Latest / Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast. / Sports Injuries of the shoulder and the science behind them

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Sports Injuries of the shoulder and the science behind them · Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast.

• 0:00
  Welcome to The Deep Dive, the show where we unpack
• 0:02
  complex topics and arm you with the essential
• 0:04
  insights you need to be truly well -informed.
• 0:08
  Today, we're plunging into a marvel of human
• 0:10
  engineering, a joint that really epitomizes both
• 0:13
  extraordinary power and, well, surprising fragility,
• 0:17
  the shoulder. It really is quite something, isn't
• 0:19
  it? It's an incredible feat of anatomy, capable
• 0:22
  of immense force and delicate precision, yet
• 0:24
  paradoxically, it's also one of the most inherently
• 0:27
  unstable joints in the human body. So how does
• 0:30
  this fundamental conflict play out, particularly
• 0:33
  in the demanding, high -stakes world of professional
• 0:35
  athletics, where every movement is pushed to
• 0:37
  its absolute limit? It's truly a fascinating
• 0:40
  paradox that incredible range of motion often
• 0:42
  comes at a cost, making the shoulder a frequent
• 0:45
  sight of injury in sports, as you know. Indeed.
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  And that's precisely why we're taking an in -depth
• 0:50
  look today. This deep dive is an exploration
• 0:53
  into the intricate world of sports -related shoulder
• 0:55
  injuries. Our aim is to provide mid -senior medical
• 0:59
  professionals like you with practical, evidence
• 1:01
  -based insights that hopefully transcend basic
• 1:04
  understanding, giving you that critical edge
• 1:06
  in diagnosis and management. And joining me today
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  to navigate this complex landscape is a truly
• 1:11
  distinguished expert in the field, Professor
• 1:13
  Mo Imam. He possesses an exceptional ability
• 1:16
  to synthesize complex orthopedic information,
• 1:19
  draw critical connections between nuanced details,
• 1:22
  and truly illuminate the broader clinical implications
• 1:24
  of these injuries. Thank you. It's a pleasure
• 1:26
  to be here and to delve into a topic that truly
• 1:28
  underpins so much of what we see in practice.
• 1:30
  Our mission today is clear. We're going to meticulously
• 1:33
  unpack the shoulder's fundamental anatomy and
• 1:35
  biomechanics, dissect common injury patterns
• 1:37
  unique to athletic demands and explore cutting
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  -edge diagnostic approaches and evolving management
• 1:43
  strategies. Ultimately, we want to enhance your
• 1:47
  diagnostic precision and elevate the efficacy
• 1:49
  of your treatment plans, optimizing outcomes
• 1:51
  for your athletic patients. You know, when we
• 1:53
  talk about the shoulder, it's this incredible
• 1:55
  paradox capable of throwing a fastball at, what,
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  100 mile of horror, yet seemingly prone to dislocation
• 2:01
  just from falling awkwardly. What is it about
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  its fundamental architecture with its five joints,
• 2:06
  eight ligaments, and 30 muscles that creates
• 2:07
  this inherent conflict, offering unparalleled
• 2:10
  mobility at the cost of inherent instability.
• 2:12
  That really is the core paradox, isn't it? The
• 2:15
  shoulder achieves its status as the most movable
• 2:18
  joint in the human body, precisely because it
• 2:21
  sacrifices inherent stability. Its primary function
• 2:25
  is to facilitate incredibly precise hand positioning
• 2:28
  in space, allowing for complex multi -directional
• 2:32
  movements. But this comes at the expense of a
• 2:35
  deep bony socket, the kind that would provide
• 2:37
  intrinsic stability like you see in the hip,
• 2:40
  for instance. Why? So it's a trade -off. Exactly.
• 2:42
  And when we consider its movements, we're talking
• 2:44
  about a full spectrum, internal and external
• 2:46
  rotations, abduction and adduction in the frontal
• 2:48
  plane, and flexion and extension in the sagittal
• 2:51
  plane. The combination of these elementary movements
• 2:54
  generates circumduction, that complex circular
• 2:56
  trajectory we see, for example, in a picture's
• 2:59
  wind -up. Crucially, the glenohumeral joint also
• 3:01
  has significant translational capabilities anterior
• 3:04
  -posterior, superior -inferior, and medial -lateral.
• 3:08
  All of this extensive range of motion is critically
• 3:10
  dependent on a balanced and synchronized interplay
• 3:12
  between both its static or passive and active
• 3:15
  or dynamic stabilizers. Without that delicate
• 3:17
  balance, the entire system falters. OK, so passive
• 3:20
  and active stabilizers working together. 1 .2
• 3:23
  static stabilizers. the passive framework. So
• 3:27
  if extreme mobility is paramount, what precisely
• 3:30
  is holding it all together? Let's delve into
• 3:32
  the static stabilizers first, starting with the
• 3:35
  bony components. What's truly fascinating about
• 3:37
  the bone geometry that contributes to this delicate,
• 3:40
  often precarious balance? Well, the bony anatomy
• 3:43
  itself is a major contributor to the shoulder's
• 3:46
  inherent instability, actually. Take the humeral
• 3:48
  head, for instance. It exhibits significant variability
• 3:51
  in shape and size. And on average, it's retroverted
• 3:54
  by about 90%. degrees, though there's quite a
• 3:56
  range. This retroversion, along with the humeral
• 3:59
  head's curvature, plays a role in how it articulates
• 4:02
  with the glenoid. And the glenoid, that's the
• 4:03
  socket part, isn't it? Yes, and it's remarkably
• 4:05
  shallow. It's pear -shaped, with an average depth
• 4:08
  of just 2 .5 millimeters in the entero -posterior
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  direction, and maybe 9 millimeters superior,
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  inferiorly. This minimal bony containment, coupled
• 4:16
  with its slight retroversion and superior inclination,
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  is a fundamental architectural compromise. It
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  grants unparalleled mobility but forces the soft
• 4:24
  tissues to do the heavy lifting for stability.
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  So the bones offer very little constraint on
• 4:28
  their own. Precisely. What's even more astounding
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  is that only a maximum of 30 % of the humeral
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  articular surface articulates with the glenoid
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  at any given time. This starkly underscores the
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  indispensable role of the soft tissue and dynamic
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  restraints. When we consider how little bone
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  -on -bone contact there is, it becomes clear
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  why even subtle changes in bony anatomy can significantly
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  influence stability. Which brings us to bony
• 4:53
  lesions after trauma. Exactly. Certain bony lesions
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  often arise after traumatic events leading to
• 4:59
  instability. The bony bankart lesion, for example,
• 5:02
  located at the anterior inferior glenoid rim.
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  It becomes clinically significant when it involves
• 5:07
  more than 20 % of the glenoid's length predisposing
• 5:10
  to recurrence. If it involves over 50 % of the
• 5:12
  glenoid, shoulder stability is reduced by more
• 5:14
  than 30%. And the classification for that? Bigliani
• 5:17
  et al. Classified it into type 1, 2, and 3 based
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  on displacement and healing. Then you have the
• 5:25
  hill -sax lesion, a compression fracture at the
• 5:28
  post -relateral aspect of the humeral head that
• 5:30
  typically occurs following an anterior dislocation.
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  And we also see reverse lesions, like the reverse
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  bony bankart lesion or the reverse hill -sax,
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  also called the McLaughlin lesion, on the anterior
• 5:41
  humeral head, which can become engaging during
• 5:43
  specific arm movements. Right, engaging, meaning
• 5:46
  it can catch on the glenoid rim. Exactly. Okay,
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  beyond the intricate bony architecture, you mentioned
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  the soft tissues play an equally crucial if not
• 5:54
  more critical, role. What are these unsung heroes
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  and how do their complex interconnections contribute
• 6:00
  to stability and, well, instability when injured?
• 6:04
  You're right. The soft tissues are absolutely
• 6:05
  vital. A key concept here, especially for understanding
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  instability, is the glenoid tract. Think of this
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  as the contact area between the glenoid and humeral
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  head. It shifts from the inframedial to the post
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  -relateral portion of the humeral head's posterior
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  articular surface during maximum external rotation,
• 6:22
  extension, and abduction. Okay, so the contact
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  zone moves. Precisely. And the glenoid tract's
• 6:27
  width is about 84 % of the glenoid's width. This
• 6:31
  means that any glenoid articular surface loss,
• 6:33
  as we see in bony bankart lesions, significantly
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  influences this crucial dimension. Why this matters
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  clinically? It precisely influences the risk
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  of Hill -Sachs lesion engagement. If the humeral
• 6:45
  head bony loss remains within the glenoid tract,
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  it's considered on track. Meaning less risk.
• 6:50
  Exactly. No possibility of the hill sacs lesion
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  overriding the glenoid rim. Conversely, if it
• 6:55
  extends over the medial margin of the glenoid
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  tract, it's off track, and the risk of engagement
• 6:59
  rises significantly. This distinction is critical
• 7:02
  for surgical planning. That makes sense. So what
• 7:04
  are the main soft tissue players? Well, looking
• 7:06
  at the soft tissue stabilizers themselves, we
• 7:09
  have the glenoid labrum, the glenohumeral capsule,
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  the glenohumeral ligaments, the rotator interval,
• 7:15
  negative intercapsular pressure, and the adhesion
• 7:17
  -cohesion mechanism. The glenoid labrum, that
• 7:21
  triangular fibrocartilaginous ring, is particularly
• 7:23
  prone to lesions. A bankard tear, affecting the
• 7:27
  anteroinferior labrum, has a high association
• 7:29
  with recurrent instability, potentially up to
• 7:32
  an 87 % recurrence after an arthroscopic bankard
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  procedure under certain conditions. That's a
• 7:37
  huge recurrence rate. It is. We also see the
• 7:39
  ALPSA anterior labral ligamentus periosteal sleeve
• 7:43
  avulsion, where the complex rolls up, displaced
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  medially and inferiorly. This potentially carries
• 7:48
  an even higher risk of re -dislocation than undisplaced
• 7:51
  bankard tears. And the capsule and ligaments?
• 7:53
  Also key. Capsular stretching is quite common
• 7:56
  in recurrent anterior instability found in up
• 7:58
  to 28 % of patients. Conversely, recurrent posterior
• 8:02
  subluxations lead to posterior capsular redundancy
• 8:05
  and increased joint volume causing posterior
• 8:07
  instability. This redundancy in various directions
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  is a very common finding in atraumatic multidirectional
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  instability. The glenohumeral ligament superior,
• 8:17
  SGHL, middle. MGHL, and especially the inferior
• 8:20
  glenohumeral ligament complex, IGHLC, primarily
• 8:24
  act at the extremes of range of motion when they
• 8:26
  are in tension. So, not so much in the midrange?
• 8:28
  Correct. In the middle ranges, the rotator cuff
• 8:30
  and long head of biceps take over more. The IGHLC
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  forms a crucial sling -like structure that moves
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  anteriorly during abduction, external rotation,
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  and extension to restrain anterior humeral head
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  translation. And AGHL lesion, humeral avulsion
• 8:43
  of the glenohumeral ligament, where the ligament
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  pulls off the humerus, has an incidence as high
• 8:47
  as 10 % and can often be missed. So another potential
• 8:50
  hidden injury. Yes. Then there's the rotator
• 8:53
  interval, that triangular space bounded by the
• 8:55
  coracoid, biceps tendon, subscapularis, and supraspinatus.
• 9:00
  It's an important inferior stabilizer. Insufficiency
• 9:03
  here can be clinically appreciated, especially
• 9:05
  in athletes when muscles are contracted. And
• 9:08
  finally, almost imperceptibly, you have mechanisms
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  like negative intracapsular pressure, a sort
• 9:14
  of suction effect, and the adhesion -cohesion
• 9:16
  effect. Like wet glass. Exactly like wet glass
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  surfaces sticking together. The articular cartilage
• 9:21
  surfaces create a subtle but critical bond through
• 9:24
  fluid -mediated mechanisms. This highlights how
• 9:27
  vital a healthy, intact cartilage surface is
• 9:30
  for maintaining that foundational stability even
• 9:33
  before the muscles kick in. 1 .3 Dynamic Stabilizers
• 9:36
  The Active Control System Okay, so the static
• 9:39
  structures provide the foundational architecture,
• 9:41
  but the shoulder is anything but static. It's
• 9:43
  constantly in motion, performing incredible feats.
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  That brings us to the Active Control System,
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  doesn't it? How do the muscles and proprioception
• 9:50
  actively coordinate to keep the shoulder in check
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  and enable its incredible mobility? Precisely.
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  The dynamic stabilizers are the real -time guardians,
• 9:59
  constantly adjusting, and their combined and
• 10:02
  synchronized roles are absolutely paramount in
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  maintaining dynamic stability. The rotator cuff
• 10:07
  muscles are the primary dynamic stabilizers here.
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  Their main function is to compress the humeral
• 10:13
  head onto the glenoid surface, centering it and
• 10:16
  dynamically tightening the capsule ligamentous
• 10:17
  structures they attach to. These four muscles,
• 10:20
  subscapularis, supraspinatus, infraspinatus,
• 10:23
  and teres minor, effectively hug the joint, creating
• 10:26
  that dynamic compression. A hugging effect. I
• 10:28
  like that. It's a good visual. And the work by
• 10:31
  Wolker and colleagues was quite compelling. They
• 10:33
  show that even a 50 % decrease in rotator cuff
• 10:36
  muscle forces resulted in nearly a 50 % increase
• 10:39
  in anterior displacement of the humeral head
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  in response to external loading. Wow, that really
• 10:43
  underscores their importance. It does. It shows
• 10:45
  just how vital their active contribution is.
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  The subscatularis, in particular, provides anterior
• 10:50
  stability, especially when the arm is in neutral
• 10:53
  rotation. Now, you mentioned impingement earlier.
• 10:56
  Can you clarify the types we see? Yes. Within
• 10:58
  this dynamic system, we often differentiate between
• 11:01
  two primary types of impingement. External impingement
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  is an abnormal contact between the coracoacromial
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  arc, that's the roof of the shoulder, and superior
• 11:09
  surface of the rotator cuff. Internal impingement,
• 11:12
  on the other hand, involves abnormal contacts
• 11:15
  between the rotator cuff's articular surface,
• 11:17
  the underside, and the posterior glenode rim.
• 11:20
  This is particularly common in throwing athletes.
• 11:23
  And the cause of internal impingement is debated.
• 11:25
  There's an ongoing discussion, yes. It's often
• 11:28
  attributed to anterior micro instability and
• 11:30
  tightness of the posterior capsule. Others highlight
• 11:33
  that postural inferior capsular contracture can
• 11:36
  result in postural superior instability, leading
• 11:39
  to a peelback of the superior labrum and rotator
• 11:41
  cuff tearing. It's likely multifactorial in many
• 11:44
  cases. What about the biceps? The long head of
• 11:47
  biceps acts as a secondary stabilizer. Its role
• 11:50
  becomes predominant and critical when a rotator
• 11:52
  cuff or capsuligmentous deficiency coexists,
• 11:55
  which we often find in patients with insufficient
• 11:57
  rotator cuff function. Then we have the scapulothoracic
• 12:00
  muscles and their rhythm. The key scapular rotators
• 12:04
  include the trapezius, rhomboids, latissimus
• 12:07
  dorsi, serratus anterior, and levator scapulae.
• 12:10
  Codman's seminal concept of scapula thoracic
• 12:13
  rhythm describes the coordinated movement between
• 12:15
  the scapula thoracic joint, essentially a sliding
• 12:18
  surface between the scapula and the rib cage
• 12:20
  and the glenohumeral joint. So the shoulder blade
• 12:23
  has to move correctly with the arm. Absolutely.
• 12:26
  The scapula rotators enable the glenoid to modify
• 12:28
  its orientation to follow the humeral head during
• 12:31
  motion. This is crucial. Dysfunction, such as
• 12:34
  weakness or imbalance in the serratus anterior,
• 12:36
  can predispose athletes to rotator cuff tendonitis
• 12:39
  or atraumatic shoulder instability. Therefore,
• 12:41
  recovering the scapula thoracic rhythm through
• 12:43
  appropriate rehabilitation of these scapula rotators
• 12:46
  is absolutely essential, particularly in younger
• 12:48
  patients. And finally, proprioception, the septum
• 12:50
  joint position. Yes, proprioception. Numerous
• 12:54
  mechanoreceptors are located within the glenohumeral
• 12:57
  joint capsule, particularly concentrated in the
• 12:59
  anterior and inferior capsule. These are activated
• 13:02
  during movement, sending crucial signals to the
• 13:05
  stabilizing muscles. Here's the profound clinical
• 13:07
  implication. Progressive instability leads to
• 13:10
  increased capsular stretch and, consequently,
• 13:13
  proprioceptive loss or disorganization. Ah, so
• 13:16
  the instability damages the feedback system.
• 13:19
  Precisely. This disorganization can then lead
• 13:21
  to muscle patterning problems, repeated dislocations
• 13:24
  and subluxations, and can even progress to bony
• 13:27
  glenoid wear and affect core stability and the
• 13:29
  full kinetic chain. This interconnected cascade
• 13:32
  strongly supports the principle that early treatment
• 13:34
  and stabilization are highly advantageous. You
• 13:37
  want to stop that negative cycle. 2 .1 shoulder
• 13:39
  injuries in overhead athletes, the kinetic chain
• 13:41
  challenge. OK, let's zoom in now on the unique,
• 13:45
  often extreme demands placed on the shoulders
• 13:47
  of overhead athletes. think pitchers, tennis
• 13:51
  players, javelin throwers. How does their specialized
• 13:54
  high -velocity movement governed by this intricate
• 13:57
  kinetic chain you mentioned lead to very specific
• 13:59
  injury patterns that differ from, say, contact
• 14:02
  athletes? The kinetic chain is indeed the cornerstone
• 14:05
  of overhead athletic performance. We define it
• 14:07
  as an orchestrated system of sequential body
• 14:10
  positions and motions, precisely designed to
• 14:12
  efficiently transfer the maximum force generated
• 14:15
  in large muscles of the core and lower leg all
• 14:17
  the way up to the hand. This provides distal
• 14:20
  arm mobility on a stable proximal base at the
• 14:22
  scapula. What's critical to understand is that
• 14:25
  even with a fully functional kinetic chain, the
• 14:27
  repetitive tremendous forces created on the glenocumeral
• 14:30
  joint during the throwing motion can still lead
• 14:32
  to micro -damage of tendons and ligaments over
• 14:34
  time. Just the sheer repetitive force. Exactly.
