Latest / Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast. / Sports Injuries to the Shoulder and Elbow

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Sports Injuries to the Shoulder and Elbow · Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast.

0:00
Welcome to the deep dive. Just take a moment
0:02
and picture the incredible raw power, the whip
0:05
-like speed, and the astonishing precision needed
0:08
for overhead sports. Imagine a perfectly thrown
0:12
fastball scorching towards home plate, the sheer
0:15
devastating force unleashed in a professional
0:18
tennis serve, or the relentless fluid, almost
0:21
hypnotic motion of an elite swimmer cutting through
0:24
the water. Yeah, it's amazing to watch. It really
0:26
is, pushing the human body to its absolute limits.
0:29
But that same intensity, that same drive for
0:31
peak performance, places tremendous, almost unbelievable
0:34
stress squarely on two key joints. The shoulder
0:38
and the elbow. That's right. And for anyone involved
0:41
in these activities, whether you're an athlete
0:42
yourself, a coach, a parent, or maybe just someone
0:45
fascinated by the mechanics of the human body
0:47
under extreme load, understanding why and how
0:50
these joints are vulnerable is, well, it's absolutely
0:53
critical. Definitely. In this deep dive, we're
0:55
going to unpack the complex world of injuries
0:57
common in these overhead athletes. Our mission
1:00
today is to act as your guides. We've taken a
1:03
stack of detailed expert sources on this very
1:06
topic, and we're going to try and cut through
1:08
the complexity, extract the most important insights,
1:11
maybe some surprising facts, and the core knowledge
1:13
you need. We're here to provide you with a clearer
1:16
picture of the unique biomechanical challenges
1:19
these athletes face, the specific problems and
1:22
injury patterns that commonly arise, how they're
1:25
diagnosed using various tools, the range of treatment
1:27
options available both non -surgical and surgical,
1:30
and, crucially, the fundamental principles of
1:33
getting these athletes back to their sport through
1:35
rehabilitation. Exactly. We'll be covering the
1:38
full spectrum, drawing directly from the information
1:40
provided in the material we have here. We'll
1:43
start with the fundamental physics and mechanics
1:44
of how an overhead throw or motion even happens,
1:47
delve into the intricate anatomy and stabilizers
1:50
of the shoulder and elbow, and then zoom in on
1:53
specific issues you hear about, like tears in
1:55
the rotator cuff or the elbow's ulnar collateral
1:58
ligament, complex problems with the shoulder
2:00
labrum, like SLAP lesions, issues with how the
2:03
shoulder blade moves scapular dyskinesis, and
2:06
even conditions affecting the bone itself, like
2:09
osteolysis or OCD. Okay, so quite a range. All
2:11
right, let's jump right in and start with the
2:13
shoulder, because the forces it endures during
2:15
an overhead motion are, well, they sound nothing
2:18
short of astronomical. When we talk about overhead
2:22
throwing, we're not just talking about generating
2:23
speed. We're talking about incredibly rapid movements
2:26
that also have to be stopped. Right, the deceleration
2:29
part. Exactly. Think about the moment right after
2:32
the ball is released. The arm is still moving
2:34
at tremendous velocity, and all that kinetic
2:36
energy needs to be dissipated, absorbed by the
2:39
body. Okay. Experts estimate that during the
2:41
deceleration phase of a baseball pitch, the angular
2:44
deceleration at the shoulder can reach an astonishing
2:47
500 ,000 degrees per second squared. Half a million
2:50
degrees per second squared? That number is hard
2:53
to even wrap your head around. What does that
2:55
level of force actually mean for the body? It
2:57
means the structures around the shoulder Joint,
3:00
the muscles, tendons, ligaments, the capsule
3:02
are absorbing immense energy to slow the arm
3:05
down safely and controllably. It really brings
3:08
you back to foundational physics, doesn't it?
3:10
Like Newton's laws of motion. Absolutely. It's
3:13
not just abstract concepts. They're fundamental
3:15
to understanding these injuries in a practical
3:18
sense. Precisely. Take Newton's third law. For
3:22
every action, there is an equal and opposite
3:24
reaction. So when the muscles generate force
3:27
to accelerate the arm, the body experiences reactive
3:30
forces. When the muscles stop the arm, eccentrically
3:33
contract, the body experiences equal and opposite
3:36
deceleration forces. These forces are transmitted
3:39
through the joints and soft tissues. If the body
3:41
isn't equipped to handle them, or if they are
3:43
applied repetitively over and over, well, something
3:47
has to give eventually. So the shoulder isn't
3:49
operating in isolation then. It's part of a bigger
3:51
system, a chain. It's exactly right. This is
3:54
where the concept of the kinetic chain becomes
3:56
absolutely vital. Effective and importantly,
4:01
injury resistant overhead motion starts far away
4:04
from the shoulder itself. It begins with generating
4:07
power from the ground, the legs, the hips, and
4:10
particularly the trunk or the core. Okay. This
4:13
energy is transferred sequentially up through
4:16
the body to the arm. Think of it like cracking
4:18
a whip. The flick starts at the handle and the
4:20
speed builds exponentially towards the tip. So
4:23
if an athlete has weakness or maybe poor coordination
4:26
in their legs or core, that energy transfer is
4:28
inefficient. Does it break down? Exactly. If
4:30
the lower body and core aren't generating and
4:33
transferring enough force, or maybe if the timing
4:34
is off even slightly, the upper body, specifically
4:38
the shoulder and elbow, has to compensate. This
4:41
puts excessive stress on those later links in
4:44
the chain, forcing them to work harder than they
4:45
were designed to, especially during those high
4:47
-force acceleration and, crucially, deceleration
4:50
phases. And the shoulder blade, the scapula,
4:53
plays a unique role here too, I understand? A
4:55
crucial one. The scapula isn't just a static
4:58
bone. It's a dynamic part of the shoulder complex.
