clavicle has been reported to be ashigh as 27% in weightlifters (Auge & Fischer 1998). Thesenumbers likely underestimate the true prevalence, as indi-viduals with minor injuries or dysfunction might not seekmedical care (Mehrberg et al 2004, Fraser-Moodie et al2008). ACJ injuries are more common in males (Beim2000, Mehrberg et al 2004, Petron & Hanson 2007, Whiteet al 2008, Fraser-Moodie et al 2008) and over half occurin the under-30 population (Kiner 2004, Mehrberg et al2004).
ANATOMY OF ACROMIO-CLAVICULAR JOINT
Fraser-Moodie et al (2008) described the ACJ as the ‘key-stone’ link between the scapula and the clavicle. It sus-pends the upper extremity from the axial skeleton (Buss& Watts 2003, Nuber & Bowen 2003, Renfree & Wright2003, Shaffer 1999). A thin capsule surrounds the diarthro-dial ACJ, which typically contains a fibrocartilaginous disk(Lemos 1998, Shaffer 1999, Beim 2000, Buss & Watts2003, Garretson & Williams 2003, Renfree & Wright 2003,Docimo et al 2008, Fraser-Moodie et al 2008, Macdonald
201© 2011 Elsevier Ltd.
DOI: 10.1016/B978-0-7020-3528-9.00014-5
& Lapointe 2008, Rios & Mazzocca 2008, White et al 2008,Simovitch et al 2009). This intra-articular disk is variable insize and shape and may sometimes undergo rapid degener-ation beginning as early as the second decade of life (Beim2000, Renfree &Wright 2003, Mehrberg et al 2004, Docimoet al 2008, White et al 2008 Simovitch et al 2009). The ACJis reinforced by the acromio-clavicular (AC) ligaments(superior, inferior, anterior and posterior), the robust cor-aco-clavicular (CC) ligaments (conoid and trapezoid), thecoraco-acromial ligament, and the delto-trapezius aponeu-rosis (Fig. 14.1) (Lemos 1998, Shaffer 1999, Beim 2000,Buss & Watts 2003, Garretson & Williams 2003, Renfree &Wright 2003, Petron & Hanson 2007, Docimo et al 2008,Fraser-Moodie et al 2008, Macdonald & Lapointe 2008,White et al 2008, Rios & Mazzocca 2008, Simovitch et al2009, White et al 2008). Dynamic stabilization is providedby the deltoid and trapezius muscles (Lizaur et al 1994,Beim 2000, Buss & Watts 2003, Renfree & Wright 2003,Garretson & Williams 2003, Petron & Hanson 2007, Mac-donald & Lapointe 2008, Rios & Mazzocca 2008, Docimoet al 2008, White et al 2008, Simovitch et al 2009).
BIOMECHANICS OF ACROMIO-CLAVICULAR JOINT
Few studies have been published on ACJ kinematics(Teece et al 2008) but more recent 3D imaging studiesthat quantify its motion suggest that movement has his-torically been underestimated (Sahara et al 2006, 2007,Fraser-Moodie et al 2008, Teece et al 2008). Sahara et al(2007) have noted that during abduction of the shoulderthere is significant rotation of the clavicle and within
the ACJ, with the clavicle acting as a screw axis (Sahara2006). For example, in the antero-posterior direction,the clavicle translated most posteriorly (1.9 � 1.3 mm)at 90� of abduction and most anteriorly (1.6 � 2.7 mm)at maximum abduction. When defining motion of thescapula with respect to the clavicle, the scapula generallyrotated about a specific screw axis passing through theinsertions of both the acromio-clavicular and the coraco-clavicular ligaments on the coracoid process (Saharaet al 2006). Teece et al (2008) found that significantmotion (internal rotation, upward rotation, and posteriortilting) occurs at the ACJ during active humeral elevation,and discussed how abnormal motions at the ACJ willaffect the position of the scapula on the thorax, andcontribute to shoulder pathology and dysfunction. Teeceet al (2008) observed during active scapular plane abduc-tion from rest to 90�, average ACJ angular values demon-strated increased internal rotation (approximately 4.3�),increased upward rotation (approximately 14.6�), andincreased posterior tilting (approximately 6.7�). Teeceet al (2008) did not analyse motion beyond 90� abduc-tion, due to technical limitations with clavicular tracking.These ACJ motions are of sufficient magnitude to warrantclinical attention with manual mobilization when thesemotions are abnormal or dysfunctional.