• 14:37
  But crucially, shoulder symptoms in overhead
• 14:40
  athletes are predominantly related to a failure
• 14:42
  of this kinetic chain, specifically at the hip
• 14:45
  joint, the trunk, and the scapula. This failure
• 14:48
  fundamentally altered shoulder biomechanics,
• 14:51
  resulting in overstress on the glenohumeral structures
• 14:53
  themselves. So the shoulder takes the hip for
• 14:55
  a problem elsewhere? Very often, yes. Consider
• 14:58
  a compelling mathematical study that demonstrated
• 15:01
  that a mere 20 % reduction in trunk kinetic energy
• 15:04
  development necessitates a compensatory 33 %
• 15:07
  increase in velocity in the distal segments,
• 15:10
  the arm, to maintain the same energy at ball
• 15:12
  impact. This vividly highlights the profound
• 15:15
  impact of proximal dysfunction on the entire
• 15:17
  system. The shoulder ends up working overtime.
• 15:20
  That's a really clear illustration. How do these
• 15:22
  athletes typically present? Well, when it comes
• 15:24
  to diagnosis, we differentiate between two primary
• 15:27
  stages of presentation. The early stage is characterized
• 15:30
  by shoulder symptoms without anatomical failure.
• 15:33
  This often presents as inflammation, perhaps
• 15:35
  what's termed a disabled throwing shoulder or
• 15:37
  pathologic kinetic chain syndrome. Most symptoms
• 15:41
  at this stage can be effectively treated non
• 15:43
  -operatively. The advanced stage, however, involves
• 15:45
  anatomical failure that necessitates evaluation
• 15:48
  through advanced imaging studies like x -ray,
• 15:51
  CT, MRI, and ultrasound to confirm the diagnosis.
• 15:54
  And what specific injuries are common in this
• 15:56
  group? Within this population, we see very specific
• 15:59
  injuries in pathomechanisms. SLAP lesions, particularly
• 16:02
  type 2 superior labrum, anterior posterior lesions,
• 16:06
  and associated biceps tendonitis are common findings.
• 16:08
  Rotator cuff injuries also present uniquely here.
• 16:12
  Articular -sided partial thickness tears of the
• 16:14
  supraspinatus and infraspinatus tendons in this
• 16:16
  population may not always be true rotator cuff
• 16:19
  tears in the traditional sense. How so? They
• 16:22
  might actually represent detachment of the superior
• 16:24
  shoulder capsule from the greater tuberosity
• 16:27
  given its substantial attachment area. High -grade
• 16:30
  partial tears, or complete tears, present more
• 16:32
  typically with positive subacromial impingement
• 16:35
  tests and decreased muscle strength. Cadaveric
• 16:38
  studies show that superior capsule tears specifically
• 16:41
  increase anterior and inferior translations.
• 16:44
  Okay, what else? Dysfunction of the anterior
• 16:46
  capsular ligament complex, whether through tearing
• 16:49
  or elongation, leads to anterior shoulder instability
• 16:53
  and can significantly disable the throwing shoulder.
• 16:56
  We also see little league shoulder or proximal
• 16:59
  humeral epiphysealysis that's a specific epiphyseal
• 17:02
  plate injury common in adolescent throwing athletes
• 17:04
  due to repetitive stress on the weaker growth
• 17:06
  plate. Beyond structural issues, neurovascular
• 17:09
  entrapment is a possibility, including superscapular
• 17:12
  nerve entrapment, as well as vascular problems,
• 17:15
  such as effort thrombosis of the axillary artery
• 17:17
  or vein, or thoracic outlet syndrome, which are
• 17:20
  often quite difficult to diagnose. Any impingement
• 17:22
  types? Yes. Short or internal impingement is
• 17:24
  a critical pathomechanism here. It's that abnormal
• 17:27
  contact between the undersurface of the rotator
• 17:29
  cuff and the posterior superior labrum and glenoid
• 17:33
  during the late cocking phase of throwing. While
• 17:35
  it can be physiological to some degree, forceful
• 17:38
  internal impingement becomes pathological and
• 17:40
  is thought to be a primary cause of posterior
• 17:42
  rotator cuff injury and type 2 SLAP lesions.
• 17:46
  What increases that forceful contact? Key factors
• 17:48
  include posterior capsule tightness, increased
• 17:50
  shoulder abduction and external rotation, decreased
• 17:53
  internal rotator muscle strength, and increased
• 17:56
  scavular internal rotation or dyskinesis. Subacromial
• 18:00
  impingement, the more classic type, is mostly
• 18:02
  diagnosed in older overhead athletes and is often
• 18:05
  associated with decreased upward scapular rotation
• 18:08
  and post or inferior capsule tightness. The peel
• 18:11
  back mechanism is a specific pathomechanism described
• 18:14
  for type II SLAP lesions, where cadaveric studies
• 18:17
  have shown excessive humeral external rotation
• 18:20
  causes increased strain on and detachment of
• 18:23
  the superior labrum. And finally, Job and colleagues
• 18:26
  postulated that capsular laxity due to repetitive
• 18:28
  microtrauma in overhead athletes may result in
• 18:31
  increased shoulder laxity with secondary pathologies,
• 18:34
  dividing this as pathologic shoulder laxity.
• 18:36
  Given these complex and often subtle injuries,
• 18:40
  how do clinicians accurately diagnose them, especially
• 18:42
  when, as you said, imaging findings can sometimes
• 18:44
  be misleading? What are the absolutely crucial
• 18:46
  elements of the physical examination for an overhead
• 18:48
  athlete? This is where precision in physical
• 18:51
  examination becomes absolutely critical, because
• 18:53
  as you noted, imaging alone can be insufficient
• 18:56
  or even misleading due to asymptomatic pathology
• 18:59
  often found in athletes. A thorough physical
• 19:03
  examination for overhead athletes must include
• 19:05
  a detailed scapular assessment. Tests like the
• 19:08
  scapula spine distance test and the elbow extension
• 19:11
  and elbow push tests help assess scapular stabilizers.
• 19:15
  What about strength? For muscle strength evaluation,
• 19:18
  we use manual muscle testing on that 0 -5 scale,
• 19:21
  assessing shoulder abduction in the full can
• 19:23
  position and external and internal rotation strength.
• 19:26
  An abnormal result is typically defined as muscle
• 19:29
  strength on the dominant side being less than
• 19:31
  that on the non -dominant side. To assess posterior
• 19:34
  tightness, we perform the combined abduction
• 19:37
  test and horizontal flexion test meticulously,
• 19:40
  with the examiner fixing the scapula to prevent
• 19:42
  compensatory movement. Capsulaxity is evaluated
• 19:45
  via load and shift testing in anterior, posterior,
• 19:48
  and inferior directions, along with the anterior
• 19:51
  apprehension and relocation tests. It's abnormal
• 19:54
  when the dominant side shows increased laxity
• 19:56
  or the subject feels instability. And impingement
• 19:58
  tests. For subacromial impingement, we perform
• 20:01
  the standard Neer, Hawkins, and Yokum tests.
• 20:04
  Pain during any of these is considered abnormal.
• 20:07
  The hyper -external rotation test has a specific
• 20:10
  role in evaluating the peelback mechanism and
• 20:12
  pathologic internal impingement. To systematically
• 20:15
  evaluate these findings, a comprehensive scoring
• 20:18
  sheet like the HERA test can be incredibly useful
• 20:20
  in practice. Okay, so the physical exam is key,
• 20:23
  but what about imaging? You mentioned caveats.
• 20:25
  Yes, regarding imaging, it's vital to reiterate
• 20:28
  why it can be misleading in throwing athletes.
• 20:29
  Yeah. While MRI or MR arthrograms are useful
• 20:33
  for detecting partial or complete rotator cuff
• 20:35
  tears and SLAP lesions, it's crucial to understand
• 20:38
  that significant amounts of shoulder pathology,
• 20:41
  especially partial thickness tears found in maybe
• 20:44
  20, 86 % of patients in some studies, can actually
• 20:47
  be present in asymptomatic athletes. So a tear
• 20:50
  on MRI doesn't automatically mean it's the source
• 20:52
  of pain. Exactly. Therefore, we must stress the
• 20:55
  critical importance of performing a thorough
• 20:57
  history and physical examination. Pain may not
• 21:00
  be directly correlated with imaging findings,
• 21:03
  and even things like SLAP tears often do not
• 21:06
  require immediate intervention, especially if
• 21:08
  they appear incidental. Clinical correlation
• 21:10
  is everything. 2 .2 scapular dyskinesis. the
• 21:14
  unstable platform. You've highlighted scapular
• 21:16
  dyskinesis several times now as a critical factor
• 21:18
  in athletic shoulder injuries. Here's where it
• 21:20
  gets really interesting for me. How does this
• 21:22
  unstable platform of the scapula fundamentally
• 21:25
  disrupt shoulder function and contribute to this
• 21:27
  cascade of injuries? And most importantly for
• 21:29
  our audience, how can we accurately spot and
• 21:31
  assess it in clinical practice? The scapula's
• 21:33
  role is truly indispensable. It's a pivotal link
• 21:36
  in the kinetic chain, as we discussed. Think
• 21:38
  of it as the central segment bridging the larger
• 21:41
  body segments, generating force the legs and
• 21:44
  trunk, with the smaller arm segments producing
• 21:46
  precision and applying that force. Skillful athletic
• 21:50
  activities demand precise, coordinated motions
• 21:53
  of the scapula and the glenohumeral joint. Any
• 21:56
  alterations in these motions, either separately
• 21:58
  or coupled, can lead to inefficient shoulder
• 22:01
  function, decreased performance, and of course
• 22:03
  increased injury risk. So what exactly is scapular
• 22:06
  dyskinesis? Well, it's defined quite simply as
• 22:09
  the loss of control of normal resting scapular
• 22:11
  position and dynamic motion. It has a surprisingly
• 22:14
  high prevalence, found in perhaps 67 -100 % of
• 22:18
  patients with shoulder injuries in some studies.
• 22:20
  That high, really? Yes, but it's crucial to clarify
• 22:23
  this. Dyskinesis is best considered a potential
• 22:26
  impairment of optimum shoulder function. If it's
• 22:28
  found alongside shoulder symptoms, it certainly
• 22:30
  warrants further evaluation to determine its
• 22:32
  contribution, but it's not automatically the
• 22:35
  sole cause. Okay, so it's a finding that needs
• 22:37
  context. What pathologies is it associated with?
• 22:40
  There are strong associations between scapular
• 22:42
  dyskinesis and various shoulder pathologies,
• 22:45
  each with fairly clear underlying mechanisms.
• 22:47
  For instance, there's a high association with
• 22:49
  labral injury. Altered scapular position and
• 22:52
  motion, things like increased internal rotation
• 22:55
  and anterior tilt, change the glenohumeral alignment.
• 22:58
  This places increased tensile strain on the anterior
• 23:00
  ligaments, increases that peelback force on the
• 23:03
  biceps labral complex, and can create pathological
• 23:06
  internal impingement. And GRRD makes this worse.
• 23:09
  These effects are certainly magnified in the
• 23:11
  presence of glenohumeral internal rotation deficit,
• 23:13
  or GRR. The fact that manually retracting the
• 23:16
  scapula can often correct symptoms found in tests,
• 23:19
  like the modified dynamic label shear test, really
• 23:22
  highlights the role of dyskinesis. What about
• 23:24
  impingement? Impingement, both internal and external,
• 23:27
  is frequently seen in throwing athletes, often
• 23:30
  secondary to other pathology. Scapular dyskinesis
• 23:33
  contributes by altering the resting and dynamic
• 23:35
  scapular position, typically a loss of acromial
• 23:38
  upward rotation, excessive scapular internal
• 23:41
  rotation, and excessive scapular anterior tilt.
• 23:45
  These positions essentially create scapular protraction,
• 23:48
  which narrows the subacromial space and has been
• 23:51
  shown to decrease rotator cuff strength. Altered
• 23:54
  muscle activation patterns like increased upper
• 23:56
  trapezius activity and delayed or decreased lower
• 23:59
  trapezius and serratus anterior firing are also
• 24:02
  implicated. And AC joint injuries. How does dyskinesis
• 24:05
  link there? AC joint injuries remove the strut
• 24:08
  function of the clavicle. This allows what's
• 24:10
  called the third translation of the scapula,
• 24:12
  meaning it moves inferiorly and medially relative
• 24:15
  to the clavicle. This changes the biomechanical
• 24:18
  axis of scapular humeral rhythm, leading to excessive
• 24:21
  scapular internal rotation and protraction, and
• 24:23
  decreased dynamic acromial elevation. This protracted
• 24:26
  scapular position is directly linked to many
• 24:28
  dysfunctional problems seen in chronic AC separations,
• 24:31
  including impingement and reduced cuff strength.
• 24:33
  So it disrupts the whole shoulder girdle mechanism.
• 24:36
  Precisely. Clavicle fractures can also lead to
• 24:39
  dyskinesis if the clavicle anatomy isn't perfectly
• 24:41
  restored. Shortened male unions or non -unions
• 24:44
  alter scapular position towards internal rotation
• 24:47
  and anterior tilt. In these cases, dyskinesis
• 24:50
  can actually serve as a crucial clinical sign
• 24:53
  of potentially harmful alteration of clavicle
• 24:55
  anatomy, helping inform the decision for operative
• 24:58
  treatment. And finally, Though rare, scapular
• 25:01
  muscle detachment, typically the lower trapezius
• 25:04
  and rhomboids, is an often missed injury that
• 25:06
  directly causes dyskinesis, usually presenting
• 25:09
  with scapular protraction and lateral translation.
• 25:12
  Given these complex implications, how do clinicians
• 25:14
  accurately evaluate the presence and impact of
• 25:16
  scapula dyskinesis on, say, the throwing athlete?
• 25:20
  What specific tests should we be incorporating
• 25:22
  into our routine examinations? Evaluating the
• 25:25
  scapula requires a comprehensive approach. We
• 25:27
  must begin with a thorough history asking about
• 25:30
  past trauma to the scapula, clavicle, or AC joint,
• 25:34
  any spinal symptoms, and previous rehab efforts.
• 25:37
  The goals of the examination are, first, to establish
• 25:40
  the presence or absence of dyskinesis, second,
• 25:43
  to determine the effect of corrective maneuvers
• 25:45
  on the patient's symptoms, and third, to investigate
• 25:48
  potential underlying causes like bony issues,
• 25:51
  joint derangement, or muscle imbalances. How
• 25:53
  do you observe it? The scapular exam should ideally
• 25:55
  be performed from the posterior aspect, with
• 25:57
  the scapula fully exposed. We visually assess
• 26:00
  resting posture for any side -to -side asymmetry
• 26:03
  or prominence of the inferior medial or medial
• 26:06
  border. The optimum position for evaluating dynamic
• 26:09
  scapular dyskinesis is during active forward
• 26:11
  flexion watching the scapula move. And the corrective
• 26:14
  tests. Crucially, we use corrective maneuvers
• 26:16
  like the scapular assistance test, or SAT, where
• 26:18
  the examiner assists upward rotation, and the
• 26:21
  scapular retraction test, or SRT, where the examiner
• 26:24
  manually retracts the scapula. A positive SAT
• 26:27
  or SRT, meaning the patient's symptoms improve
• 26:30
  with the correction, strongly indicates that
• 26:32
  scapular dyskinesis is directly involved in producing
• 26:35
  those symptoms and highlights the immediate need
• 26:37
  for early scapular rehabilitation. What else
• 26:40
  should be checked? We also perform corcoid -based
• 26:42
  inflexibility assessment through palpation of
• 26:44
  the pectoralis minor and shorthead of the biceps,
• 26:47
  noting tenderness and top bands. Proximal kinetic
• 26:51
  chain screening, using tests like the one leg
• 26:53
  stability series, is useful to assess core and
• 26:55
  lower extremity contributions. And of course,
• 26:59
  a thorough glenohumeral exam is crucial for evaluating
• 27:01
  internal derangement and AC joint instability,
• 27:04
  paying special attention to assessing GRD and
• 27:07
  labral injuries, as both are frequently associated
• 27:09
  with dyskinesis. Remember, for accurate GRD measurements,
• 27:13
  the patient must be supine, with a second examiner
• 27:15
  stabilizing the scapula. So if the scapula is
• 27:18
  such a critical player, how do we get it back
• 27:20
  in the game effectively? What does this mean
• 27:22
  for rehabilitation to ensure not just recovery,
• 27:25
  but optimal athletic performance? Well, it means
• 27:27
  rehabilitation must absolutely start with optimizing
• 27:31
  the anatomy first. You can't effectively rehabilitate
• 27:34
  around a significant structural problem. Local
• 27:37
  issues like nerve injury or scapular stabilizer
• 27:39
  muscle detachment require repair or muscle transfer.
• 27:42
  Similarly, bony and tissue derangement issues,
• 27:45
  AC joint or clavicle injury, labral injury, rotator
• 27:47
  cuff disease, glenohumeral instability must be
• 27:50
  surgically addressed before effective rehabilitation
• 27:52
  can truly proceed. Get the foundation right first.
• 27:55
  Exactly. Once that foundation is set, we follow
• 27:59
  a comprehensive protocol. often based on established
• 28:01
  approaches like those from Ellen Becker and Cools.
• 28:04
  We typically begin with kinetic chain exercises
• 28:06
  focusing on the trunk and hips, starting from
• 28:09
  and ending at the ideal position of hip and trunk
• 28:12
  extension. These can often be initiated preoperatively.
• 28:16
  For flexibility, we address specific areas of
• 28:18
  tightness, particularly the anterior coracoid,
• 28:20
  the pectoralis minor, and shorthead of biceps
• 28:23
  and shoulder rotation. Exercises like the open
• 28:26
  book and corner stretch for the coracoid muscles
• 28:28
  and the sleeper and cross -body stretch for shoulder
• 28:30
  rotation are common recommendations. And the
• 28:32
  strengthening part. Periscapular strengthening
• 28:34
  is paramount. We emphasize achieving a position
• 28:38
  of scapular retraction as this is the most effective
• 28:41
  position to maximize the scapula's stabilizing
• 28:44
  roles. Exercises like the scapular pinch or trunk
• 28:47
  extension with scapular retraction can be done
• 28:50
  standing to simulate normal activation sequences.
