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