PATHOLOGY OF ACROMIO-CLAVICULAR JOINT
Box 14.1 contains pathologies that may affect the ACJ(Hutchinson & Ahuja 1996, Magee & Reid 1996, Auge &Fischer 1998, Lemos 1998, Shaffer 1999, Lehtinen et al1999, Santis et al 2001, Debski et al 2001, Garretson &Williams 2003, Renfree & Wright 2003, Kiner 2004Walton et al 2004, Simovitch et al 2009). The ACJ canbe acutely injured by direct blows to the shoulder or fallson an upper extremity (ligament sprain/separations/ dis-locations). The ACJ is also vulnerable to repetitive overuse(osteolysis and degenerative joint disease) (Lemos 1998,Debski et al 2001, Kiner 2004, Nuber & Bowen 2003, Pet-ron & Hanson 2007, Rios & Mazzocca 2008, Macdonald& Lapointe 2008, Simovitch et al 2009).
Acute injuries to the ACJ typically involve a direct fallonto the outer aspect of the shoulder, usually with thearm adducted (Beim 2000, Buss & Watts 2003, Garretson& Williams 2003, Rudzki et al 2003, Petron & Hanson2007, Fraser-Moodie et al 2008, Simovitch 2009). Thisforce drives the acromion inferiorly under the clavicle.The greater stability of the sternoclavicular joint (discussedin the following chapter) results in the majority of theimpact dissipated in the ACJ structures which leads to a sys-tematic failure of stabilizing structures with progressiveforce (Beim 2000, Bradley & Elkousy 2003, Rudzki et al2003, Petron & Hanson 2007, Fraser-Moodie et al 2008,
Coracoacromialligament
Lesser tuberosity
Bicipital groove
Coracoclavicular ligament
Trapezoidligament
Conoidligament
Coracoid process
Fig 14.1 Normal anatomy of the acromio-clavicular joint.
Part | 3 | The shoulder region
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Macdonald & Lapointe 2008, Rios & Mazzocca 2008,Simovitch et al 2009). The downward force with this injuryinitially stretches the AC ligaments; then, as the forcecontinues, the AC ligaments tear and the CC ligaments arestressed (Tom et al 2009). As the downward force con-tinues the CC ligaments tear, followed by the muscleattachments of the deltoid and trapezius muscles, resultingin a complete disruption to the ACJ (Tom et al 2009).
These sequential acute injuries have been defined anddescribed by Tossy et al (1963). Rockwood et al (1996)modified and expanded these injury types to the systemcommonly used today (Fig 14.2):
• Type I: AC ligament sprain, CC ligament intact,deltoid and trapezius muscles intact
• Type II: AC ligaments & ACJ disrupted, CC ligamentsprain, deltoid and trapezius muscles intact
• Type III: AC ligaments & ACJ disrupted and displaced,CC ligaments disrupted with CC interspace 25–100%larger than normal shoulder, deltoid and trapeziusmuscles usually detached;
• Type IV: AC ligaments disrupted & ACJ displaced,clavicle displaced posteriorly, CC ligaments disruptedwith wider CC interspace, deltoid and trapeziusmuscles detached
• Type V: AC & CC ligaments disrupted, ACJ grosslydisplaced (100–300% more than normal shoulder),deltoid and trapezius muscles detached
• Type VI: AC & CC ligaments disrupted & ACJdisplaced, clavicle displaced inferiorly, deltoid andtrapezius muscles detached (Tossy et al 1963,Simovitch et al 2009, Tom et al 2009)
A less common mechanism of acute injury to the ACJwould involve a fall onto an outstretched hand, or a directblow to the elbow. These mechanisms drive the humeral
head superiorly into the acromion (Beim 2000, Garretson& Williams 2003, Petron & Hanson 2007, White et al2008). These indirect forces may result in the same injurypatterns described above (Simovitch et al 2009), or mayspare the CC ligaments when the scapula is driven superi-orly and medially injuring the AC ligaments in isolation(Mehrberg et al 2004, White et al 2008). Additionally theACJ may be injured by a traction force applied to the upperextremity (Beim 2000, Garretson & Williams 2003).