• 28:53
  Once scapular control is achieved, we integrate
• 28:56
  scapular rotator cuff exercises, such as punches
• 28:59
  and shoulder dumps. These stimulate rotator cuff
• 29:01
  activation off a stabilized scapula and are performed
• 29:04
  in various planes using different resistance
• 29:06
  types. We particularly exploit the transverse
• 29:09
  plane for many activities and progressing towards
• 29:11
  sport. Finally, when strength and stabilization
• 29:14
  are achieved through controlled supervised rehabilitation,
• 29:17
  we implement a three area focus for effective
• 29:19
  transition back to sport. This involves one,
• 29:22
  lower extremity muscle power and endurance, two,
• 29:26
  integrated sports specific exercise to improve
• 29:28
  proprioception and muscle education, and three,
• 29:31
  upper extremity power and endurance using high
• 29:33
  repetition long lever exercises. This holistic
• 29:36
  progressive approach is absolutely vital for
• 29:38
  the athlete's full recovery and return to optimal
• 29:41
  performance. Okay, let's switch gears now. Moving
• 29:44
  from the precision -demanding overhead sports
• 29:46
  to the sheer force and collision inherent in
• 29:49
  sports like rugby, American football, and ice
• 29:51
  hockey, how do these high -energy impacts fundamentally
• 29:55
  change the injury landscape for the shoulder?
• 29:58
  What's particularly unique about the reckonisms
• 30:00
  and the apparently high frequency of concomitant
• 30:03
  injuries? It's a completely different dynamic,
• 30:05
  absolutely, driven by direct force and high -energy
• 30:08
  impacts. First, it might be useful to make a
• 30:10
  key distinction. Collision sports involve athletes
• 30:13
  purposely hitting or colliding with each other
• 30:15
  or inanimate objects, often with great force,
• 30:18
  like rugby, American football, ice hockey. Contact
• 30:21
  sports technically involve routine contact, but
• 30:24
  with lesser force, maybe like basketball or football.
• 30:27
  While collision implies greater risk, the terms
• 30:30
  are often used pretty synonymously in the literature.
• 30:32
  Right, but the forces involved are generally
• 30:34
  higher in collision sports. Definitely. And because
• 30:37
  of the physical nature of these sports, musculoskeletal
• 30:40
  injuries are incredibly frequent. The shoulder
• 30:42
  consistently ranks among the most common injury
• 30:45
  sites. Glenohumeral instability and rotator cuff
• 30:48
  injuries are particularly prevalent. Crucially,
• 30:51
  shoulder dislocation and instability account
• 30:54
  for the majority of playtime loss. Hetty and
• 30:57
  colleagues, for instance, reported a mean of
• 30:59
  81 days absent from play for shoulder dislocation
• 31:02
  in professional rugby union. That's a significant
• 31:05
  chunk of a season. 81 days. Wow. And the mechanisms.
• 31:08
  Different from throwing. Yes. Quite different.
• 31:11
  Shoulder injuries here can result from a direct
• 31:13
  blow to the shoulder itself, or indirectly from
• 31:16
  landing heavily on the affected shoulder. What's
• 31:18
  striking is that the tackling event alone is
• 31:20
  responsible for staggering 65 % of all shoulder
• 31:23
  injuries in rugby. The tackle itself. Yes. Video
• 31:27
  analysis studies, like one by Creighton and colleagues
• 31:29
  in elite rugby players, have identified three
• 31:32
  common mechanisms during tackles. The triscorer,
• 31:36
  high -proflection of the outstretched ball -carrying
• 31:38
  arm, the tackler, extension of the abducted arm
• 31:41
  behind the player during a tackle, and direct
• 31:44
  impact, a direct blow to the side of the shoulder.
• 31:47
  Posterior glenohumeral instability can also result
• 31:49
  from a blocking injury, as seen perhaps with
• 31:52
  an American football lineman blocking with the
• 31:53
  arm flexed and internally rotated. And you mentioned
• 31:56
  concomitant injuries are common. Yes, this brings
• 31:59
  us to a really unique aspect, the high incidence
• 32:02
  of concomitant injuries. Complex injuries involving
• 32:06
  multiple structures often occur after just a
• 32:08
  single traumatic event in these boards. Tischer
• 32:11
  and colleagues found that a significant 18 .2%,
• 32:14
  almost 1 in 5, of AC joint injuries exhibited
• 32:18
  concomitant intraarticular injuries that actually
• 32:20
  necessitated additional surgical intervention.
• 32:23
  This underscores the importance of appreciating
• 32:25
  that when a contact athlete presents with a shoulder
• 32:27
  injury, there is a strong likelihood of multiple
• 32:30
  coexisting pathologies that need addressing.
• 32:32
  You can't just focus on the most obvious injury,
• 32:34
  3 .2 rotator cuff injuries in contact athletes.
• 32:37
  Rotator cuff injuries are prevalent across all
• 32:39
  sports as you said but how do they specifically
• 32:41
  manifest and more importantly how are they managed
• 32:44
  differently in a contact athlete where direct
• 32:46
  impact is a constant threat compared to say an
• 32:49
  overhead thrower where it's more overuse? The
• 32:51
  manifestation and management in contact athletes
• 32:53
  indeed have distinct characteristics. In this
• 32:56
  population, rotator cuff injuries range from
• 32:59
  simple contusions right through to full thickness
• 33:01
  tears. It's noteworthy that contusions alone
• 33:04
  accounted for nearly half 47 % of all shoulder
• 33:07
  injuries in one study of a North American professional
• 33:10
  football team. So simple bruising is very common.
• 33:13
  And the tears themselves? Usually traumatic?
• 33:15
  Yes. For full thickness tears, the predominant
• 33:18
  mechanism of injury is traumatic. and they are
• 33:21
  typically associated with shoulder dislocations
• 33:23
  or subluxations. This differs from the microtrauma
• 33:27
  and overuse patterns often seen in overhead athletes.
• 33:30
  Tambay and colleagues reported that approximately
• 33:32
  half of professional rugby players with full
• 33:34
  -thickness rotator cuff tears also had concomitant
• 33:37
  labral injuries or bony bankart lesions, again
• 33:40
  highlighting that multi -injury pattern common
• 33:42
  in contact sports. So how do you manage them?
• 33:45
  Is surgery always needed for a tear? Not necessarily.
• 33:48
  When it comes to management strategy, Cuff contusions
• 33:51
  and partial tears can often be managed non -operatively.
• 33:54
  This typically includes pain control, a structured
• 33:57
  rotator cuff strengthening program, and perhaps
• 34:00
  consideration of subacromial corticosteroid injections
• 34:03
  for athletes with persistent bursal inflammation
• 34:05
  and pain. Surgical management is generally indicated
• 34:08
  for patients who don't respond to these conservative
• 34:10
  treatments, and certainly for those with full
• 34:13
  thickness cuff tears, especially in younger,
• 34:15
  active individuals. The advancements in arthroscopic
• 34:18
  techniques have been transformative here. They
• 34:21
  enable successful treatment of cuff tears in
• 34:23
  contact athletes with minimal soft tissue damage,
• 34:25
  allowing for a confident repair of the rotator
• 34:27
  cuff, and importantly, any associated pathology
• 34:30
  found at the same time. And the outcomes? Can
• 34:33
  they get back to playing rough sports? The outcomes
• 34:35
  are actually very encouraging. In that series
• 34:38
  by Tambi and colleagues I mentioned, an excellent
• 34:40
  91 .7 percent, that's 10 out of 11, of the elite
• 34:43
  rugby players were able to return to their pre
• 34:45
  -injury level of competition relatively early,
• 34:49
  on average around 4 .8 months after arthroscopic
• 34:51
  rotator cuff repair. That's impressive. It demonstrates
• 34:54
  that with the right surgical approach and rehabilitation,
• 34:57
  even significant injuries in these high -demand
• 35:00
  athletes can be effectively managed, allowing
• 35:02
  a return to collision sports. 3 .3 glenohumeral
• 35:06
  joint instability, a common challenge. Glenohumeral
• 35:10
  joint instability. This sounds like a really
• 35:13
  common and often disabling injury for the contact
• 35:15
  athlete, with implications that could potentially
• 35:18
  sideline careers. What are the key considerations
• 35:21
  when making treatment plans for these high stakes
• 35:23
  athletes, particularly regarding surgical timing
• 35:26
  and the specific techniques used? This is perhaps
• 35:29
  one of the most critical and complex decisions
• 35:31
  we face when treating contact athletes. While
• 35:33
  anterior instability comprises the majority of
• 35:36
  shoulder instability cases overall, recent studies
• 35:39
  indicate that posterior instability is actually
• 35:41
  increasing in this group and can account for
• 35:43
  as much as 10 -30 % of traumatic instability
• 35:46
  in contact athletes. So posterior instability
• 35:49
  is more common than we might think in this group.
• 35:51
  It appears so. And interestingly, posterior instability
• 35:54
  is also often associated with anterior instability
• 35:57
  and superior labral tears in these athletes,
• 35:59
  adding to the complexity. So the big question.
• 36:03
  Operate early or try non -operative first, especially
• 36:06
  if it happens midseason. Exactly. The choice
• 36:09
  between early surgery or non -operative treatment
• 36:12
  must be highly tailored to the individual athlete.
• 36:15
  especially for mid -season injuries. It's a decision
• 36:18
  that involves carefully weighing numerous factors.
• 36:20
  We have to consider the type of sport, the level
• 36:23
  of competition, the athlete's playing position
• 36:26
  and age. The specific path anatomy, things like
• 36:29
  significant glenoid bone loss or engaging hill
• 36:32
  -sax lesion, are major factors. Then there's
• 36:35
  the timing of the injury within the competitive
• 36:36
  season, the athlete's own career goals, and even
• 36:39
  the expectations from coaching staff or family
• 36:41
  members. It's a multifaceted discussion. And
• 36:44
  surgery usually means the season's over? Yes.
• 36:47
  It's important to acknowledge that surgical stabilization
• 36:49
  typically sidelines athletes for 4 -6 months,
• 36:52
  which is usually a season ending. This poses
• 36:54
  a significant dilemma for an in -season player
• 36:56
  and their team. So what does non -operative management
• 36:59
  look like if they want to finish the season?
• 37:01
  For non -operative in -season management, we
• 37:04
  can use accelerated rehabilitation protocols.
• 37:06
  These are designed for athletes strongly motivated
• 37:09
  to play through the season, reserving surgery
• 37:11
  for the off -season. These protocols minimize
• 37:14
  immobilization, perhaps none, or up to seven
• 37:17
  days max, and initiate supervised rehabilitation
• 37:19
  from day one, as tolerated. This starts with
• 37:23
  gentle range of motion exercises and cryotherapy,
• 37:26
  followed by rotator cuff and periscapular muscle
• 37:28
  strengthening once full ROM is achieved without
• 37:31
  discomfort. Sport -specific drills follow later.
• 37:34
  Can they play with a brace? Return to play with
• 37:36
  a motion -limiting brace was considered when
• 37:38
  specific comprehensive criteria are met. Little
• 37:41
  or no pain, the athletes' subjective feeling
• 37:43
  of stability, near -normal ROM, strength, and
• 37:46
  functional ability. But does it work? What are
• 37:48
  the recurrence rates? That's the major downside.
• 37:50
  Studies highlight significant recurrence rates
• 37:52
  with this approach. Buss and colleagues reported
• 37:54
  that while most athletes managed non -operatively
• 37:56
  return to play, 41 % experienced recurrence.
• 38:00
  Buttoni and colleagues reported an even higher
• 38:02
  recurrence rate of 75 % in their cohort treated
• 38:06
  non -operatively. 75%. That's very high. It underscores
• 38:10
  the challenges of managing significant instability
• 38:12
  non -operatively in contact athletes trying to
• 38:15
  continue playing. So when is surgery definitely
• 38:18
  the better option? Well, surgical treatment is
• 38:20
  indicated for failure of non -operative treatment,
• 38:23
  obviously. Or, importantly, the presence of high
• 38:26
  risk factors from the outset, such as significant
• 38:28
  glenoid bone loss or an engaging hill -sax lesion.
• 38:32
  These warrant early surgical intervention to
• 38:34
  prevent further damage and recurrence. And the
• 38:37
  type of surgery, has that changed? Yes, it has
• 38:40
  evolved. Historically, open bankart repair with
• 38:43
  a capsular shift was considered the gold standard
• 38:46
  for contact athletes due to its perceived robustness.
• 38:49
  However, with the development of new implants
• 38:52
  and significant advancements in arthroscopic
• 38:54
  surgical techniques, arthroscopic stabilization
• 38:56
  has gained enormous popularity and now offers
• 38:59
  comparable outcomes in many cases, with potentially
• 39:02
  less morbidity. But arthroscopy isn't always
• 39:04
  successful. No, and it's crucial to understand
• 39:07
  the risk factors for surgical failure, particularly
• 39:09
  with arthroscopy. Burkhart and De Beer famously
• 39:12
  reported a much higher recurrence rate after
• 39:14
  arthroscopic bankart repair for patients with
• 39:16
  significant glenoid bone loss and engaging heel
• 39:19
  sacs lesions. These critical bone defects compromised
• 39:23
  the procedure. Which brings us back to the glenoid
• 39:25
  tract concept. Exactly. Yamamoto and colleagues'
• 39:28
  glenoid tract concept is now invaluable for guiding
• 39:31
  clinical decision making in these cases. Remember,
• 39:34
  it defines the contact zone between the humerus
• 39:36
  and glenoid. If a Hill Sachs lesion remains within
• 39:39
  the glenoid track, on track, there is no risk
• 39:43
  of engagement. However, if it extends immediately
• 39:45
  over the glenoid track, off track, there is a
• 39:48
  high risk of engagement during functional movement,
• 39:51
  making simple soft tissue repair likely to fail.
• 39:53
  So what do you do for those off track or large
• 39:56
  bony defects? To address large humeral head defects,
• 39:59
  off -track hill sacks, surgical options include
• 40:02
  humeral head osteochondral allograft, or the
• 40:04
  infraspinatus rumbolisage procedure, where the
• 40:07
  infraspinatus tendon is sewn into the defect
• 40:09
  to prevent engagement. For significant glenoid
• 40:12
  bone loss, the Littarjet procedure is often considered.
• 40:16
  This involves transferring the coracoid process
• 40:18
  with its attached tendons to the front of the
• 40:20
  glenoid. How does Littarjet work? It provides
• 40:23
  stability through three key effects. a bone graft
• 40:26
  effect restoring the glenoid surface, a sling
• 40:29
  effect from the conjoined tendon acting like
• 40:31
  a hammock, and a capsular repair effect. It's
• 40:34
  important to acknowledge, though, that these
• 40:35
  are non -anatomic procedures and are associated
• 40:38
  with reported complication rates ranging from
• 40:40
  5 % to 30%, so patient selection and technical
• 40:43
  execution are key. Comprehensive algorithms exist
• 40:46
  now to help guide the management decisions based
• 40:48
  on these factors. 4 .1 acromioclavicular joint
• 40:51
  injuries, a persistent problem. Okay, let's move
• 40:54
  slightly away from the main ball and socket joint.
• 40:56
  Often overshadowed by the glenohumeral joint,
• 40:59
  the AC joint plays a subtle yet absolutely critical
• 41:02
  role in shoulder function, especially in those
• 41:04
  kinetic chain movements we talked about. Its
• 41:07
  injuries, however, seem notoriously tricky to
• 41:09
  classify and manage, particularly in contact
• 41:12
  athletes. What's crucial for us to understand
• 41:14
  about AC joint anatomy, its common injury patterns,
• 41:17
  and how do we accurately diagnose and approach
• 41:20
  treatment for these persistent problems? You've
• 41:23
  hit on a crucial point about the AC joint's often
• 41:25
  underestimated importance. It's a robust synovial
• 41:28
  articulation connecting the clavicle to the scapula,
• 41:32
  featuring an intraarticular fibrocartilaginous
• 41:34
  disc, though that disc rapidly degenerates beyond
• 41:37
  the fourth decade, typically. Its primary stabilizers
• 41:40
  are the dynamic muscles crossing the joint, the
• 41:42
  deltoid and trapezius, and the static ligaments.
• 41:45
  The acromioclavicular, AC ligaments providing
• 41:47
  anterior -posterior stability, and the coracoa
• 41:50
  collicular, CC ligaments, the conoid and trapezoid,
• 41:52
  providing vertical stability. And both sets of
• 41:54
  ligaments are important. Critically important,
• 41:57
  it's vital to understand that these injuries
• 41:59
  rarely occur in isolation, highlighting the importance
• 42:02
  of anatomic reconstruction of both the AC and
• 42:05
  CC ligaments for maximum healing strength if
• 42:07
  surgery is undertaken. Codman famously observed
• 42:10
  that the AC joint moves very little, but in many
• 42:13
  planes, and crucially, an intact ACJ is essential
• 42:16
  for scapula motion to be synchronously coupled
• 42:19
  with arm motion. Ah, so it links the clavicle
• 42:22
  and scapular movements. Precisely. If the ACJ
• 42:24
  is fixed, say with screws or plates, motion will
• 42:26
  be lost, limiting shoulder function, or the hardware
• 42:29
  will eventually fail due to this obligatory coupling
• 42:32
  of clavicle rotation with scapular motion. This
• 42:35
  is clinically significant, as long -standing
• 42:37
  type 3 AC joint injuries complete peers of both
• 42:40
  ligaments, lead to scapular dyskinesis in 71
• 42:43
  % of patients, often presenting as the so -called
• 42:45
  S -I -C -K scapular syndrome. So how do these
• 42:48
  injuries usually happen? Ethiologically, AC joint
• 42:51
  injuries typically result from a direct blow
• 42:53
  to the point of the shoulder, the lateral acromion,
• 42:56
  or indirectly from landing hard on the affected
• 42:59
  shoulder, driving the acromion and scapula inferiorly
• 43:02
  and anteriorly. This causes the clavicle to be
• 43:05
  relatively displaced superiorly, leading to sequential
• 43:08
  tearing of the AC and then the CC ligaments.
• 43:12
  In classification, you mentioned it's tricky.
• 43:14
  Yes, classification of AC joint injuries using
• 43:17
  the widely used Rockwood classification, types
• 43:19
  ISI based on displacement, is challenging because
• 43:22
  relying solely on radiographs has proven unreliable
• 43:25
  for determining the true pathological classification
• 43:28
  and guiding treatment. This led to the ISACOS
• 43:30
  upper limb committee's 2014 consensus document,
• 43:34
  which diversified the contentious type 3 injuries.
• 43:36
  The ones were both AC and CC ligaments are torn,
• 43:39
  but displacement varies into type I. functionally
• 43:42
  stable and type I functionally unstable. Based
• 43:45
  on clinical factors, not just x -rays. Exactly.
• 43:48
  This distinction is based on clinical factors
• 43:50
  assessed three to six weeks post -injury, including
• 43:52
  things like ongoing pain, especially over the
• 43:55
  anterior acromeon, rotator cuff, or medial scapular
• 43:58
  area, weakness during rotator cuff testing, decreased
• 44:01
  flexion and abduction ROM, and demonstrable scapular
• 44:05
  dyskinesis on observation. How do they look clinically?