Rios & Mazzocca (2008) describe an acute ‘internalderangement’ whereby the intra-articular disk is torn.Magee & Reid (1996) propose that intra-articular diskinjuries are implicated in the ‘clicking’ that is sometimesheard and in some of the post-traumatic pain syndromesfollowing ACJ injuries.
Although many ACJ injuries are due to a sudden force,repetitive loads may also cause injury to the region. Non-contact sports such as cycling, baseball, and weightliftinghave been associated with degenerative ACJ injuries(Bowen & Nuber 2003). For example, the compressiveforces across the ACJ that are created during repeatedforceful contraction by the deltoid, trapezius, and pectora-lis major muscles may contribute to osteolysis of the distalclavicle (Nuber & Bowen 2003, Renfree & Wright 2003).This repetitive stress to the subchondral bone can causefatigue fractures and a hypervascular response leading toabsorption of bone and an eventual clinically relevantosteolysis. The sequelae include demineralization, osteope-nia, subchondral cyst formation, and distal clavicle erosion(Nuber & Bowen 2003). It is often noted that the ACJ isrequired to transmit large loads across a very small surfacearea and this may contribute to failure with repetitive activ-ity and overuse (Shaffer 1999, Beim 2000, Nuber & Bowen2003, Renfree & Wright 2003, Docimo et al 2008).
In addition, degeneration of the ACJ intra-articular diskcommences in the second decade of life and may be sig-nificant by the fourth decade (Garretson & Williams2003). An incomplete fibrocartilaginous disk may play asignificant role in the development of arthrosis (Beim2000, Powell & Huijbregts 2006, Docimo et al 2008). Pri-mary osteoarthritis and post-traumatic arthritis are notedto be prevalent in 50–60% of asymptomatic elderlyindividuals (Shaffer 1999, Docimo et al 2008, Rios &Mazzocca 2008). ACJ arthrosis, joint degradation, maybe idiopathic, or result from injury and/or instability ofthis joint (Rios & Mazzocca 2008). The ACJ is also proneto inflammatory, septic, and crystalline arthropathy(Garretson & Williams 2003, Renfree & Wright 2003).
DIAGNOSIS OF ACROMIO-CLAVICULAR JOINT
The clinical presentation of an individual with acute ACJinjury typically involves a history of one of the mechan-isms of injury described above: direct trauma to the
Box 14.1 Pathologies/dysfunctions affecting theacromio-clavicular joint
Traumatic conditions:
• separation/dislocation (types I–VI)
• fracture
• sub-acromial bursitis
• rotator cuff pathology
Infectious conditions:
• septic arthritis
Inflammatory conditions:
• rheumatoid arthritis
• systemic lupus erythematosus
• ankylosing spondylitis
• gout
Degenerative joint disease:
• osteoarthritis
• osteolysis
Chapter | 14 | Acromio-clavicular joint
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shoulder with the arm adducted, fall onto an outstretchedhand or elbow, or a traction injury to the upper extremity(Hutchinson & Ahuja 1996, Lemos 1998, Beim 2000,Buss & Watts 2003, Garretson & Williams 2003, Petron& Hanson 2007, Macdonald & Lapointe 2008, Rios &Mazzocca 2008, White et al 2008, Simovitch et al 2009).Individuals with isolated ACJ lesions typically note painover the anterior and/or superior aspect of the shoulder.
Although the pain is often localized to the region directlyover the ACJ, it may radiate to the anterolateral neck, thetrapezius-supraspinatus region, and to the anterolateraldeltoid (Gerber et al 1998, Shaffer 1999, Petron &Hanson 2007, Macdonald & Lapointe 2008, Rios &Mazzocca 2008, Fraser-Moodie et al 2008).
Swelling, ecchymosis/erythema, and deformity, if pres-ent, are easily observed as the ACJ is just under the skin
Normal
Type I Type II
Type III Type IV
Type V Type VI
Conjoined tendonof biceps and coracobrachialis
Fig 14.2 Types I–VI acromio-clavicular joint sprain.
Part | 3 | The shoulder region
204
(Hutchinson & Ahuja 1996, Shaffer 1999, Beim 2000,Mehrberg et al 2004, Petron & Hanson 2007, Fraser-Moodie et al 2008, Macdonald & Lapointe 2008,White et al 2008, Simovitch et al 2009, Tom et al 2009).Tenderness on palpation of the ACJ is reported as a com-mon clinical finding associated with ACJ dysfunction(Hutchinson & Ahuja 1996, Magee & Reid 1996, Shaffer1999, Beim 2000, Tallia & Cardone 2003, Buss & Watts2003, Nuber & Bowen 2003, Mehrberg et al 2004, Waltonet al 2004, Brukner & Khan 2006, Petron & Hanson 2007,White et al 2008, Docimo et al 2008, Fraser-Moodie et al2008, Macdonald & Lapointe 2008, Rios & Mazzocca2008, Park et al 2009, Simovitch et al 2009, Tom et al2009). A number of physical examination tests have beenproposed to stress the structures of the ACJ and assist inthe clinical diagnosis of ACJ pathology. These includethe active compression test (also known as O’Brien’s sign)(Fig 14.3) (O’Brien et al 1998, Maritz & Oosthuizen,2002, Chronopoulos et al 2004, Walton et al 2004),cross-body adduction test (also known as Scarf sign) (Fig14.4) (Maritz & Oosthuizen 2002, Chronopoulos et al2004), acromio-clavicular resisted extension test (Fig14.5) (Chronopoulos et al 2004), ACJ tenderness test(Maritz & Oosthuizen 2002, Walton et al 2004), and Pax-inos sign (Fig 14.6) (Walton et al 2004, Brukner & Khan2006). Table 14.1 provides psychometric data on theseclinical tests.
Powell & Huijbregts (2006) noted that research evi-dence supports the inclusion of the following tests, withthe following interpretation, for the diagnosis of painfulACJ dysfunction:
• A negative finding on ANY of the following testswould rule out ACJ dysfunction: cross-body adductiontest; tenderness on palpation of the ACJ; Paxinos sign
• A positive finding on ANY of the following testswould rule in ACJ dysfunction: active compressiontest; the cross-body adduction test; acromio-clavicularresisted extension test
• A positive finding on ALL three tests used to rule in ACJdysfunction (the cross-body adduction stress, activecompression, and resisted acromio-clavicular extensiontests) may be relevant when considering a medical-surgical referral and associated higher-risk interventions
A number of authors note the value of ACJ local anaes-thetic injections to assist and/or confirm the involvementof ACJ dysfunction in the clinical presentation when other
Fig 14.3 Active compression test: (A) maximal internal rotation: the client stands with the involved arm straight and forwardflexed to 90�. The arm is then horizontally adducted 10–15� and maximally internally rotated. The client then resists a downwardforce applied by the examiner to the distal arm. (B) Maximal external rotation: the test is then repeated in the same position withthe arm maximally externally rotated: O’Brien et al (1998) did not quantify the amount of force used. This test is consideredpositive for ACJ dysfunction if the pain is localized to the ACJ on the first position and relieved or eliminated on the secondposition. Pain ‘deep inside the shoulder’, with or without a click, in the first position and eliminated or reduced in the secondposition is considered indicative of a glenoid labrum tear (from Powell & Huijbregts 2006, with permission).
Fig 14.4 Cross-body adduction test: the client’s arm isforward flexed to 90� and then horizontally adducted acrossthe body. Literature is unclear on whether this test isactive or passive. This test is considered positive if it causes painlocalized to the ACJ (from Powell & Huijbregts, 2006, withpermission).