• 44:08
  In clinical examination, complete AC joint disruptions,
• 44:11
  Rockwood grades III, present with that classical
• 44:13
  obvious deformity or step off. These may be locked,
• 44:16
  meaning not easily reducible in limiting scapular
• 44:18
  excursion, or shocked, unstable, but easily reducible.
• 44:22
  For less obvious disruptions, grade III -II,
• 44:25
  cross arm adduction often accentuates the injury,
• 44:27
  displacing the clavicle superiorly and posteriorly.
• 44:29
  The diagnostic triad of ACJ injury include the
• 44:32
  point tenderness directly over the joint, ACJ
• 44:35
  pain with cross -arm adduction, and importantly
• 44:37
  pain relief by local anesthetic injection into
• 44:39
  the joint. The Paxinos test can also be helpful.
• 44:42
  What about x -rays? Is there a specific view?
• 44:45
  For radiographic evaluation, the Zonka view,
• 44:48
  a 15 -degree cephalid tilt view, is considered
• 44:50
  the most accurate for visualizing the AC joint
• 44:53
  itself, though its an intra -observer reliability
• 44:57
  is acknowledged to be poor. Standard shoulder
• 45:00
  views often don't show it well. While CT scans
• 45:03
  are best for appreciating static bony displacement,
• 45:06
  clinical assessment can be equally reliable.
• 45:08
  MRI can be useful for assessing soft tissue damage,
• 45:11
  particularly the ligaments in acute scenarios.
• 45:13
  Management of AC joint injuries often sparks
• 45:16
  significant debate, doesn't it? Particularly
• 45:18
  regarding when to opt for non -operative versus
• 45:20
  operative approaches, especially considering
• 45:22
  the high functional demands and career implications
• 45:24
  for athletes. What's the current thinking and
• 45:26
  what principles guide that decision -making process?
• 45:29
  The management philosophy for AC joint injuries
• 45:31
  has definitely been shifting. Recent evidence
• 45:34
  increasingly supports initial primary non -operative
• 45:36
  treatment for even complete EC joint dislocations,
• 45:39
  type 3 and some higher grades. Reviews report
• 45:42
  successful outcomes in around 88 % of patients
• 45:45
  treated nonoperatively, comparable to operative
• 45:47
  groups in many studies. This really underscores
• 45:50
  that the grade of AC joint injury alone should
• 45:53
  not be the primary determinant for defining treatment
• 45:55
  options, due to that poor correlation with clinical
• 45:58
  symptoms we discussed. Patient function and symptoms
• 46:00
  are more important. So what does non -operative
• 46:03
  treatment involve? For non -operative treatment,
• 46:06
  particularly acute injuries less than a week
• 46:08
  old, initial management involves simple analgesia,
• 46:11
  topical ice therapy, and rest in a sling, primarily
• 46:14
  for comfort. A supportive broad -arm sling is
• 46:17
  generally preferred over a collar and cuff. The
• 46:20
  fling should typically be discarded once symptoms
• 46:22
  settle, usually within one week. Rehabilitation
• 46:25
  then follows a structured protocol, like Gladstone
• 46:27
  and colleagues' four -phase protocol. This progresses
• 46:30
  from phase one, pain control, immediate protective
• 46:33
  ROM isometrics, to phase two, isotonic strengthening,
• 46:37
  phase three, unrestricted functional participation,
• 46:39
  neuromuscular control, and finally phase four,
• 46:42
  return to activity with sports -specific drills.
• 46:44
  When can they return to contact sports? Contact
• 46:47
  sports and heavy lifting can usually be started
• 46:49
  as comfortable, typically around 6 -12 weeks
• 46:52
  post -injury. However, it's important to counsel
• 46:54
  patients that local discomfort may persist with
• 46:57
  activity for up to six months. And those concerning
• 47:00
  statistics from Cox show that a large proportion
• 47:02
  of athletes remain symptomatic at six months,
• 47:05
  particularly with grade three injuries, and 30
• 47:07
  % of overhead athletes were unable to continue
• 47:10
  at the same level of sport after non -operative
• 47:12
  treatment. So non -operative isn't always the
• 47:15
  final answer for high -demand individuals. When
• 47:17
  is surgery indicated? Surgical treatment is typically
• 47:20
  reserved for patients with high functional demands
• 47:22
  who remain symptomatic, those with a clinically
• 47:24
  symptomatic locked or unstable, shocked scapula,
• 47:28
  and patients who simply fail to improve after
• 47:30
  an initial three to six weeks of appropriate
• 47:32
  non -operative symptomatic management. The aim
• 47:35
  of surgery is to achieve a painless, stable shoulder
• 47:38
  with adequate mobility, strength, and muscle
• 47:40
  control, allowing the individual to return to
• 47:43
  their desired level of activity. And the surgical
• 47:45
  techniques. You mentioned over 100 historically.
• 47:47
  Yes. Historically, the proliferation of over
• 47:50
  100 different surgical techniques indicated a
• 47:53
  lack of consensus on the optimal treatment. Techniques
• 47:56
  like the Weaver -Dunn procedure, which involved
• 47:59
  transferring the coracochromial ligament, only
• 48:01
  reproduced about 25 % of the native cc ligament
• 48:04
  strength and had high failure rates. Hook plates
• 48:07
  provided stable reduction but could cause rotator
• 48:09
  cuff impingement and required secondary removal,
• 48:12
  often performing worse than cc ligament fixation.
• 48:14
  So what's the trend now? Current surgical trends
• 48:17
  are moving firmly towards anatomical restoration
• 48:19
  of both the CC and AC ligaments, often with some
• 48:22
  form of biological enhancement, using strong
• 48:25
  constructs that allow for early mobilization
• 48:27
  and reduce the risk of re -displacement. Choricoclavicular
• 48:31
  fixation has evolved from the original Bosworth
• 48:33
  screw to modern suture button constructs, like
• 48:36
  the dog bone or tightrope systems, now using
• 48:39
  multiple buttons and strong tape sutures for
• 48:41
  increased strength and arthroscopic amenability.
• 48:44
  Free graft augmentation or reconstruction, using
• 48:47
  tending grafts like Hercilus or Semitindinosis,
• 48:50
  placed in an anatomic position to reconstruct
• 48:52
  the trapezoid and conoid ligaments, has shown
• 48:54
  ultimate failure loads equivalent to native intact
• 48:56
  cc ligaments, although graft fixation itself
• 48:59
  remains a technical challenge. Loop reconstruction
• 49:02
  techniques, using synthetic ligaments like LARS
• 49:05
  or Surgilig, are purported to allow early post
• 49:07
  -operative functional treatment and potentially
• 49:09
  earlier recovery, with improved implant technology
• 49:12
  minimizing older issues like clavicular osteolysis.
• 49:16
  Repair and reinforcement of the superior AC ligament
• 49:18
  is also often combined with these techniques
• 49:20
  to improve horizontal stability. And your preferred
• 49:22
  technique? Our preferred technique involves the
• 49:25
  use of a strong synthetic polyethylene tetra
• 49:28
  -trophallate ligament. Specifically, the lyre's
• 49:30
  ligament. We use an anatomical construct, passing
• 49:33
  it through drill holes in the clavicle and around
• 49:35
  the coracoid, combined with a reefing repair
• 49:38
  of the ACJ capsule and the overlying delta trapecial
• 49:41
  fascia. This lyre's ligament actually exceeds
• 49:44
  the tensile strength of native CC ligaments and
• 49:46
  encourages fibroblast and collagen in growth.
• 49:49
  We've also modified this by adding a further
• 49:51
  figure of 8 loop around the coracoid and or over
• 49:53
  the ACJ via a drill hole in the acromeon to further
• 49:56
  improve horizontal stability and overall construct
• 49:59
  strength. Our own results with this have been
• 50:01
  positive, showing a low 2 % loss of reduction.
• 50:03
  And rehabilitation after surgery, is it milestone
• 50:06
  based? Absolutely. Postoperative rehabilitation
• 50:10
  is crucial, and progression through the phases
• 50:12
  is not time -based, but strictly milestone -based,
• 50:15
  depending entirely on the patient's responses
• 50:17
  and ability to progress safely. Phase 1 involves
• 50:20
  protective, gentle pendulum exercises and passive
• 50:24
  range of motion. Phase 2 progresses to light
• 50:26
  resistance and sport -specific rehabilitation
• 50:29
  including plyometrics and perturbation training.
• 50:32
  Phase 3 focuses intensely on regaining scapula
• 50:35
  and glenohumeral stability and control. and return
• 50:38
  to sport. Sport -specific rehabilitation commences
• 50:41
  within weeks. Return to sport participation and
• 50:44
  competition is graduated, always requiring input
• 50:46
  from the surgeon, the therapist, and the strength
• 50:48
  and conditioning coaches. Typically, this is
• 50:51
  achieved within three to four months for contact
• 50:53
  athletes, and perhaps six to nine months for
• 50:55
  overhead athletes, though some, like horse riders
• 50:57
  and cyclists, often return in less than three
• 50:59
  months. 4 .2 sternoclavicular joint injuries,
• 51:03
  the body's most stable joint, Right, if the AC
• 51:05
  joint can be subtly tricky, the sternoclavicular
• 51:08
  or SC joint presents a different challenge altogether.
• 51:11
  It's often described as inherently the most stable
• 51:14
  joint in the body, yet its injuries can be incredibly
• 51:16
  deceptive, even potentially life -threatening.
• 51:20
  What makes the SC joint so incredibly stable?
• 51:22
  What are the subtle diagnostic clues we should
• 51:25
  never miss? And how do their distinct characteristics
• 51:28
  dictate management, especially the really urgent
• 51:30
  ones? The SE joint is truly an anomaly in its
• 51:33
  stability. Despite having largely incongruent
• 51:36
  articular surfaces and a small contact area,
• 51:39
  it is extremely stable due to very robust static
• 51:42
  and dynamic stabilizers. Its static stabilizers
• 51:44
  include the inherent, albeit limited, congruity
• 51:47
  of the articular surfaces, the extremely strong
• 51:49
  anterior and posterior sternoclavicular ligaments.
• 51:52
  are the most important for anterocollectural
• 51:54
  stability. The intraarticular fibrocartilaginous
• 51:57
  disc, which divides the joint and acts a bit
• 51:58
  like a knee meniscus, and the interclavicular
• 52:01
  and costoclavicular ligaments. Dynamic stabilizers
• 52:03
  include the surrounding musculotendin assemblo,
• 52:06
  particularly the sternoplidomastoid, subclavius,
• 52:08
  and pectoralis major muscles. And there's a key
• 52:11
  point about younger patients. Yes. This is a
• 52:13
  crucial developmental point for clinicians. The
• 52:16
  epiphysis or growth plate of the medial end of
• 52:19
  the clavicle is the last epiphysis in the body
• 52:21
  to close, usually between 25 and 31 years old.
• 52:24
  This is critically relevant because significant
• 52:27
  traumatic injuries in patients younger than 25
• 52:29
  are far more likely to result in a displaced
• 52:32
  medial -physiol fracture, a growth plate injury,
• 52:35
  rather than a true SC joint dislocation, simply
• 52:38
  because the physis is inherently weaker than
• 52:40
  the incredibly strong SC joint ligaments before
• 52:43
  it fuses. So always consider a physio fracture
• 52:46
  in younger patients with apparent SCJ disruption.
• 52:49
  Absolutely. The SC joint itself moves in three
• 52:51
  planes. retraction, protraction, elevation, depression,
• 52:54
  and rotation coordinated with AC joint movement
• 52:56
  to optimally position the glenoid. How do we
• 52:59
  diagnose these injuries? What should we look
• 53:01
  for? When unraveling SCJ injuries, a detailed
• 53:03
  history is vital. Acute injuries typically involve
• 53:07
  a high -energy mechanism, like a direct blow
• 53:09
  or fall. Chronic problems may follow previous
• 53:12
  trauma or activity changes. In younger patients,
• 53:15
  Atraumatic instability can present with pain,
• 53:17
  clicking, or recurrent dislocation without a
• 53:20
  specific injury, and it's worth asking about
• 53:22
  connective tissue disorders like Ehlers -Danlos
• 53:25
  or Marfan's. On inspection, we look for deformity
• 53:28
  or muscle wasting compared to the other side.
• 53:31
  Palpation involves checking the SEC joint for
• 53:33
  swelling, differentiating between soft tissue
• 53:35
  swelling like effusion or synovitis, and hard
• 53:38
  swelling from a chronic dislocation or osteophytes,
• 53:41
  and assessing tenderness. We assess movements
• 53:43
  of the SE joint in all three planes. Protraction,
• 53:46
  retraction, arms forward. Elevation, depression,
• 53:49
  arms abducted. And rotation, arms abducted, elbows
• 53:51
  flexed. We palpate the anterior joint during
• 53:53
  movement for abnormal motion or clicking, which
• 53:56
  might suggest degenerative changes or disc pairs.
• 53:59
  In cases of instability, the medial clavicle
• 54:01
  may sublux or dislocate anteriorly. And imaging.
• 54:04
  CT seems key here. Yes, for imaging, while X
• 54:08
  -rays, AP, lateral, can be helpful, a CT scan
• 54:11
  is undoubtedly the investigation of choice. It
• 54:14
  accurately assesses the position of the medial
• 54:16
  clavicle relative to the sternum and crucially
• 54:18
  differentiates a true dislocation from a physio
• 54:21
  fracture. And most importantly, for posterior
• 54:23
  dislocations where there's any concern for mediastinal
• 54:26
  compromise, a CT angiogram should be undertaken
• 54:29
  as a matter of urgency to visualize the great
• 54:31
  vessels like the aorta and subplavian vessels
• 54:34
  and the tracheosophagus in relation to the displaced
• 54:36
  medial clavicle. So CT angio for suspected posterior
• 54:39
  dislocations. What about MRI? MRI offers poorer
• 54:43
  bony resolution compared to CT, but can effectively
• 54:46
  demonstrate ligamentous structures, intraarticular
• 54:49
  disc injuries, and the adjacent neurovascular
• 54:51
  anatomy if needed. Okay, what are the most concerning
• 54:54
  types of SC joint injuries, particularly those
• 54:56
  posterior dislocations you mentioned? How do
• 54:58
  their distinct, often life -threatening characteristics
• 55:01
  dictate management, including the need for urgent
• 55:04
  intervention and specialized surgical considerations?
• 55:07
  SC joint instability can be classified by direction,
• 55:10
  anterior, posterior, severity, sprain, subluxation,
• 55:14
  dislocation, or chronicity, acute, recurrent,
• 55:17
  persistent. But the Stanmore Triangle Classification
• 55:20
  is also useful as it considers the cause. Type
• 55:23
  I traumatic, type II atraumatic structural laxity,
• 55:27
  and type III non -structural muscle patterning.
• 55:29
  Let's focus on type one, the traumatic ones.
• 55:32
  Type A traumatic structural instability involves
• 55:34
  those high energy, high stakes injuries. Traumatic
• 55:37
  SE joint dislocations are rare, less than 1 %
• 55:40
  of upper limb injuries, usually resulting from
• 55:42
  significant force. The force is often indirect,
• 55:45
  transferred along the clavicle from a blow to
• 55:47
  the shoulder. A protracted scapula at impact
• 55:50
  increases the likelihood of posterior dislocation.
• 55:53
  A retracted scapula anterior dislocation. Like
• 55:56
  frequently, a direct anterior blow to the clavicle
• 55:58
  can drive the medial end posteriorly into the
• 56:01
  mediastinum. And posterior dislocation is a dangerous
• 56:03
  one. Acute posterior dislocations are a particular
• 56:06
  concern. Yes, due to their potential to cause
• 56:10
  mediastinal compromise, making them a potential
• 56:12
  medical emergency. Clinicians must be extremely
• 56:15
  vigilant for features such as dysphagia, difficulty
• 56:18
  swallowing, dyspnoea, shortness of breath, stridor
• 56:22
  hoarseness, or vascular symptoms like venous
• 56:24
  congestion or edema of the ipsilateral arm. These
• 56:28
  suggest pressure on the great vessels or the
• 56:30
  tracheosophagus. While these complications are
• 56:33
  rare, they can be devastating and their probability
• 56:36
  increases the longer the dislocation remains
• 56:38
  unreduced. How are they managed based on direction
• 56:41
  and timing? Management strategies depend critically
• 56:43
  on the direction and timing. Undisplaced ligamentous
• 56:46
  sprains, grade 1, and subluxations, grade 2,
• 56:48
  as well as minimally displaced medial -fusel
• 56:51
  fractures, are typically treated conservatively
• 56:53
  with reassurance, analgesia, ice, and a short
• 56:56
  period of immobilization in a sling for comfort.
• 56:58
  Patients are advised to avoid re -injury for
• 57:00
  about three months. What about acute anterior
• 57:03
  dislocations? For acute anterior dislocations,
• 57:06
  usually within 48 hours, a closed reduction under
• 57:09
  sedation or general anesthetic can be attempted
• 57:11
  by applying posterior pressure. However, the
• 57:15
  SC joint often re -dislocates immediately or
• 57:17
  soon after, with recurrence rates over 50%. Because
• 57:21
  of this high recurrence rate and the fact that
• 57:23
  anterior dislocations rarely cause long -term
• 57:25
  functional issues, most surgeons adopt a wait
• 57:28
  -and -see policy. Symptoms typically settle with
• 57:30
  conservative management over three to six months.
• 57:32
  Surgery is considered only in unusual situations,
• 57:35
  with significant, persistent symptoms despite
• 57:37
  adequate non -operative management and after
• 57:39
  -muscle patterning issues have been excluded.
• 57:41
  And acute posterior dislocations, urgent reduction.
• 57:44
  Yes, for acute posterior dislocations, again,
• 57:47
  ideally within 48 hours, there is a much greater
• 57:50
  imperative to reduce and maintain reduction due
• 57:53
  to that risk of mediastinal compromise. Closed
• 57:55
  reduction is undertaken under general anesthetic,
• 57:58
  often with fluoroscopy guidance, and involves
• 58:00
  specific maneuvers like placing a bolster between
• 58:03
  the scapulae, applying traction and extension
• 58:05
  to the abducted arm, and sometimes using a towel
• 58:07
  clip to grip and pull the medial clavicle anteriorly.
• 58:10
  Success rates for closed reduction are challenging,
• 58:13
  perhaps around 56 % within 48 hours, dropping
• 58:16
  significantly after that. Crucially, the on -site
• 58:19
  cardiothoracic surgeon should always be informed
• 58:21
  prior to booking for closed reduction due to
• 58:24
  the potential need for immediate open reduction
• 58:26
  if closed reduction fails or vascular complications
• 58:29
  arise during the attempt. What happens after
• 58:31
  successful reduction? Post -reduction, a figure
• 58:34
  of eight brace is often used for about four weeks
• 58:36
  to maintain scapular retraction and reduce stress
• 58:38
  on the joint, and contact sports are avoided
• 58:41
  for three, six months. When is open surgery needed?