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associated shoulder injuries may be present (Parlington &Broome 1998, Shaffer 1999, Maritz & Oosthuizen 2002,Nuber & Bowen 2003, Tallia & Cardone 2003, Waltonet al 2004, Chronopoulos et al 2004, Codsi 2007,Docimo et al 2008, Rios & Mazzocca 2008, Park et al2009) and some consider it the criterion reference (goldstandard) for the diagnosis of ACJ injury/pathology(Parlington & Broome 1998, Maritz & Oosthuizen 2002,Walton et al 2004, Chronopoulos et al 2004). If painceases with injection, only the ACJ is involved if pain
decreases with injection, then other pathologies likelyco-exist; if pain is unaffected, the ACJ is likely notinvolved (Parlington & Broome 1998, Shaffer 1999,Maritz & Oosthuizen 2002, Tallia & Cardone 2003,Walton et al 2004, Chronopoulos et al 2004, Codsi2007, Docimo et al 2008, Rios & Mazzocca 2008, Parket al 2009). However, injection into the ACJ is noted tohave its challenges. It may be unsuccessful, particularlywith injection targeting, due to its variable anatomy, varia-bility in the obliquity of the joint, the small intra-articular
Fig 14.5 Acromio-clavicular resisted extension test: theclient’s shoulder is flexed to 90�, then combined with maximalinternal rotation and 90� of elbow flexion. The client is thenasked to horizontally abduct the arm against resistance. Thistest is considered positive if it causes pain at the ACJ (fromPowell & Huijbregts, 2006, with permission).
Fig 14.6 Paxinos sign: the patient sits with the arm relaxedby his/her side. The examiner’s thumb is placed under thepostero-lateral aspect of the acromion; the index and longfingers (same or contralateral hand) are then placed superior tothe mid-portion of the ipsilateral clavicle. The thumb applies anantero-superior force concurrently while the fingers apply aninferior force. This test is considered positive if it causes orincreases pain localized to the ACJ (from Powell & Huijbregts,2006, with permission).
Table 14.1 Psychometric data for ACJ physical examination tests (Powell & Huijbregts 2006)
Active compression Cross-bodyadduction
AC resistedextension
ACJtenderness
Paxinossign
Accuracy 0.531; 0.922; 0.973 0.792 0.842 0.531 0.651
Sensitivity 0.161; 0.412; 0.684; 1.03 0.772;1.04 0.722 0.954; 0.961 0.71
Specificity 0.901; 0.933; 0.952 0.792 0.852 0.11 0.51
Positive predictive value 0.292; 0.621; 0.923 0.22 0.22 0.521 0.611
Negative predictive value 0.521; 0.972;1.03 0.982 0.982 0.711 0.71
Positive likelihood ratio 1.61; 8.22; 13.33 3.72 4.82 1.11 1.61
Negative likelihood ratio 0.03; 0.62; 0.91 0.32 0.32 0.41 0.41
1Walton & Sadi (2008);2Chronopoulos et al (2004)3O’Brien et al (1998);4Maritz & Oosthuizen (2002)
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region, and substantial joint space narrowing whendiminished by osteophyte formation (Shaffer 1999, Par-lington & Broome 1998, Bisbinas et al 2006, Codsi2007, Rios & Mazzocca 2008). Parlington & Broome(1998) noted that non-image guided intra-articular infil-trations were placed successfully in the ACJ in only 16/24 (67%) of cadaveric shoulders. Bisbinas et al (2006)found that only 40% of ACJ injections will be placed inthe joint if performed without imaging guidance.
As a general principle, imaging is only necessary when itwill change management. For acute injuries, history andclinical examination will usually rule out a fracture or anACJ injury severe enough to require surgical interventionand therefore imaging is often not recommended. If afracture cannot be ruled out, or if the injury may benefitfrom surgery, standardized radiographs are essential toboth the diagnosis and classification (Shaffer 1999,Fraser-Moodie et al 2008, Nuber & Bowen 2003, Docimoet al 2008, White et al 2008, Simovitch et al 2009). Theseroutine images include: true AP views, axillary views, andthe Zanca view (10–15� cephalic tilt) (Shaffer 1999, Beim2000, Garretson & Williams 2003, Nuber & Bowen 2003,Mehrberg et al 2004, Rios & Mazzocca 2008, Docimo et al2008, Fraser-Moodie et al 2008, Macdonald & Lapointe2008, White et al 2008, Simovitch et al 2009). Ideallyviews would be taken of the uninvolved shoulder to pro-vide normative comparison images (Shaffer 1999, Beim2000, Garretson & Williams 2003, Simovitch et al2009). Although stress views of the ACJ have beendescribed to differentiate between Type II and Type IIIinjuries, they are costly, uncomfortable, rarely add diag-nostic information, do not affect management, and arethus no longer recommended for routine use (Shaffer1999, Beim 2000, Buss & Watts 2003, Garretson &Williams 2003, Petron & Hanson 2007, Rios & Mazzocca2008, White et al 2008, Simovitch et al 2009). Rios &Mazzocca (2008) proposed the use of an AP radiographof the involved shoulder with the arm adducted acrossthe chest as a prognostic tool. Normal positioning, wherethe acromion does not overlap the clavicle, indicates a sta-ble joint and directs the clinician to non-surgical manage-ment. Superimposition of the acromion and distal claviclesuggests instability and may indicate the need for surgicalintervention (Rios & Mazzocca 2008).
Contrary to acute injuries, standardized radiographs areoften essential to both the diagnosis and classification ofnon-acute injuries (Shaffer 1999, Nuber & Bowen 2003,Docimo et al 2008, Fraser-Moodie et al 2008, Whiteet al 2008, Simovitch et al 2009). Computed tomographycan be utilized when investigating arthritic osseouschanges (joint narrowing, erosions, subchondral cysts)(Docimo et al 2008, Macdonald & Lapointe 2008). Someauthors recommend magnetic resonance imaging andultrasound when investigating capsular hypertrophy, effu-sions, subchondral edema, subchondral fractures, andligamentous/aponeurosis injury (Shaffer 1999, Nuber &
Bowen 2003, Petron & Hanson 2007, Docimo et al2008, Fraser-Moodie et al 2008, Macdonald & Lapointe2008). A recent study utilized ultrasound to identifyabnormal movements in an injured ACJ that were notidentified on standard imaging or stress radiographs(Peetrons & Bedard 2007, Rios & Mazzocca 2008). Iso-tope bone scanning may be useful in discriminating thesource of symptoms (Shaffer 1999, Nuber & Bowen2003, Fraser-Moodie et al 2008). Walton et al (2004)found bone scans had relatively high sensitivity (82%)and specificity (70%) in the diagnosis of ACJ-related pain.
MANAGEMENT OF ACROMIO-CLAVICULAR JOINT
The goals of treatment for ACJ injuries are achieving pain-less range of motion of the shoulder, obtaining fullstrength, and exhibiting no limitation in activity (Fraser-Moodie et al 2008, Macdonald & Lapointe 2008, Whiteet al 2008). Conservative management is considered thestandard of care for non-acute ACJ dysfunction and fortypes I and II ACJ injuries (Magee & Reid 1996, Bradley& Elkousy 2003, Buss & Watts 2003, Hootman 2004,Mehrberg et al 2004, Petron & Hanson 2007, Spencer2007, Ceccarelli et al 2008, Docimo et al 2008, Fraser-Moodie et al 2008, Macdonald & Lapointe 2008, Rios &Mazzocca 2008, White et al 2008, Tom et al 2009).Although there is some controversy over the treatmentsof type III injuries, most authors now favour non-surgicalintervention (Magee & Reid 1996, Bradley & Elkousy2003, Buss & Watts 2003, Rudzki et al 2003, Hootman2004, Mehrberg et al 2004, Brukner & Khan 2006, Petron& Hanson 2007, Spencer 2007, Ceccarelli et al 2008, Fra-ser-Moodie et al 2008, Macdonald & Lapointe 2008, Rios& Mazzocca 2008, White et al 2008, Simovitch et al 2009,Tom et al 2009, Murena et al 2009). Treatment of type IIIACJ injuries is dependent on the injury severity and activ-ity level of the patient. Surgical intervention is recom-mended for types IV, V, and VI and for protracted pain/disability with ACJ dysfunction (Urist 1963, Bradley &Elkousy 2003, Hootman 2004, Mehrberg et al 2004,Macdonald & Lapointe 2008, Petron & Hanson 2007,Rabalais & McCarty 2007, Rios & Mazzocca 2008, Whiteet al 2008, Simovitch et al 2009).