• 58:44
  Open reduction and reconstruction are indicated
• 58:46
  for failed closed reductions, delayed presentations,
• 58:49
  more than a few days, or chronic posterior dislocations
• 58:52
  that cause significant functional deficit or
• 58:55
  carry a high risk of erosion into vital structures.
• 58:58
  Since the normal capsular and ligamentous stabilizers
• 59:00
  are usually damaged and only partially referable,
• 59:04
  additional reconstruction is typically required
• 59:05
  to maintain the reduction. Historically, wires
• 59:08
  and pins were used but were abandoned due to
• 59:11
  lethal complications like introthoracic migration.
• 59:14
  Current trends favor reconstruction using autograft,
• 59:17
  like palmaris longus or semitendinosus tendon,
• 59:20
  or allograft. A figure of eight reconstruction
• 59:23
  technique, where the graft is shuttled through
• 59:25
  drill holes in the sternum and clavicle, tensioned
• 59:28
  and sutured, is considered biomechanically superior.
• 59:31
  Synthetic ultra -strong braided sutures can also
• 59:33
  be used to augment the graft. And those medial
• 59:36
  -physial fractures and under -25s. Reiterate
• 59:38
  that these are fractures, not true dislocations.
• 59:41
  CT confirms the diagnosis. Most are un - or minimally
• 59:44
  displaced and managed non -operatively with immobilization.
• 59:47
  Open reduction is reserved only for those rare
• 59:49
  cases with mediastinal compressive symptoms.
• 59:51
  Briefly, what about the other types of instability?
• 59:54
  Type 2 in -traumatic structural instability,
• 59:56
  or hypermobility, is due to capsular laxity,
• 59:59
  often bilateral, and frequently seen with generalized
• 1:00:02
  ligamentous laxity syndromes. Patients present
• 1:00:05
  with pain, clicking, and medial clavicle subluxation
• 1:00:08
  prominence, usually less painful than traumatic
• 1:00:10
  instability. This is managed non -operatively
• 1:00:13
  initially, with physiotherapy focusing on muscle
• 1:00:15
  patterning. Surgery might be considered for failed
• 1:00:18
  rehab. SCJ disc pathologies can cause pain and
• 1:00:21
  clicking, potentially treated with arthroscopic
• 1:00:23
  resection. SCJ osteoarthritis is common, especially
• 1:00:27
  in middle -aged women, managed conservatively
• 1:00:29
  first. NSAIDS, ICE, activity modification, steroid
• 1:00:33
  injections. If that fails, surgical options include
• 1:00:36
  resection of the medial end of the clavicle,
• 1:00:38
  increasingly done arthroscopically. And finally,
• 1:00:41
  type 3 muscle patterning instability involves
• 1:00:43
  poorly coordinated neuromuscular control causing
• 1:00:45
  instability. This must be addressed with physiotherapy
• 1:00:48
  and biofeedback before consiching any stabilization
• 1:00:50
  surgery. Botulinum toxin might even be used preoperatively
• 1:00:53
  to temporarily weaken offending muscles and protect
• 1:00:55
  a surgical repair. 5 .1 clavicle fractures. More
• 1:00:58
  than just a broken collarbone. Okay, let's move
• 1:01:00
  on to clavicle fractures. They're incredibly
• 1:01:03
  common, aren't they? Accounting for a significant
• 1:01:06
  portion of upper limb injuries. Yet, the approach
• 1:01:09
  to managing them seems to have evolved dramatically
• 1:01:11
  from the historical conservative norms. What's
• 1:01:14
  the latest evidence on when to manage these conservatively
• 1:01:16
  versus surgically, and why does this distinction
• 1:01:19
  matter so much for athletes, especially when
• 1:01:21
  considering complications like non -union and
• 1:01:23
  malunion? Yes, clavicle fractures are very common.
• 1:01:26
  And the clavicle itself, that saw -shaped bone,
• 1:01:29
  is the only skeletal attachment of the scapula
• 1:01:31
  to the torso. This means a clavicle injury profoundly
• 1:01:34
  affects the entire shoulder biomechanics, disrupting
• 1:01:37
  that strut function. It's the first bone to ossify
• 1:01:40
  in the fetus, but its sternal end is the last
• 1:01:43
  epiphysis to fuse, as we discussed, around the
• 1:01:45
  25th year. Cervical factors make up perhaps up
• 1:01:48
  to 5 % of all fractures in the adult population,
• 1:01:51
  and the vast majority, 70 -80%, occur in the
• 1:01:54
  mid -shaft, which is the thinnest and most exposed
• 1:01:56
  segment. Who gets them most often? Incidence
• 1:01:59
  is highest in males under 20, often due to sports
• 1:02:01
  injuries, which account for about 45 % of cases
• 1:02:04
  in recent studies. Also, in polytrauma patients,
• 1:02:08
  early fixation of high -energy clavicle fractures
• 1:02:10
  is increasingly recognized for reducing ITU length
• 1:02:14
  of stay and facilitating mobilization. How do
• 1:02:16
  they typically present? Diagnosis is usually
• 1:02:19
  straightforward clinically. The typical mechanism
• 1:02:21
  is a fall onto the shoulder or a direct blow,
• 1:02:23
  resulting in a compressive axial force. If displaced,
• 1:02:27
  the fracture can shorten due to unopposed muscle
• 1:02:29
  action. The sternocleidomastoid muscle pulls
• 1:02:31
  the medial fragments superiorly and posteriorly,
• 1:02:34
  while Pectoralis major in deltoid pull the lateral
• 1:02:38
  fragment inferiorly and medially leading to that
• 1:02:40
  characteristic tautic or draw shoulder deformity
• 1:02:43
  and shortening. Careful assessment of the overlying
• 1:02:45
  skin for tinting by sharp fragments is crucial.
• 1:02:48
  Clinical measurement of clavicle length difference
• 1:02:49
  compared to the uninjured side and a thorough
• 1:02:52
  neurological examination are essential. Can we
• 1:02:54
  predict who might have problems healing? We can
• 1:02:56
  use a prognostic index to predict non -union
• 1:02:59
  risk. Factors like older age, female sex, shortening
• 1:03:03
  of greater than two centimeters, complete fracture
• 1:03:05
  displacement, being a smoker, and significant
• 1:03:08
  comminution are all negative predictive factors
• 1:03:11
  for union. So, for example, a 60 -year -old woman
• 1:03:14
  with a displaced, comminuted mid -shaft fracture
• 1:03:17
  has an approximate 75 % projected probability
• 1:03:20
  of non -union at 12 weeks if treated non -operatively.
• 1:03:24
  This clearly informs the management discussion.
• 1:03:26
  Right. So how has management changed? especially
• 1:03:29
  for displaced fractures. Well, undisplaced mid
• 1:03:32
  -shaft fractures, Robinson type 2a, are traditionally
• 1:03:35
  and still currently treated conservatively, usually
• 1:03:37
  with a broad arm sling, and they generally unite
• 1:03:40
  with excellent function. However, the management
• 1:03:42
  of displaced mid -shaft fractures has been the
• 1:03:44
  focus of the shift. Historically, these were
• 1:03:47
  also treated conservatively based on the belief
• 1:03:49
  that most heal well functionally, even if they
• 1:03:51
  unite in a shortened position. But this has been
• 1:03:54
  strongly challenged by more recent high -quality
• 1:03:56
  studies indicating significantly higher non -union
• 1:03:58
  rates than previously thought and potentially
• 1:04:00
  poorer functional outcomes, especially in younger
• 1:04:03
  active individuals. What about non -operative
• 1:04:05
  treatment itself, Sling or Figure of Eight? The
• 1:04:08
  broad arm sling is the most frequently used non
• 1:04:11
  -operative treatment now. It offers better patient
• 1:04:13
  satisfaction scores than the figure of eight
• 1:04:15
  bandage, which was also shown in some studies
• 1:04:18
  to have a higher non -union rate, possibly due
• 1:04:20
  to distracting forces. Crucially though, neither
• 1:04:24
  sling type can reliably reduce or hold the reduction
• 1:04:27
  of a displaced, shortened fracture. This means
• 1:04:30
  that conservative treatment for a significantly
• 1:04:32
  displaced fracture always results in some degree
• 1:04:34
  of malunion or healing in a shortened position.
• 1:04:37
  The sling is really just used for comfort until
• 1:04:40
  pain settles. So the push is towards surgery
• 1:04:42
  for displaced ones? Yes. The paradigm shift has
• 1:04:45
  been towards considering primary operative treatment
• 1:04:47
  for displaced mid -shaft fractures, particularly
• 1:04:50
  in active patients. Evidence from large trials,
• 1:04:53
  like those from the Canadian Orthopedic Trauma
• 1:04:55
  Association and UK trials, demonstrated that
• 1:04:58
  open reduction and internal fixation significantly
• 1:05:00
  reduced non -union rates down to around 2 % versus
• 1:05:04
  15 % non -operatively and were associated with
• 1:05:07
  better functional outcome scores and faster return
• 1:05:09
  to function. But is the function better if they
• 1:05:12
  do unite non -operatively? That's a key point.
• 1:05:16
  The improved outcome scores in the surgical groups
• 1:05:19
  primarily resulted from preventing non -union
• 1:05:21
  and malunion. There was actually little functional
• 1:05:24
  difference reported between surgically and conservatively
• 1:05:27
  managed fractures that did go on to unite, although
• 1:05:30
  union occurred faster with surgery. We must also
• 1:05:33
  acknowledge the higher complication rates infection,
• 1:05:35
  hardware issues, need for removal, and greater
• 1:05:38
  expense associated with surgical intervention.
• 1:05:40
  So the treatment choice really needs to be individualized,
• 1:05:44
  carefully weighing the benefits of preventing
• 1:05:46
  non -malunion against the risks of surgery, considering
• 1:05:48
  the patient's activity level and expectations.
• 1:05:51
  When surgery is indicated for clavicle fractures,
• 1:05:54
  what are the preferred techniques? What are their
• 1:05:56
  advantages and disadvantages? And what specific
• 1:05:59
  complications do clinicians need to be aware
• 1:06:01
  of? When surgery is indicated, plate fixation
• 1:06:04
  via open reduction and internal fixation, or
• 1:06:07
  IF, is the most common surgical intervention
• 1:06:10
  worldwide. Doing the technique, meticulous care
• 1:06:13
  is taken to identify and preserve the supraclavicular
• 1:06:16
  nerve branches overlying the clavicle. Modern
• 1:06:19
  anatomically contoured locking plates allow for
• 1:06:21
  precise anatomical restoration and are designed
• 1:06:24
  to be less prominent than older plates. Plates
• 1:06:27
  are typically placed on the superior surface,
• 1:06:29
  which is biomechanically advantageous and generally
• 1:06:31
  requires minimal soft tissue detachment if done
• 1:06:34
  carefully. Interfragmentary lag screw techniques
• 1:06:37
  can be used prior to plating to provide compression
• 1:06:39
  and stabilize oblique or butterfly fragments.
• 1:06:42
  Anterior plating is another option some surgeons
• 1:06:44
  prefer, arguing it reduces plate prominence.
• 1:06:47
  What are the downsides of plating? Complications
• 1:06:49
  include infection, though typically low, around
• 1:06:52
  1 to 5 percent, hardware prominence causing irritation,
• 1:06:55
  quite common, hardware failure, less common with
• 1:06:58
  modern plates, and the potential need for plate
• 1:07:01
  removal later on, which means a second operation.
• 1:07:04
  Reoperation rates are inherently higher with
• 1:07:06
  surgical treatment compared to non -operative
• 1:07:08
  treatment simply because of the possibility of
• 1:07:10
  hardware removal. What about rods or nails inside
• 1:07:13
  the bone? Intramedullary IM fixation is another
• 1:07:16
  technique. Its theoretical advantages include
• 1:07:19
  less soft tissue stripping, relative protection
• 1:07:22
  of the supraclavicular nerves, smaller incisions,
• 1:07:25
  and potentially shorter operating times. Historically,
• 1:07:28
  rigid pins or nails were used but were largely
• 1:07:31
  abandoned due to serious complications, including
• 1:07:34
  intra -thoracic migration. Modern techniques
• 1:07:37
  use elastic titanium nails, like ten nails, which
• 1:07:40
  provide a three -point fixation within the bone
• 1:07:42
  medulla and allow the fracture to heal primarily
• 1:07:45
  by callus formation. While potentially offering
• 1:07:48
  a rapid return to sport for some athletes, these
• 1:07:51
  nails are axially and rotationally less stable
• 1:07:53
  than clade fixation and significantly weaker
• 1:07:56
  biomechanically. They are generally not suitable
• 1:07:59
  for highly committed fractures and usually require
• 1:08:01
  removal once the fracture has healed. Beyond
• 1:08:04
  the initial healing phase, what are the long
• 1:08:06
  -term complications clinicians should be vigilant
• 1:08:08
  for with clavicle fractures, especially non -union
• 1:08:11
  and malunion? How do these complications impact
• 1:08:13
  an athlete's function and potentially their career?
• 1:08:15
  Long -term complications are indeed a significant
• 1:08:18
  concern, especially for high -demand individuals
• 1:08:20
  like athletes. While historically believed to
• 1:08:23
  be low, the non -union rate for displaced mid
• 1:08:26
  -shaft clavicle fractures treated non -operatively
• 1:08:29
  is now recognized as being significant, around
• 1:08:32
  15 .1 % in some meta -analyses compared to just
• 1:08:36
  2 .2 % in operatively treated fractures. And
• 1:08:39
  the risk factors are displacement, Yes. Risk
• 1:08:42
  factors for non -union include increasing age,
• 1:08:45
  female sex, initial shortening greater than two
• 1:08:47
  centimeters, complete fracture displacement,
• 1:08:50
  smoking, and significant combination. Non -union
• 1:08:52
  typically results from a failure of mechanical
• 1:08:54
  stability, too much movement at the fracture
• 1:08:56
  site, which prevents the conversion of soft callus
• 1:08:58
  to hard bone. Management of an established non
• 1:09:01
  -union requires achieving rigid fixation, usually
• 1:09:03
  with plate fixation, and often providing biological
• 1:09:06
  stimulation, for example, through judit decortication,
• 1:09:09
  drilling the medullary canals, or adding bone
• 1:09:11
  graft. Plate fixation offers reliable results
• 1:09:13
  with high union rates for non -unions. What about
• 1:09:16
  malunion, healing in the wrong position? Malunion,
• 1:09:19
  or healing with significant shortening or angulation,
• 1:09:22
  was previously considered primarily a cosmetic
• 1:09:24
  concern with good functional tolerance. However,
• 1:09:28
  more recent patient -reported outcome measures
• 1:09:31
  clearly show that significant malignans can cause
• 1:09:33
  persistent pain, a subjective loss of strength,
• 1:09:37
  rapid fatigue ability during overhead activities,
• 1:09:39
  and cosmetic concerns. How does it affect the
• 1:09:42
  biomechanics? The biomechanical consequences
• 1:09:45
  are quite profound. Shortening a rotational deformity
• 1:09:48
  of the clavicle's lever arm leads to a relative
• 1:09:50
  scapular protraction, altering the orientation
• 1:09:53
  of the glenoid and potentially causing scapular
• 1:09:55
  winging or abnormal scapulothoracic rhythm. This
• 1:09:58
  can decrease the resting tension of the shoulder
• 1:10:00
  girdle muscles, alter the force balance around
• 1:10:03
  the shoulder, leading to perceived weakness and
• 1:10:05
  decreased endurance, particularly affecting overhead
• 1:10:07
  activities which are critical for many athletes.
• 1:10:10
  Melunion has also been linked to symptomatic
• 1:10:12
  arthrosis, developing later at the AC and SC
• 1:10:15
  joints, and sometimes neurovascular problems
• 1:10:17
  or thoracic outlet syndrome due to bony encroachment
• 1:10:20
  on the brachial plexus or subclavian vessels.
• 1:10:23
  This could be especially profound in overhead
• 1:10:25
  athletes. Can Melunion be treated? Treatment
• 1:10:28
  for symptomatic Melunion typically starts with
• 1:10:30
  targeted physiotherapy focusing on scapular control
• 1:10:32
  and strengthening. If symptoms persist, despite
• 1:10:36
  this, surgical corrective osteotomy, essentially
• 1:10:38
  re -breaking the bone, restoring its length and
• 1:10:40
  alignment, and fixing it with a plate, can be
• 1:10:43
  considered after thorough preoperative planning,
• 1:10:45
  often involving CT scans and potentially 3D modeling.
• 1:10:49
  What about fractures at the ends of the clavicle?
• 1:10:51
  Briefly, lateral third fractures near the AC
• 1:10:54
  joint are classified based on their relationship
• 1:10:56
  to the corcaclavicular ligaments. Displacement
• 1:10:59
  occurs if these ligaments are torn, leading to
• 1:11:02
  high non -union rates, perhaps 22 -44 % non -operatively
• 1:11:06
  for unstable types. Undisplaced fractures are
• 1:11:09
  treated non -operatively while displaced. Unsafe
• 1:11:11
  fractures often require surgical intervention
• 1:11:14
  using various techniques like hook plates, distal
• 1:11:16
  clavicle plates, or CC ligament reconstruction
• 1:11:19
  augmentation. Medial third fractures near the
• 1:11:22
  SC joint are rare. less than 5 % of clavicle
• 1:11:25
  fractures, and due to the strong surrounding
• 1:11:27
  ligamentous structures, rarely displaced significantly.
• 1:11:31
  Most are treated conservatively. Displaced fractures
• 1:11:33
  require careful neurovascular assessment due
• 1:11:35
  to the close proximity of vital structures posteriorly.
• 1:11:38
  Expeditious reduction, potentially open, in a
• 1:11:41
  setting with vascular or thoracic surgical expertise
• 1:11:43
  available is crucial, if any compromise is evident.
• 1:11:46
  So pulling it all together for the high -performing
• 1:11:48
  athlete, when is surgical intervention truly
• 1:11:50
  indicated for a clavicle fracture to safeguard
• 1:11:52
  their career and functional longevity? It's a
• 1:11:55
  synthesis of all those factors. For young, high
• 1:11:57
  -demand athletes, particularly those whose sports
• 1:11:59
  demand repetitive or forceful overhead activity,
• 1:12:03
  non -union and significant malunion, especially
• 1:12:05
  two -centimeter shortening, are generally poorly
• 1:12:08
  tolerated and can be career limiting due to the
• 1:12:11
  functional deficits we discussed, pain, weakness,
• 1:12:14
  fatigue, altered mechanics. Therefore, for athletes
• 1:12:17
  presenting with significantly displaced, shortened,
• 1:12:20
  or segmental mid -shaft clavicle fractures, early
• 1:12:23
  operative fixation is often the preferred strategy.