Conservative management can involve rest, splinting/bracing, physical therapy (including, but not limited tomanual therapy, active rehabilitation, taping, modalitiesincluding cold, heat, ultrasound, laser, electrical stimula-tion, and iontophoresis), ACJ corticosteroid injections,and anti-inflammatory and/or analgesic medication(Magee & Reid 1996, Shaffer 1999, Bradley & Elkousy2003, Buss & Watts 2003, Rudzki et al 2003, Lemos &Tolo 2003, Buttaci et al 2004, Mehrberg et al 2004,Brukner & Khan 2006, Codsi 2007, Petron & Hanson
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2007, Spencer 2007, Docimo et al 2008, Fraser-Moodieet al 2008, Macdonald & Lapointe 2008, White et al2008, Rios & Mazzocca 2008, Simovitch et al 2009, Tomet al 2009). A structured active rehabilitation programmethat involves the strengthening of the shoulder girdlemuscles, including the deltoid, trapezius, sternocleido-mastoid, and subclavius, as well as the rotator cuff andperiscapular stabilizers, is recommended to prevent on-going disability in individuals with AJC dysfunction/injury (Shaffer 1999, Bradley & Elkousy 2003, Buss &Watts 2003, Fraser-Moodie et al 2008, Simovitch et al2009).
The literature suggests 80–90% of conservatively man-aged individuals have good/satisfactory outcomes withregards to strength, motion, and return to pre-injury levelsof function (Rudzki et al 2003, Hootman 2004, Macdonald& Lapointe 2008, Rios & Mazzocca 2008, White et al 2008,Simovitch et al 2009). These studies used a variety of ‘con-servative treatments’. Simovitch et al (2009) proposed thatnon-surgical management often translates into benignneglect and suggested that inadequate rehabilitationexplains some of the failures seen in non-surgical manage-ment. First, a good/satisfactory outcome in 80–90% ofindividuals does not necessarily mean these subjects arefree of pain or dysfunction (Bjerneld et al 1983, Rawes &Dias 1996, Schlegel et al 2001): up to one-third of thosewith type I and type II ACJ injuries had pain on activityat longer term follow-up (Galpiri et al 1985, Rawes & Dias1996). Bergfeld et al. (1978) found that 30% of individualswith type I ACJ injury and 42% of individuals with type IIACJ injury reported clicking and pain with push-ups anddips. An additional 9% and 23% of individuals with typeI and II injuries, respectively, reported severe pain and lim-itation of activities. Mouhsine et al (2003) reported similarresults noting 27% of individuals with type I & II ACJ inju-ries treated non-surgically developed chronic ACJ symp-toms at a mean of 26 months post injury and requiredsubsequent surgery. Unsatisfactory results have beenreported in 10% to 50% of individuals undergoing conser-vative management, at times leading to a change of joband/or modification of recreational activities, even poten-tially requiring subsequent surgery (Fraser-Moodie et al2008). These results underscore the need for investigatorsand clinicians to provide detailed information about ‘con-servative management’ when reporting their results, justas a proper evaluation of studies on pharmaceuticalsrequire details on type, dose, and frequency.
The importance of adequate rehabilitation was shownin a study of the non-surgical management of type IIIACJ injuries (Simovitch et al 2009). Glick et al (1977)investigated 35 unreduced ACJ dislocations that weremanaged conservatively in a professional and competitiverecreational athletic population and noted all individualswho had a supervised rehabilitation programme werepain-free. They concluded that the predominant reasonfor persistent pain and disability after a type III ACJ injury
managed conservatively was inadequate rehabilitation.This proposition is supported by Gurd (1941) who notedthat the shoulder can function normally despite an absentclavicle, as long as the shoulder girdle muscles arestrengthened and maintained.
Despite the success of conservative treatment for thevast majority of injuries, there are indications for surgery.These include: ACJ tenderness with (1) evident abnormalsigns on ACJ imaging results such as those seen on typesIV, V & VI ACJ injuries, (2) a lack of response to conserva-tive management, and (3) an unwillingness or inability tomodify or refrain from demanding physical activity (over-head sports, weight training, manual labour) (Shaffer1999, Schwarzkopf et al 2008, White et al 2008). Whenindicated, surgical outcomes are also successful but tendto have higher rates of complications, longer convales-cence, and longer time away from work and sports(Petron & Hanson 2007, Spencer 2007). There are manysurgical options for managing ACJ dysfunction and injury,including but not limited to open or arthroscopic proce-dures, distal clavicle resection, primary fixation of theACJ, secondary stabilization of the ACJ via a linkagebetween the clavicle and coracoid process, dynamic stabi-lization of the ACJ via a musculo-tendinous (inferiorlydirected force) transfer from distal clavicle to the coracoidprocess, ligament transfers and soft tissue reconstructions,and anatomic reconstruction (Magee & Reid 1996, Shaffer1999, Bradley & Elkousy 2003, Buss & Watts 2003, Nuber& Bowen 2003, Kwon & Iannotti 2003, Mehrberg et al2004, Buttaci et al 2004, Docimo et al 2008, Petron &Hanson 2007, Rabalais & McCarty 2007, Macdonald &Lapointe 2008, White et al 2008, Simovitch et al 2009,Murena et al 2009, Tom et al 2009).