• 1:12:26
  The goal here is to facilitate a predictable
• 1:12:28
  union, restore normal anatomy, and allow for
• 1:12:31
  an early, high -quality recovery, maximizing
• 1:12:33
  their chances of returning to peak performance
• 1:12:35
  and preserving their athletic careers. It's about
• 1:12:37
  minimizing the risk of those long -term complications.
• 1:12:40
  5 .2 pectoralis major ruptures. The power lifter's
• 1:12:43
  scourge. Okay, from bone to the sheer power of
• 1:12:47
  muscle. Let's turn our attention now to the pectoralis
• 1:12:50
  major. Ruptures of this muscle might seem a bit
• 1:12:52
  niche perhaps, but they are absolutely critical
• 1:12:54
  injuries for power athletes, aren't they? What's
• 1:12:57
  the classic mechanism of injury here? What are
• 1:13:00
  the telltale clinical signs we need for accurate
• 1:13:02
  diagnosis? And how does early recognition influence
• 1:13:06
  management and outcomes? Yes, pectoralis major,
• 1:13:09
  or PM, tendon ruptures predominantly occur in
• 1:13:12
  young adult males, typically between 20 and 40
• 1:13:14
  years of age, who engage in strenuous physical
• 1:13:17
  activity. Most classically, these ruptures happen
• 1:13:20
  during the eccentric phase, the lowering phase
• 1:13:21
  of the bench press maneuver in weight training.
• 1:13:24
  This is when the muscle is eccentrically loaded
• 1:13:26
  while in extension and abduction. So the muscle
• 1:13:28
  is lengthening under load. Exactly. That's when
• 1:13:31
  it's most vulnerable. However, other high -demand
• 1:13:34
  activities, such as rugby tackling, wrestling,
• 1:13:37
  martial arts like jujitsu, boxing, and gymnastics,
• 1:13:40
  have also been reported as causes. Importantly,
• 1:13:43
  there appears to be an association with the use
• 1:13:45
  of anabolic steroids. Animal studies suggest
• 1:13:47
  these substances can lead to alterations in collagen
• 1:13:50
  structure, making tendons potentially weaker
• 1:13:52
  or more brittle, and cause disproportionate increases
• 1:13:55
  in muscle strength relative to tendon strength,
• 1:13:58
  effectively lowering the stress required to cause
• 1:13:59
  a rupture. Interesting. Can you remind us of
• 1:14:02
  the anatomy and function? Certainly. The pectoralis
• 1:14:06
  major muscle comprises two main heads, a clavicular
• 1:14:09
  head, up apart, and a larger sternal head. lower
• 1:14:13
  part arising from the ribcage sternum and external
• 1:14:15
  oblique aponeurosis. These heads merge laterally
• 1:14:18
  to form a broad, flat tendon that twists on itself
• 1:14:21
  and inserts into the lateral lip of the occipital
• 1:14:24
  groove on the proximal humeral shaft. Functionally,
• 1:14:27
  the pectoralis major is a powerful adductor,
• 1:14:29
  an internal rotator of the arm, with the clavicular
• 1:14:32
  head contributing to forward flexion. While it
• 1:14:35
  might not be essential for mundane daily activities,
• 1:14:37
  it is an absolute necessity for maximal power
• 1:14:39
  production in strenuous and sporting endeavors.
• 1:14:42
  As mentioned, the muscle is under maximum stress
• 1:14:45
  when eccentrically loaded in extension and abduction,
• 1:14:48
  and it's typically the lower sternal segments
• 1:14:49
  that tend to fail first in a predictable sequence,
• 1:14:52
  often tearing off the humerus. How do patients
• 1:14:54
  usually present it? Is it obvious? Patients typically
• 1:14:57
  present early and can often recall the exact
• 1:14:59
  mechanism and time of injury quite vividly. They
• 1:15:02
  frequently describe hearing or feeling a distinct
• 1:15:05
  snap or pop at the time of rupture. However,
• 1:15:08
  despite this clear history, the diagnosis can
• 1:15:11
  sometimes still be missed initially, perhaps
• 1:15:13
  mistaken for a simple strain leading to delayed
• 1:15:16
  presentation for specialist treatment. What are
• 1:15:18
  the key signs on examination? In the acute setting,
• 1:15:21
  physical examination usually reveals varying
• 1:15:23
  degrees of swelling and bruising ecomosis, over
• 1:15:27
  the upper arm and chest wall, often tracking
• 1:15:29
  down the arm. Crucially, in both acute and chronic
• 1:15:32
  settings, several pathognomonic features are
• 1:15:35
  usually evident when compared carefully to the
• 1:15:37
  contralateral, uninjured side. There might be
• 1:15:40
  a visible or palpable defect. a dropped nipple
• 1:15:42
  sign on the affected side, a medially retracted
• 1:15:45
  pectoralis muscle belly, especially when contracting
• 1:15:47
  the muscle, and a noticeable loss of the sharp
• 1:15:49
  definition of the anterior axillary fold. How
• 1:15:52
  can you accentuate these signs? These features
• 1:15:54
  can often be accentuated by passively abducting
• 1:15:57
  the arm or, more effectively, with attempted
• 1:16:00
  resistive deduction or internal rotation, asking
• 1:16:03
  the patient to push their hand inwards against
• 1:16:05
  resistance. It's worth noting that partial tears
• 1:16:08
  may not present with all these signs so clearly,
• 1:16:11
  and acute swelling can sometimes obscure some
• 1:16:13
  findings, necessitating a high index of suspicion,
• 1:16:16
  especially with the typical history. While ultrasound
• 1:16:20
  can be a useful dynamic adjunct, particularly
• 1:16:23
  in experienced hands, magnetic resonance imaging,
• 1:16:26
  MRI, is generally considered the preferred imaging
• 1:16:29
  modality. MRI not only confirms the diagnosis,
• 1:16:33
  but provides vital information for surgical planning.
• 1:16:35
  It can show the precise location of the tear,
• 1:16:38
  tendon off bone, musculatendinous junction, or
• 1:16:41
  intramuscular, the degree of tendon retraction,
• 1:16:43
  the quality of the remaining tissue, and the
• 1:16:45
  presence of any intact portions of the tendon
• 1:16:48
  and partial tears. It is important, however,
• 1:16:50
  to specifically request a dedicated MRI sequence
• 1:16:53
  that visualizes the entire pectoralis major muscle
• 1:16:56
  and tendon as a standard shoulder MRI sequence
• 1:16:59
  focusing only on the glenohumeral joint might
• 1:17:01
  miss the injury or not show its full extent.
• 1:17:03
  So what's the optimal management for these tears
• 1:17:05
  and athletes? Is surgery usually recommended?
• 1:17:08
  And what are the long -term prospects for them
• 1:17:10
  getting back to sport and regaining their pre
• 1:17:11
  -injury power levels? The key factors determining
• 1:17:14
  the most appropriate management and the subsequent
• 1:17:16
  outcome really are the patient's age and activity
• 1:17:19
  level, the chronicity of the injury, how long
• 1:17:21
  ago it happened, and the precise location and
• 1:17:24
  extent of the tear along the muscle tendon unit.
• 1:17:27
  Who gets non -operative treatment? Non -operative
• 1:17:29
  management is primarily reserved for frail, elderly
• 1:17:32
  patients with a very sedentary lifestyle, or
• 1:17:35
  perhaps for very partial tears with minimal symptoms
• 1:17:39
  in lower demand individuals. It often results
• 1:17:42
  in acceptable functional outcomes in this specific
• 1:17:45
  low demand population. But for athletes? For
• 1:17:48
  young, active, and high demand patients, which
• 1:17:50
  includes virtually all competitive athletes,
• 1:17:53
  surgical repair is unequivocally the treatment
• 1:17:55
  of choice. This consistently yields the best
• 1:17:58
  long -term outcomes and demonstrably superior
• 1:18:01
  functional results, particularly regarding strength
• 1:18:03
  and power compared to non -operative treatment.
• 1:18:06
  The best outcomes with the highest chance of
• 1:18:08
  restoring near -normal anatomy and function are
• 1:18:10
  achieved with early direct surgical repair, preferably
• 1:18:13
  within the first few weeks of injury before significant
• 1:18:16
  tendon retraction and scarring occur. Can surgery
• 1:18:19
  still be done later if the diagnosis was missed?
• 1:18:22
  Yes, surgery can still be considered and often
• 1:18:25
  yields good results even in selected cases where
• 1:18:27
  diagnosis has been delayed or even in long -standing
• 1:18:30
  chronic cases particularly if the athlete has
• 1:18:32
  a significant functional deficit or ongoing pain.
• 1:18:35
  A direct repair back to the bone is usually possible
• 1:18:38
  using various fixation techniques, including
• 1:18:40
  suture anchors, cortical buttons, or transosseous
• 1:18:43
  sutures through drill holes in the humerus. Currently,
• 1:18:46
  no single technique has been clearly shown to
• 1:18:48
  be definitively superior to others. In chronic
• 1:18:51
  settings where direct repair is impossible due
• 1:18:54
  to excessive retraction or poor tissue quality,
• 1:18:57
  additional releases or grafting techniques using
• 1:18:59
  allograft or autograft tendon may be employed
• 1:19:01
  to bridge the gap. What's the rehab like after
• 1:19:04
  surgery? Postoperative rehabilitation involves
• 1:19:07
  an initial period of rest and protection, typically
• 1:19:09
  in a sling, often for three to six weeks, depending
• 1:19:12
  on the repair security. Active hand, wrist, and
• 1:19:15
  elbow exercises are usually allowed immediately.
• 1:19:18
  Early controlled passive or active assisted range
• 1:19:20
  of motion for the shoulder is often initiated
• 1:19:22
  within a safe range determined at surgery, with
• 1:19:25
  movements like external rotation and abduction
• 1:19:27
  generally avoided or limited initially to protect
• 1:19:30
  the repair. The sling is gradually weaned off,
• 1:19:34
  followed by a structured progression aimed at
• 1:19:36
  restoring active motion, then strength, and finally
• 1:19:39
  power. And the return to sport. Return to sports
• 1:19:42
  and unrestricted activity, including heavy lifting
• 1:19:44
  and contact, is usually achieved somewhere between
• 1:19:46
  three to six months from the time of surgery,
• 1:19:49
  though some protocols might extend this further
• 1:19:50
  for maximal strength activities. High return
• 1:19:53
  to sport rates are generally reported after successful
• 1:19:56
  surgical repair, underscoring the effectiveness
• 1:19:58
  of this approach for maintaining an athletic
• 1:20:00
  career that relies on upper body power. Okay,
• 1:20:03
  moving beyond acute injuries now, let's consider
• 1:20:06
  the long game. The cumulative, relentless toll
• 1:20:09
  of high -level sport can, unfortunately, lead
• 1:20:12
  to degenerative conditions like glenohumeral
• 1:20:15
  arthritis. This can be absolutely devastating
• 1:20:18
  for an athlete's career, potentially ending it
• 1:20:20
  prematurely. How exactly does arthritis tend
• 1:20:23
  to develop in this unique, high -demand population?
• 1:20:26
  And what are the often subtle diagnostic clues
• 1:20:29
  that clinicians might inadvertently miss, possibly
• 1:20:31
  leading to delayed treatment? For athletes, the
• 1:20:52
  primary aim of management when arthritis develops
• 1:20:54
  is generally to maximize function and performance
• 1:20:56
  while prolonging their careers for as long as
• 1:20:58
  safely possible. Is it the same type of arthritis
• 1:21:00
  we see in the general older population? Not usually.
• 1:21:04
  When we look at the etiology, primary osteoarthritis...
• 1:21:07
  The wear and tear type, with no obvious preceding
• 1:21:10
  cause, while it certainly occurs in older or
• 1:21:12
  lower demand individuals, is actually relatively
• 1:21:15
  rare in younger, high -level athletes. Its precise
• 1:21:18
  etiology in this specific group remains somewhat
• 1:21:20
  unclear. Interestingly, rotator cuff cares are
• 1:21:23
  uncommon in primary glenohumeral arthritis, unlike
• 1:21:26
  in the hip or knee. Secondary arthritis, however,
• 1:21:28
  is the predominant form we see in the athletic
• 1:21:30
  population. This stems from symptomatic chondral
• 1:21:33
  damage that occurs secondary to other problems,
• 1:21:35
  particularly trauma and most commonly acute or
• 1:21:38
  recurrent instability. So instability is a big
• 1:21:40
  risk factor. A huge risk factor. Patients who
• 1:21:43
  have suffered even a single shoulder dislocation
• 1:21:46
  have up to a 20 times greater risk of developing
• 1:21:49
  glenohumeral arthritis later in life compared
• 1:21:51
  to the general population. Repetitive overhead
• 1:21:54
  activities like those in the dominant arms of
• 1:21:57
  tennis players or throwing athletes often lead
• 1:21:59
  to conditions like internal impingement, which
• 1:22:02
  is associated with occult or hidden chondral
• 1:22:04
  trauma that can predispose to arthritis over
• 1:22:07
  time. Other less common causes include osteonecrosis,
• 1:22:11
  of vascular necrosis, osteochondritis dissecans,
• 1:22:15
  or the sequelae of previous joint infection.
• 1:22:17
  Is there any risk from treatments themselves?
• 1:22:20
  Yes. A critical, albeit rare, iatrogenic cause
• 1:22:22
  that needs mentioning is chondrolysis rapid cartilage
• 1:22:25
  destruction. There was a strong association identified,
• 1:22:28
  particularly during the 2000s, with the use of
• 1:22:31
  intraarticular pain infusion pumps, delivering
• 1:22:33
  continuous local anesthetic, especially bupophocaine,
• 1:22:36
  after arthroscopic surgery. This led to fulminant
• 1:22:39
  chondrolysis and devastating extensive clenohumeral
• 1:22:41
  arthritis developing in young patients within
• 1:22:44
  months of their index procedure. But not from
• 1:22:46
  single injections. It is crucial to note that
• 1:22:48
  this association has not been clearly established
• 1:22:50
  with standard single -shot injections of local
• 1:22:53
  anesthetic, which are commonly and safely used.
• 1:22:57
  Heightened awareness of the risks associated
• 1:22:58
  with continuous infusion pumps should hopefully
• 1:23:01
  significantly reduce any future incidents of
• 1:23:04
  this catastrophic complication. How do we diagnose
• 1:23:07
  arthritis in athletes? You mentioned subtle clues.
• 1:23:11
  Yes. Diagnosis requires clinicians to be particularly
• 1:23:13
  astute because the signs and symptoms can indeed
• 1:23:16
  be understated or non -specific initially. The
• 1:23:19
  athlete with early glenohumeral arthritis may
• 1:23:22
  present with complaints that demand careful diagnostic
• 1:23:24
  assessment to pinpoint the underlying cause.
• 1:23:26
  There's a real risk of narrowly focusing on more
• 1:23:29
  common shoulder pathologies often seen in athletes,
• 1:23:31
  things like partial thickness, rotator cuff tears,
• 1:23:34
  biceps tendinopathy, subacromial bursitis, or
• 1:23:37
  labral tears, which can potentially delay the
• 1:23:39
  diagnosis and appropriate management of the underlying
• 1:23:41
  chondral damage, significantly impacting the
• 1:23:44
  athlete's career trajectory. So we need to think
• 1:23:46
  beyond the usual suspects. Exactly. It's crucial
• 1:23:50
  to actively elicit those understated symptoms,
• 1:23:53
  perhaps subtle episodes of instability they might
• 1:23:55
  downplay, or just a slightly reduced ability
• 1:23:58
  to undertake previously performed tasks at their
• 1:24:00
  usual intensity or duration. Classic symptoms
• 1:24:04
  of more established arthritis include night pain,
• 1:24:07
  often described as a deep ache associated with
• 1:24:09
  inability to sleep on the affected side, and
• 1:24:12
  mechanical symptoms like clicking, grinding,
• 1:24:14
  or even transient locking with sudden sharp pain
• 1:24:17
  that limits activity. We must also emphasize
• 1:24:19
  that athletes may be functionally disabled by
• 1:24:21
  symptoms that wouldn't necessarily significantly
• 1:24:24
  affect the average member of the public. They
• 1:24:26
  often continue to play and function at a high
• 1:24:28
  level, but report a gradual deterioration in
• 1:24:31
  their capability to perform at their expected
• 1:24:33
  peak level. That subtle decline can be the first
• 1:24:36
  sign. What about the physical exam? Physical
• 1:24:39
  examination findings to look for include periscapular
• 1:24:41
  muscle wasting due to disuse or pain inhibition
• 1:24:45
  and crepitus during movement. which may be audible
• 1:24:47
  or just palpable by the examiner. The joint line
• 1:24:50
  itself may be painful on palpation, with posterior
• 1:24:54
  joint line tenderness often cited as a more specific,
• 1:24:57
  though not definitive, sign of underlying caudal
• 1:24:59
  damage. Range of motion restriction, particularly
• 1:25:02
  a loss of external rotation, both active and
• 1:25:05
  passive, and a painful arc of motion are also
• 1:25:07
  common findings. And imaging. How useful is MRA
• 1:25:10
  here? For imaging, standard radiographs are the
• 1:25:12
  essential initial investigation. AP radiographs
• 1:25:15
  are used to describe the degree of arthritis
• 1:25:17
  reliably using classifications like the Samuelson
• 1:25:20
  and Pareto classification, which categorizes
• 1:25:22
  patients into mild, moderate, and severe based
• 1:25:24
  on osteophyte size, glenohumeral joint space
• 1:25:27
  narrowing, and surface irregularity. While MRI
• 1:25:31
  and CT scans also play a role, their limitations
• 1:25:33
  in this context are key. Chondral surfaces in
• 1:25:36
  the glenohumeral joint are much thinner, around
• 1:25:38
  1 .5 millimeters on average, compared to the
• 1:25:40
  knee, which can be up to 10 millimeter. This
• 1:25:42
  makes visualizing subtle early chondral lesions
• 1:25:45
  challenging. Magnetic resonance imaging, MRI,
• 1:25:48
  scanning for arthritis, even with specialized
• 1:25:50
  cartilage sequences or FRN arthrography, actually
• 1:25:53
  lacks sensitivity and specificity for detecting
• 1:25:55
  these subtle early chondral lesions reliably.
• 1:25:57
  However, more profound full -thickness chondral
• 1:25:59
  loss is more easily evident. Computed tomography
• 1:26:02
  CT scans are particularly helpful for quantifying
• 1:26:04
  glenoid bone loss or wear patterns, especially
• 1:26:07
  if there are metal artifacts from previous surgery
• 1:26:08
  obscuring MRI, and 2D -3D reconstructions can
• 1:26:12
  assist with exact localization of osteophytes
• 1:26:14
  or loose bodies. So if imaging is limited for
• 1:26:16
  early stages, what's the gold standard? Due to
• 1:26:19
  these inherent limitations of non -invasive imaging
• 1:26:22
  modalities in accurately diagnosing subtle chondral
• 1:26:25
  damage, diagnostic arthroscopy unfortunately
• 1:26:28
  remains the gold standard for definitive diagnosis
• 1:26:30
  and staging, particularly in joints like the
• 1:26:32
  shoulder with inherently thinner articular cartilage
• 1:26:35
  layers. It allows direct visualization and probing
• 1:26:38
  of the cartilage surfaces. 6 .2 management strategies.
• 1:26:42
  Career -focused approaches. When we approach
• 1:26:45
  the management of an athlete grappling with glenohumeral
• 1:26:47
  arthritis, the objective, as you said, isn't
• 1:26:50
  merely to reduce pain. It's intricately woven
• 1:26:53
  with preserving their career, if possible. How
• 1:26:56
  do we strategically stratify treatment options?
• 1:26:59
  What are the specific nuances within each category,
• 1:27:02
  ranging from maintaining function to salvaging
• 1:27:04
  what's possible and ultimately facing those difficult
• 1:27:06
  career -ending decisions? This really requires
• 1:27:09
  a truly athlete -centered approach. because the
• 1:27:12
  principles and goals of managing glenohumeral
• 1:27:14
  arthritis in athletes are fundamentally different
• 1:27:17
  from those in the general older patient population.
• 1:27:20
  The professional athlete's primary aim is generally
• 1:27:23
  to maintain a career at the highest possible
• 1:27:25
  level for as long as possible. whereas recreational
• 1:27:28
  athletes may accept modifying their activities
• 1:27:30
  or lowering their participation level. Therefore,
• 1:27:34
  a solid understanding and appropriate management
• 1:27:36
  of the patient's specific aims, goals, and expectations
• 1:27:39
  are absolutely critical to achieving a positive
• 1:27:42
  outcome in this challenging degenerative condition.
• 1:27:46
  Athletes must be educated about their condition,
• 1:27:48
  taught how to interpret their symptoms, and actively
• 1:27:50
  participate in their management plan. Treatment
• 1:27:53
  options can be broadly categorized as palliative,
• 1:27:56
  reparative, restorative, and reconstructive.
• 1:27:59
  Let's start with options aiming to maintain their
• 1:28:01
  career. Okay. Career -maintaining options are
• 1:28:04
  generally appropriate for athletes with early
• 1:28:06
  or moderate stage arthritis who are aiming to
• 1:28:08
  continue performing at the highest possible level.
• 1:28:11
  The objective here is to mitigate symptoms that
• 1:28:13
  limit high -level function. These options are
• 1:28:16
  generally less invasive with lower morbidity
• 1:28:18
  and often achieve successful short to medium
• 1:28:21
  -term outcomes, though the underlying natural
• 1:28:23
  history of arthritis will ultimately determine
• 1:28:25
  longer -term career impacts. For professional
• 1:28:28
  athletes, awareness of the World Anti -Doping
• 1:28:30
  Agency, WADA, regarding allowed medications is,
• 1:28:33
  of course, essential. What does non -operative
• 1:28:36
  management involve here? First -line therapy
• 1:28:38
  includes activity modification, which might mean
• 1:28:40
  adjusting training load or technique rather than
• 1:28:43
  stopping completely, and the use of appropriate
• 1:28:45
  non -steroidal anti -inflammatory drugs, NSAIs,
• 1:28:49
  to decrease inflammation and improve function
• 1:28:51
  within WADA limits, if applicable. What about
• 1:28:53
  injections? Steroids, PRP. Injections, such as
• 1:28:57
  corticosteroids, hyaluronic acid, viscose supplementation,
• 1:29:01
  and platelet -rich plasma, PRP, can potentially
• 1:29:04
  provide short -term pain relief and can also
• 1:29:06
  act as a diagnostic tool, confirming the joint
• 1:29:09
  as the pain source. Crucially, injections must
• 1:29:12
  be performed under sterile conditions, ideally
• 1:29:15
  with fluoroscopic or ultrasound guidance, to
• 1:29:17
  ensure accurate intraarticular placement. And
• 1:29:20
  perhaps most importantly, injections should never
• 1:29:23
  be used simply as short -term solutions to get
• 1:29:25
  an athlete. through game or competition. This
• 1:29:28
  approach can have devastating consequences by
• 1:29:30
  masking pain, the body's protective mechanism,
• 1:29:33
  potentially leading to accelerated chondral degeneration.
• 1:29:36
  Corticosteroids themselves can also suppress
• 1:29:38
  collagen synthesis. So what is the goal of injections,
• 1:29:41
  then? The objective should be to provide temporary
• 1:29:43
  dampening of synovitis and pain to allow the
• 1:29:46
  athlete to engage more effectively in a structured
• 1:29:48
  strengthening and rehabilitation program, not
• 1:29:50
  to enable an immediate return to high impact
• 1:29:52
  activity while the joint is still inflamed or
• 1:29:54
  unstable. and physiotherapy, still core. Physiotherapy
• 1:29:58
  forms the absolute core of non -operative treatment.
• 1:30:02
  It must be individualized and sport -job specific,
• 1:30:05
  focusing on pain reduction, maintenance of range
• 1:30:08
  of motion, especially combating capsular contracture,
• 1:30:11
  and targeted strengthening. As arthritic shoulders
• 1:30:14
  often develop associated scapular dyskinesis,
• 1:30:17
  a tailored program focusing on scapular stabilization
• 1:30:19
  and regaining excellent scapular humeral rhythm
• 1:30:21
  is paramount. This should be combined with isometric
• 1:30:24
  strengthening and passive stretching. Hydrotherapy
• 1:30:27
  can also play a key role due to water's buoyancy
• 1:30:29
  and resistance properties. What if non -operative
• 1:30:32
  measures aren't enough? Arthroscopy. Yes, in
• 1:30:34
  patients with earlier stage disease who fail
• 1:30:36
  conservative measures, arthroscopic debridement
• 1:30:38
  and chondroplasty can be considered. This involves
• 1:30:41
  smoothing down unstable chondral flaps or frayed
• 1:30:44
  cartilage, which are thought to be pain generators.
• 1:30:46
  Best outcomes are generally seen in patients
• 1:30:48
  with congruent joints, meaning the joint surfaces
• 1:30:50
  still match reasonably well, minimal osteophyte
• 1:30:53
  or cyst formation, and relatively shallow lesions,
• 1:30:55
  less than two centimeters squared, affecting
• 1:30:57
  only one side of the joint, usually the humeral
• 1:30:59
  head. Adjunctive procedures performed at the
• 1:31:02
  time of arthroscopy can include lavage, washing
• 1:31:05
  out debris and inflammatory mediators, and removal
• 1:31:07
  of loose bodies. As the disease progresses, anterior
• 1:31:10
  capsule contracture can develop, leading to decreased
• 1:31:13
  external rotation and increased load on the posterior
• 1:31:15
  chondral surfaces. More comprehensive arthroscopic
• 1:31:18
  procedures for advanced disease might include
• 1:31:20
  a full -capsular release, subacromial decompression
• 1:31:23
  if needed, glenohumeral chondroplasty, AC joint
• 1:31:26
  excision, humeral osteoplasty, reshaping bone
• 1:31:28
  spurs, osteophyte resection, biceps tenodesis
• 1:31:32
  if the biceps tendon is involved, and even axillary
• 1:31:34
  nerve neuralysis if nerve irritation is suspected.
• 1:31:37
  Some promising results have shown these more
• 1:31:39
  comprehensive arthroscopic approaches, sometimes
• 1:31:41
  termed comprehensive arthroscopic management
• 1:31:43
  or CAM, can potentially delay the need for arthroplasty
• 1:31:47
  by up to two years in around 85 % of selected
• 1:31:49
  patients. What about options when things are
• 1:31:52
  more severe? Career salvaging options. These
• 1:31:55
  options come into play when career maintaining
• 1:31:57
  strategies are becoming less successful. or for
• 1:31:59
  more severe or symptomatic degenerative disease.
• 1:32:03
  While high -impact activity might still be possible
• 1:32:05
  after some of these, the overall success rates
• 1:32:08
  in a high -load athletic environment are certainly
• 1:32:10
  more circumspect. Athletes' expectations must
• 1:32:13
  be carefully managed as they may not recover
• 1:32:16
  sufficient function or symptom control to return
• 1:32:18
  to their desired pre -injury level. What procedures
• 1:32:21
  fall into this category? Microfracture is one.
• 1:32:24
  The principle borrowed from knee surgery is to
• 1:32:27
  penetrate the subchondral bone plate to stimulate
• 1:32:30
  a healing response from the bone marrow, leading
• 1:32:32
  to fibrocartilage formation over the defect.
• 1:32:35
  It requires meticulous surgical technique and
• 1:32:37
  a very slow, tailored rehabilitation protocol
• 1:32:40
  involving restricted weight bearing or loading.
• 1:32:43
  While successful in the knee for certain lesions,
• 1:32:45
  the literature supporting its use in the shoulder
• 1:32:47
  is minimal. Best outcomes, anecdotally, are reported
• 1:32:50
  for smaller, isolated humeral -side lesions in
• 1:32:53
  young, active patients. A potential advantage
• 1:32:56
  is that it doesn't appear to compromise future
• 1:32:58
  reconstructive options like arthroplasty. What
• 1:33:00
  about grafting, like cartilage transplants? Chondral
• 1:33:04
  or osteochondral grafting techniques are designed
• 1:33:06
  for more focal chondral lesions. Modalities include
• 1:33:09
  osteochondral allograft transplantation, using
• 1:33:12
  donor tissue, primary autograft transfer, OATS
• 1:33:15
  procedure, taking plugs from a non -weight -bearing
• 1:33:17
  area, staged autologous chondrocyte implantation,
• 1:33:21
  ACI, growing the patient's own cartilage cells
• 1:33:23
  in a lab and re -implanting them, or the use
• 1:33:26
  of synthetic scaffolds to encourage cartilage
• 1:33:28
  regrowth. Osteochondral grafting for humeral
• 1:33:31
  head defects has theoretical advantages but can
• 1:33:33
  have significant donor site morbidity if using
• 1:33:35
  autograft or availability issues with allograft.
• 1:33:38
  Reports specifically in the shoulder athlete
• 1:33:39
  population are limited. Biological resurfacing?
• 1:33:42
  What's that? This involves resurfacing an arthritic
• 1:33:45
  glenoid surface using biological tissues instead
• 1:33:48
  of a plastic component. Tissues used have included
• 1:33:51
  enfolded anterior capsule, allografts like fascia
• 1:33:54
  lata or Achilles tendon, or commercially available
• 1:33:56
  dermal tissue matrices or biologic patches. It's
• 1:34:00
  designed as a potential bone preserving alternative
• 1:34:03
  to prosthetic glenoid replacement, particularly
• 1:34:05
  in younger patients. It's typically an open procedure
• 1:34:08
  requiring prolonged rehabilitation, although
• 1:34:10
  advanced arthroscopic techniques are developing.
• 1:34:12
  Sporadic reports looking specifically at athletes
• 1:34:14
  show some good outcomes in the first couple of
• 1:34:16
  years, but long -term durability is still under
• 1:34:18
  investigation. And joint fusion. Arthrodesis.
• 1:34:22
  Seems drastic. Arthrodesis, or surgical fusion
• 1:34:25
  of the glenohumeral joint, has largely been consigned
• 1:34:28
  to historical significance for primary glenohumeral
• 1:34:30
  arthritis by the success of prosthetic implants.
• 1:34:34
  It's now mainly reserved for situations like
• 1:34:35
  failed arthroplasty, deep infection, or certain
• 1:34:38
  neurological injuries. However, it holds a unique
• 1:34:41
  albeit small niche place for a very specific
• 1:34:44
  subgroup of athletes. Despite creating a fused,
• 1:34:47
  immobile glenohumeral joint, a successfully united
• 1:34:50
  arthrodesis does allow patients to return to
• 1:34:53
  almost any desired level of sport, including
• 1:34:55
  full impact and heavy loading, as there are no
• 1:34:58
  implant -related restrictions or concerns about
• 1:35:00
  wear or loosening. Thus, for certain patients,
• 1:35:03
  perhaps those involved in heavy manual labor
• 1:35:05
  or specific high -impact sports, especially on
• 1:35:07
  their non -dominant side who prioritize the ability
• 1:35:10
  to perform high -impact or loading activities
• 1:35:12
  over achieving a functional range of motion,
• 1:35:14
  arthrodesis should potentially be discussed as
• 1:35:16
  an alternative to arthroplasty. It's a tradeoff
• 1:35:19
  between motion and unrestricted activity. Finally,
• 1:35:22
  the career -ending options. Yes. Inevitably,
• 1:35:25
  sometimes the damage is too extensive or symptoms
• 1:35:27
  too severe for career preservation. Activity
• 1:35:30
  modification, meaning the complete cessation
• 1:35:32
  of the specific sporting activities that exacerbate
• 1:35:35
  pain, is often the first line of management advised
• 1:35:38
  in many patients with advanced arthritis. But
• 1:35:41
  for a professional or serious recreational athlete,
• 1:35:44
  this is often the last resort. and, by definition,
• 1:35:47
  a career -ending decision regarding that sport.
• 1:35:50
  This difficult decision is typically made due
• 1:35:52
  to intractable pain significantly affecting quality
• 1:35:55
  of life, stiffness severely limiting function
• 1:35:57
  and performance, or the realization, often after
• 1:36:00
  failed attempts at salvaging procedures, that
• 1:36:03
  continued high -level sporting activity will
• 1:36:04
  significantly compromise their long -term joint
• 1:36:07
  health and overall quality of life. provides
• 1:36:14
  the most consistently positive and reproducible
• 1:36:16
  outcomes for pain relief and functional improvement
• 1:36:19
  in older patients with advanced arthritis. Modern
• 1:36:22
  implants and techniques are excellent. Options
• 1:36:25
  include heme arthroplasty, replacing only the
• 1:36:28
  humal head, sometimes with reaming of the glenoid,
• 1:36:30
  the ream and run technique, or total shoulder
• 1:36:33
  arthroplasty, replacing both surfaces. Cementless
• 1:36:36
  resurfacing arthroplasty is another option that
• 1:36:38
  aims to preserve bone stock and potentially offer
• 1:36:40
  easier revision surgery later, which is a consideration
• 1:36:43
  in younger patients. While short and medium term
• 1:36:46
  results of arthroplasty are generally positive
• 1:36:48
  even for younger active patients compared to
• 1:36:50
  their preoperative state, this must be weighed
• 1:36:52
  against the generally superior overall results
• 1:36:55
  and longer implant survival, typically seen with
• 1:36:57
  stem total shoulder arthroplasty in older populations.
• 1:37:01
  Crucially, however, for the professional or high
• 1:37:03
  -level recreational athlete, prosthetic arthroplasty
• 1:37:06
  is realistically only an option following the
• 1:37:08
  end of their competitive career. A prosthetic
• 1:37:10
  joint simply cannot tolerate the high forces,
• 1:37:13
  repetitive impacts, and extreme ranges of motion
• 1:37:15
  required by the vast majority of upper limb athletic
• 1:37:18
  pursuits without risking early failure, loosening,
• 1:37:21
  or fracture. It demands significant permanent
• 1:37:24
  activity adjustment and is, by definition, a
• 1:37:27
  career -ending decision for these athletes regarding
• 1:37:29
  high impact or high -demand sports. Finally,
• 1:37:31
  let's talk about the ultimate objective for any
• 1:37:34
  injured athlete, achieving a safe, effective,
• 1:37:37
  and hopefully sustainable return to play. What
• 1:37:39
  are the core evidence -based principles guiding
• 1:37:42
  modern rehabilitation after shoulder injury or
• 1:37:44
  surgery? And crucially, how do we objectively
• 1:37:46
  measure readiness moving beyond just a patient
• 1:37:49
  feeling better to making truly robust data -driven
• 1:37:51
  decisions about their return? This is absolutely
• 1:37:54
  where the science of recovery comes in, moving
• 1:37:56
  beyond just letting nature take its course. Effective
• 1:37:59
  rehabilitation extends far beyond simple pain
• 1:38:02
  management and reduction of inflammation, though
• 1:38:05
  those are important initial steps. It must encompass
• 1:38:08
  the meticulous restoration of optimal muscle
• 1:38:10
  strength and balance around the shoulder girdle,
• 1:38:13
  achieving functional joint range of motion specific
• 1:38:15
  to the athlete's needs, and crucially, a carefully
• 1:38:19
  managed progression to functional movements that
• 1:38:21
  precisely replicate the demands of the athlete's
• 1:38:24
  specific sport. This entire progression from
• 1:38:27
  early protection to high -level function is underpinned
• 1:38:30
  by a fundamental requirement for meticulous joint
• 1:38:32
  control. This necessitates explicit attention
• 1:38:35
  to restoring proprioceptive awareness, ensuring
• 1:38:39
  dynamic stabilization from the rotator cuff and
• 1:38:41
  scapular muscles, developing feed -forward mechanisms
• 1:38:44
  through anticipatory muscle responses before
• 1:38:46
  movement occurs, and training reactive muscle
• 1:38:49
  function to cope with unexpected perturbations
• 1:38:51
  during athletic activity. So it's much more than
• 1:38:54
  just strength and flexibility. Much more. And
• 1:38:57
  return -to -play decisions, therefore, absolutely
• 1:39:00
  must be based on objective measurements and criteria,
• 1:39:03
  not just time elapsed or subjective feeling.