A wide variety of surgical techniques have beendescribed, but none have been shown to be significantlysuperior (Fraser-Moodie et al 2008). The later mini-mally-invasive techniques are reported to show promise,but well-designed prospective studies need to be per-formed (Fraser-Moodie et al 2008, White et al 2008).Timing of surgery is controversial with some authorsadvocating early reconstruction and others advocatingsurgery be reserved for chronic symptomatic patients(Weinstein et al 1995, Bradley & Elkousy 2003, Buss &Watts 2003). Weinstein et al (1995) noted a trend to bet-ter outcomes when ligament reconstruction was donewithin the first 3 weeks after injury. Dumontier et al(1995) found no difference between early (< 3 weeks)and late ligamentous reconstruction.
The evaluation of success or failure for a surgical inter-vention must include complications. Surgical complica-tions include, but are not limited to: hardware failureand migration, neurovascular injury, infection, fracture,and osteolysis (Shaffer 1999, Bradley & Elkousy 2003,Kwon & Iannotti 2003, Lemos & Tolo 2003, Nuber &Bowen 2003, Rudzki 2003, Petron & Hanson 2007,Fraser-Moodie et al 2008, Rios & Mazzocca 2008, White
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et al 2008, Simovitch et al 2009). Many surgical optionsexist for the ACJ region and their goal is to minimizesymptoms and maximize long-term function (Bradley &Elkousy 2003, Kwon & Iannotti 2003). Bradley & Elkousy(2003) note there is no correlation in the literaturebetween anatomic reduction and improvements in pain,strength or motion. Fraser-Moodie et al (2008) note thateven though the many varied surgical techniques record alow rate of failure the multiplicity of procedures, the lack ofa generally-accepted surgical method, and the number ofreports outlining the specific surgical complications inferthat all ACJ surgical techniques carry a substantial risk of fail-ure of the implant, leading to re-subluxationof the joint. Par-tial re-subluxation is not necessarily associated with pooroutcomes and is oftenmanaged conservatively (Fraser-Moo-die et al 2008). Complete re-subluxation is associated withresidual symptoms, and there are reports of successful revi-sion operations (Fraser-Moodie et al 2008).
CONCLUSION
The vast majority of ACJ injuries are minor (Grades I–II,with CC ligaments intact) and recover fully with adequateconservative management. Studies comparing adequate
rehabilitation to surgery for Grade III injuries (CCligaments disrupted) also support the role of adequaterehabilitation as the primary treatment. The more severeinjuries (e.g. posterior or inferior displacement of the clav-icle) are rarer and there is some research suggesting theseinjuries should be treated surgically. Areas that are mostlikely to benefit from more research include:
• Long-term prognosis: Studying the sequelae of ACJinjury with validated relevant outcome measures(Hootman 2004).
• Diagnostic testing: Study of the validity of the newerdiagnostic manoeuvres such as Paxinos sign and thecross-arm adduction AP radiographs (Rios &Mazzocca 2008) and understanding how best tocombine the results of different tests for makingmanagement decisions.
• Conservative treatment: The comparison of differenttypes of supervised rehabilitation in the managementof types I, II and III ACJ injury and in chronic ACJdysfunction (Hootman 2004, Spencer 2007,Macdonald & Lapointe 2008, Ceccarelli et al 2008,Simovitch et al 2009).
• Surgical treatment: The timing of surgicalinterventions, including whether there are sometimesindications for early surgical intervention with type IIIACJ injury (Rios & Mazzocca 2008).
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