• 1:39:05
  This involves a thorough evaluation of the athlete's
• 1:39:09
  overall health status, a clear assessment of
• 1:39:11
  the remaining participation risk, risk of re
• 1:39:14
  -injury or further damage, and consideration
• 1:39:16
  of extrinsic factors like equipment, playing
• 1:39:19
  surface or game intensity. McCarty and colleagues
• 1:39:22
  outlined what might be considered ideal criteria
• 1:39:24
  for return to play following shoulder stabilization
• 1:39:27
  surgery, which provide a good framework. Little
• 1:39:30
  or no pain, the patient's subjective impression
• 1:39:33
  of stability, feeling confident in the shoulder,
• 1:39:35
  near normal range of motion compared to the other
• 1:39:37
  side, near normal strength, often defined as
• 1:39:40
  90 % of the contralateral side, demonstrated
• 1:39:42
  normal functional ability in sport -specific
• 1:39:44
  tests, and execution of normal sport -specific
• 1:39:47
  skills without deficit or compensation. And the
• 1:39:50
  kinetic chain comes back into play here. Indispensably
• 1:39:52
  so. The kinetic chain concept is fundamental
• 1:39:55
  to effective rehabilitation, especially for overhead
• 1:39:58
  athletes. Remember, it's that open -linked system
• 1:40:01
  of segments, lower limbs, torso, scapula, GH
• 1:40:04
  joint, upper limb operating in a proximal to
• 1:40:07
  distal sequence to generate and transfer high
• 1:40:09
  velocity or force to the distal segment, the
• 1:40:12
  hand. The final velocity or force achieved depends
• 1:40:15
  on the contribution of each segment and the smooth
• 1:40:18
  interaction between them. Therefore, when assessing
• 1:40:20
  and rehabilitating the overhead athlete, each
• 1:40:23
  segment of the kinetic chain needs to be assessed
• 1:40:25
  to ensure it possesses the required range of
• 1:40:27
  movement and muscular control. Any break or inefficiency
• 1:40:30
  in that chain will overload another segment,
• 1:40:32
  often the shoulder. The scapula, as we've discussed,
• 1:40:35
  plays that pivotal role as a critical link, permitting
• 1:40:38
  effective force transfer from the trunk and legs
• 1:40:40
  and ensuring optimal glenohumeral joint alignment.
• 1:40:43
  This highlights the paramount need to identify
• 1:40:45
  and include correction of any suboptimal movement
• 1:40:48
  strategies elsewhere in the kinetic chain within
• 1:40:50
  the shoulder rehabilitation process. Fixing the
• 1:40:53
  shoulder in isolation often isn't enough. You
• 1:40:55
  also mentioned an alternating pattern of mobility
• 1:40:58
  and stability. Yes, that's a crucial concept
• 1:41:00
  within the kinetic chain, often attributed to
• 1:41:03
  physical therapists like Greg Cook and Michael
• 1:41:05
  Boyle. It suggests that optimal performance requires
• 1:41:08
  a balance between stability and mobility at different
• 1:41:10
  joints, often following an alternating pattern
• 1:41:13
  of the body. For example, The ankle needs mobility,
• 1:41:17
  the knee requires stability, the hip needs mobility,
• 1:41:20
  the lumbar spine needs stability, the thoracic
• 1:41:22
  spine requires mobility, the scapula needs stability
• 1:41:25
  as a platform, and the glenohumeral joint itself
• 1:41:28
  needs mobility. Dysfunction often occurs when
• 1:41:31
  a joint that should be mobile becomes stiff,
• 1:41:33
  forcing the adjacent joint that should be stable
• 1:41:36
  to compensate with excessive movement leading
• 1:41:38
  to injury. That makes sense. Are there specific
• 1:41:40
  screening tools for this? Integrating these components
• 1:41:43
  leads to the use of specific screening tools
• 1:41:45
  designed to assess these different segments.
• 1:41:48
  Examples commonly used include tests for thoracic
• 1:41:51
  rotation, like the locked lumbar rotation test,
• 1:41:54
  thoracic extension, example combined elevation
• 1:41:56
  test, shoulder internal and external rotation
• 1:41:59
  range, assessing GRD and total arc, hip internal
• 1:42:02
  and external rotation, and tests for core trunk
• 1:42:05
  endurance, like extensor, lateral, and flexor
• 1:42:07
  endurance tests. These help identify limitations
• 1:42:10
  throughout the chain. One of the most talked
• 1:42:12
  about concepts in athlete rehab, particularly
• 1:42:15
  for throwers, is glenohumeral internal rotation
• 1:42:18
  deficit, or GIRD, which you touched on earlier.
• 1:42:20
  Can you explain precisely what it is again, why
• 1:42:23
  it matters as a potential injury risk factor,
• 1:42:25
  and how we should measure it accurately in a
• 1:42:27
  clinical setting? Yes, glenohumeral internal
• 1:42:29
  rotation deficit, or GIRD, is a very common adaptive
• 1:42:33
  change observed specifically in overhead athletes,
• 1:42:35
  particularly throwers. It is characterized by
• 1:42:38
  a functional increase in glenohumeral external
• 1:42:40
  rotation on the dominant throwing side, coupled
• 1:42:43
  with a compensatory decrease in internal rotation
• 1:42:46
  on that same side. The total arc of rotational
• 1:42:49
  motion might remain similar side to side, but
• 1:42:52
  the arc itself is shifted posteriorly. The underlying
• 1:42:55
  mechanism is often thought to be adaptive tightness
• 1:42:57
  or contracture of the posterior inferior glenohumeral
• 1:43:01
  ligament PIGHL complex and the posterior inferior
• 1:43:04
  capsule, developed over time due to repetitive
• 1:43:06
  throwing motions. This tightness can lead to
• 1:43:09
  a post or superior shift of the point of clenocumeral
• 1:43:12
  articulation and the center of rotation during
• 1:43:14
  throwing. Why is this potentially problematic?
• 1:43:17
  From a clinical significant standpoint, increasing
• 1:43:19
  GRD, specifically a significant loss of internal
• 1:43:22
  rotation compared to the non -dominant side or
• 1:43:25
  compared to the total arc, may be associated
• 1:43:27
  with an increased injury risk in throwing athletes.
• 1:43:30
  It's thought to contribute to conditions like
• 1:43:32
  internal impingement and SLAP cares by altering
• 1:43:35
  joint mechanics. How do we measure it reliably?
• 1:43:38
  We assess GIRD relative to the total arc of motion
• 1:43:41
  of the glenohumeral joint. Total arc measured
• 1:43:44
  glenohumeral internal rotation plus measured
• 1:43:46
  glenohumeral external rotation. It's crucial
• 1:43:49
  to measure this accurately usually with the patient's
• 1:43:52
  supine, the shoulder abducted to 90 degrees,
• 1:43:54
  and the scapula stabilized by the examiner or
• 1:43:57
  an assistant to prevent scapula thoracic motion
• 1:44:00
  compensating for true glenohumeral rotation loss.
• 1:44:03
  It has been proposed that a healthy shoulder
• 1:44:05
  should ideally present with around a 180 -degree
• 1:44:08
  total arc of motion, or perhaps more functionally
• 1:44:11
  relevant, the total arc of motion should be roughly
• 1:44:13
  equal bilaterally within 510 degrees. While there's
• 1:44:18
  ongoing debate and research, generally accepted
• 1:44:20
  thresholds for concern often include a side -to
• 1:44:22
  -side difference of greater than 20 degrees for
• 1:44:24
  internal rotation loss, or a loss of total rotational
• 1:44:27
  range of motion greater than 510 percent compared
• 1:44:30
  to the contralateral side. These values are often
• 1:44:32
  considered potentially pathological and warrant
• 1:44:35
  intervention like targeted stretching. More specific
• 1:44:38
  predictive findings for injury risk have been
• 1:44:40
  proposed in certain populations, such as a loss
• 1:44:42
  of greater than 25 degrees into internal rotation
• 1:44:45
  in baseball players, or a loss of 20 degrees
• 1:44:48
  internal rotation combined with a 5 % loss in
• 1:44:50
  total ROM, doubling the risk for injury in professional
• 1:44:53
  baseball pitchers in one study. However, it's
• 1:44:56
  important to acknowledge that some studies have
• 1:44:57
  not found a direct or consistent association
• 1:44:59
  between GRD measurements alone and subsequent
• 1:45:02
  injury. So, while GRD is an important factor
• 1:45:05
  to assess and address particularly significant
• 1:45:07
  deficits, it should be considered as part of
• 1:45:09
  the broader clinical picture on kinetic chain
• 1:45:11
  assessment, not as an isolated risk factor. 7
• 1:45:14
  .2 Objective Strength and Proprioception Assessment
• 1:45:17
  Beyond range of motion measures like GID, accurately
• 1:45:20
  assessing shoulder strength and proprioception
• 1:45:22
  is absolutely crucial for making those safe return
• 1:45:25
  to play decisions. How do we get truly objective,
• 1:45:29
  reliable data on these parameters? How do we
• 1:45:32
  move beyond just subjective clinical impressions
• 1:45:35
  feel strong, given the known limitations of traditional
• 1:45:38
  methods like manual muscle testing? That's a
• 1:45:40
  vital question for evidence -based practice.
• 1:45:42
  When it comes to shoulder strength assessment,
• 1:45:44
  While standard manual muscle testing, MMT, using
• 1:45:47
  the Euro -5 Oxford scale, has good clinical utility
• 1:45:50
  for detecting growth weakness, it is inherently
• 1:45:53
  highly subjective. MMT is significantly prone
• 1:45:56
  to user error and bias, especially at the higher
• 1:45:59
  grades, grade four and five, where distinguishing
• 1:46:02
  subtle but potentially clinically significant
• 1:46:04
  weakness can be very difficult. It's often hard
• 1:46:06
  to present objective, quantifiable data using
• 1:46:09
  this method, and the results can be heavily influenced
• 1:46:11
  by the examiner's own experience and strength
• 1:46:13
  relative to the patient. So what's a better alternative
• 1:46:16
  for objective data? We strongly advocate for
• 1:46:19
  the use of handheld dynamometers. HHD has a much
• 1:46:22
  more objective and reliable method of strength
• 1:46:24
  evaluation. It's far superior to MMT for quantifying
• 1:46:28
  strength and crucially for evaluating subtle
• 1:46:30
  changes in muscle strength caused by injury dysfunction
• 1:46:33
  or rehabilitation progress. HHD provides objective
• 1:46:37
  numerical data, for example in kilograms or pounds
• 1:46:39
  of force, that can be tracked over time and compared
• 1:46:41
  to the contralateral side or normative data.
• 1:46:43
  It's particularly useful for assessing specific
• 1:46:46
  scapular stabilizer muscles, like the upper middle
• 1:46:48
  and lower trapezius and the serratus anterior,
• 1:46:51
  by resisting specific movements in standardized
• 1:46:53
  test positions. What about endurance, not just
• 1:46:55
  peak strength? Beyond peak strength, assessing
• 1:46:58
  muscular endurance is also incredibly important,
• 1:47:01
  especially in athletes performing repetitive
• 1:47:03
  tasks. Shoulder muscle fatigue has been proposed
• 1:47:06
  to be strongly associated with repeated arm use
• 1:47:08
  and the subsequent development of rotator cuff
• 1:47:10
  disorders and instability. The mechanism for
• 1:47:13
  this is postulated to be due to fatigue causing
• 1:47:16
  altered timing and coordination of the local
• 1:47:18
  muscle system around the shoulder girdle. Fatigue
• 1:47:21
  muscles absorb less energy before elongation,
• 1:47:24
  increasing the risk of tissue strain and injury
• 1:47:26
  during subsequent forceful movements. Enduris
• 1:47:29
  can be assessed using time tests or repetitions
• 1:47:31
  against submaximal resistance. Okay, and proprioception,
• 1:47:35
  that sense of joint position, how do we measure
• 1:47:36
  that objectively? Proprioception assessment is
• 1:47:39
  equally important, but perhaps even more challenging
• 1:47:41
  to quantify reliably in a standard clinical setting.
• 1:47:45
  We define proprioception as a sensory -offerant
• 1:47:48
  feedback mechanism that mediates joint position
• 1:47:51
  and movement sensibility with modular reflex
• 1:47:53
  stabilization. Essentially, it's the body's kinesthetic
• 1:47:57
  sense knowing where your joint is in space without
• 1:47:59
  looking. Why does it matter? Well, those mechanoreceptors
• 1:48:03
  within the capsule -laboral complex or on the
• 1:48:05
  shoulder, which detect joint position and movement,
• 1:48:08
  can be damaged due to local tissue trauma from
• 1:48:10
  injury or surgery. This can lead to significant
• 1:48:12
  deficiencies in joint proprioception. Reduced
• 1:48:15
  joint proprioception has been proposed as a significant
• 1:48:17
  contributing factor to functional instability
• 1:48:19
  and re -injury, as the joint doesn't know where
• 1:48:22
  it is as accurately, impairing protective muscle
• 1:48:25
  responses. How can we test it clinically without
• 1:48:27
  expensive equipment? While many high -tech laboratory
• 1:48:30
  devices exist, like isokinetic dynamometry with
• 1:48:33
  proprioceptive modes or electronic motion tracking
• 1:48:35
  devices, these are often costly and impractical
• 1:48:37
  for routine clinical use. However, we can advocate
• 1:48:41
  for more utilitarian, clinically applicable methods.
• 1:48:44
  The assessment of proprioception using reproduction
• 1:48:46
  of passive positioning is a valid and established
• 1:48:48
  method. This often involves joint angular replication
• 1:48:51
  tests. Typically, the examiner passively places
• 1:48:55
  the patient's injured shoulder into a specific
• 1:48:57
  angle or position. The patient consciously registers
• 1:48:59
  this position, often with eyes closed, the arm
• 1:49:02
  is returned to the resting start position, and
• 1:49:04
  the subject is then asked to actively replicate
• 1:49:06
  the test position as accurately as possible.
• 1:49:09
  The difference between the target angle and the
• 1:49:11
  reproduced angle is measured. This assesses the
• 1:49:13
  function of both static joint receptors and dynamic
• 1:49:15
  muscle spindles, shoulder joint stabilizers,
• 1:49:18
  and their input to position sets. Other practical
• 1:49:20
  open and closed kinetic chain exercises used
• 1:49:23
  in rehabilitation also challenge proprioception,
• 1:49:26
  such as attempting to hold a specific joint angle
• 1:49:28
  with eyes closed, or contralateral limb mirroring
• 1:49:31
  exercises where the patient tries to mirror the
• 1:49:34
  position or movement of their uninjured arm with
• 1:49:36
  their injured arm while keeping their eyes closed.
• 1:49:40
  These practical methods provide valuable clinical
• 1:49:42
  insights into an athlete's proprioceptive capabilities
• 1:49:45
  and help guide rehabilitation. 7 .3 Conclusion
• 1:49:49
  of Rehab Principles So, to synthesize all of
• 1:49:53
  that, effective rehabilitation for the athletic
• 1:49:55
  shoulder demands a truly profound understanding
• 1:49:58
  of sport -specific biomechanics and the demands
• 1:50:00
  placed on the joint. It requires a comprehensive
• 1:50:03
  biomechanical screening process, looking beyond
• 1:50:06
  the shoulder itself to assess the entire kinetic
• 1:50:08
  chain for any contributing deficits. We must
• 1:50:10
  utilize objective measurement tools for tracking
• 1:50:12
  progress in strength, endurance, range of motion,
• 1:50:16
  and proprioception. And fundamentally, there
• 1:50:18
  must be a commitment to a criterion -based milestone
• 1:50:21
  -driven progression through rehabilitation phases,
• 1:50:24
  rather than relying on rigid time -based protocols
• 1:50:26
  that don't account for individual variation in
• 1:50:29
  healing and response. This integrated objective
• 1:50:32
  and holistic approach is absolutely essential
• 1:50:34
  to guide a safe, effective, and sustainable return
• 1:50:37
  to play, ultimately protecting an athlete's career
• 1:50:39
  and their long -term joint health. This has been
• 1:50:41
  an incredibly comprehensive deep dive, truly
• 1:50:44
  unraveling the immense complexity of the shoulder.
• 1:50:47
  We've journeyed from its intricate anatomy and
• 1:50:49
  biomechanics right through to the diverse injury
• 1:50:52
  patterns seen in both overhead and contact athletes,
• 1:50:55
  and explored the nuanced, constantly evolving
• 1:50:58
  landscape of diagnosis and treatment. I feel
• 1:51:01
  we've moved far beyond a superficial understanding
• 1:51:03
  today, providing a framework for truly informed
• 1:51:06
  clinical decisions when faced with these challenging
• 1:51:08
  injuries. Indeed. And I think if there's one
• 1:51:11
  key takeaway for orthopedic professionals listening,
• 1:51:14
  it's that a deep understanding of the shoulder's
• 1:51:16
  interconnectedness, its role within the entire
• 1:51:18
  kinetic chain, is not just academic. It is absolutely
• 1:51:22
  paramount for effective practice. Because it
• 1:51:24
  allows for more precise diagnoses. Precisely.
• 1:51:26
  It helps identify those often mis -contributing
• 1:51:29
  factors, like subtle scapular dyskinesis or seemingly
• 1:51:33
  minor bony changes that can have major downstream
• 1:51:35
  effects. And ultimately it leads to the implementation
• 1:51:38
  of more effective, targeted, and often career
• 1:51:41
  -preserving interventions that truly address
• 1:51:43
  the unique demands and biomechanics of each individual
• 1:51:45
  athlete. It allows for more precise diagnoses,
• 1:51:48
  the identification of often missed contributing
• 1:51:51
  factors like scapular dyskinesis or subtle bony
• 1:51:54
  changes, and the implementation of more effective
• 1:51:57
  career -preserving interventions that truly address
• 1:52:00
  the unique demands of each athlete. Absolutely.
• 1:52:03
  Perhaps the biggest challenge for us as clinicians
• 1:52:05
  moving forward isn't just treating the injury
• 1:52:07
  we see on the scan or find in theater. It's about
• 1:52:10
  truly understanding and interpreting the unique
• 1:52:13
  athletic blueprint of each individual patient.
• 1:52:16
  That incredibly delicate balance of their innate
• 1:52:18
  constitutional factors like laxity, the acquired
• 1:52:21
  adaptations they've developed through years of
• 1:52:23
  sport, and their specific kinetic chain movement
• 1:52:26
  patterns. How do we continue to refine our ability
• 1:52:29
  to read that complex blueprint, not just so we
• 1:52:31
  can react effectively to injury, but so we can
• 1:52:33
  proactively support our athletes, manage their
• 1:52:36
  load, and guide them through the long, demanding
• 1:52:38
  arc of their careers and, importantly, beyond,
• 1:52:41
  into a healthy, active life afterwards. A powerful
• 1:52:44
  thought to consider indeed. How do we read that
• 1:52:48
  blueprint better? Thank you. If you found this
• 1:52:51
  deep dive insightful and valuable, please do
• 1:52:53
  take a moment to rate and share our deep dive
• 1:52:56
  with a colleague who might also benefit from
• 1:52:58
  these crucial insights. Professor Moimam, thank
• 1:53:01
  you so much for sharing your profound expertise
• 1:53:03
  and invaluable contributions to this incredibly
• 1:53:05
  detailed discussion today. It's been my pleasure.
• 1:53:07
  Thank you for having me. And to you, our listener,
• 1:53:10
  thank you for joining us on the deep dive. We
• 1:53:12
  encourage you to continue your own deep dives
• 1:53:15
  into knowledge. Until next time.