5:01
It needs to move in a coordinated way on the
5:04
rib cage protract, retract, rotate upward to
5:06
provide a stable base. Think of it as the launch
5:10
platform for the humerus, the upper arm bone.
5:12
Right, a platform. This stable platform allows
5:15
the humeral head, the ball of the shoulder joint,
5:18
to rotate through the extreme ranges of motion
5:20
required for overhead activities without putting
5:23
undue stress on the static stabilizers like the
5:26
ligaments and capsule. If the scapula's movement
5:29
or stability is compromised, a condition often
5:31
called scapular dyskinesis, the mechanics of
5:34
the main shoulder joint the glenohumeral joint
5:37
are disrupted, significantly increasing the risk
5:39
of injury. It makes sense. Now, experts often
5:42
break down the overhead throwing motion into
5:44
distinct phases to analyze the mechanics. It
5:46
happens incredibly fast, less than two seconds
5:48
total, apparently, but there's a lot going on
5:50
in that short time. There's tremendous complexity
5:53
packed into that brief window, absolutely. The
5:55
phases typically described are the windup, early
5:57
cocking, late cocking, acceleration, deceleration,
6:01
and follow through. The wind -up and early cocking
6:03
are really preparatory, getting the body and
6:05
arm into position. The arm elevates to about
6:08
90 degrees of abduction, maybe a bit more. Muscles
6:10
like the deltoid and the rotator cuff muscles,
6:13
supraspinatus, infraspinatus, teres minor, start
6:16
engaging. Late cocking feels like the point of
6:19
maximum load, almost like stretching a rubber
6:21
band to its limit. It really is. This phase culminates
6:25
in maximal external rotation at the shoulder,
6:27
often reaching 170 to an incredible 180 degrees
6:30
in elite throwers. At the same time, the scapula
6:33
retracts and rotates upwards, helping to stabilize
6:36
the shoulder in this extreme position. Critically
6:38
at this point, the humeral head actually translates
6:40
forward slightly on the glenoid socket. Muscles
6:43
like the supraspinatus, infraspinatus, and teres
6:45
minor are working intensely here, contracting
6:47
isometrically or slightly eccentrically, and
6:50
the subscapularis, a powerful internal rotator
6:52
at the front, starts preparing for the next phase,
6:55
building up elastic energy. Okay, then acceleration
6:57
is the explosive part, the release. You're right.
6:59
It's a very rapid transition from that eccentric
7:02
pre -stretch to powerful concentric muscle activity.
7:06
The shoulder internally rotates at tremendous
7:08
speed. The scapula protracts, moving forward
7:11
around the rib cage, maintaining that stable
7:13
platform as the arm whips forward. Big muscles
7:15
like the pectoralis major, latissimus dorsi,
7:18
and the serratus anterior are driving this explosive
7:20
motion. And then immediately you have to slam
7:22
on the brakes, stop all that momentum. That leads
7:25
into deceleration and follow through. Yes, and
7:28
these are arguably the most demanding phases.
7:31
biomechanically speaking. They rely heavily on
7:34
eccentric muscle contractions. That's muscles
7:36
lengthening while under tension to slow the arm
7:38
down safely and prevent injury. Right. Lengthening
7:41
under load. Experts consistently point to the
7:43
deceleration phase as having the absolute highest
7:46
forces acting on the shoulder joint. This is
7:48
when the rotator cuff, particularly the posterior
7:50
rotator cuff muscles like infraspinatus and teres
7:53
minor, is under maximum stress and most vulnerable
7:56
to injury due to that massive eccentric load.
7:59
So it's not throwing the ball that tears it,
8:01
it's stopping the arm after throwing? Very often,
8:04
yes. Or at least that's where the cumulative
8:05
damage really occurs. Any kinetic energy that
8:08
didn't efficiently transfer to the ball has to
8:11
be absorbed by the athlete's arm and body. And
8:14
if the core and lower body haven't efficiently
8:16
dissipated energy earlier in the kinetic chain...
8:19
Then the shoulder and elbow take the hit? Precisely.
8:22
The forces landing on the shoulder and elbow
8:24
become even greater here. Muscles like the teres
8:26
minor, posterior deltoid, and middle deltoid
8:29
are highly active in deceleration, working eccentrically.
8:33
The teres minor, a key posterior stabilizer,
8:36
actually shows some of the highest activity levels
8:38
of any shoulder muscle during this phase. Interesting.
8:41
This makes the posterior joint structures, the
8:43
back of the rotator cuff, the posterior capsule
8:46
particularly susceptible to injury during deceleration,
8:49
the torque, the twisting force on the humerus
8:52
during deceleration can reach values around 15
8:55
,000 inch pounds. 15 ,000 inch pounds. Can you
8:58
put that in perspective? Well, it's difficult
9:00
to make a perfect analogy, but imagine trying
9:02
to stop a 1 ,250 pound weight that's attached
9:06
to a one foot lever arm connected to your shoulder.
9:09
That's the kind of force those muscles are dealing
9:11
with, albeit very briefly. Wow. OK, that really
9:14
makes those deceleration forces tangible. So
9:16
what are the key structures actually holding
9:18
that joint together and allowing that incredible
9:21
motion under such extreme stress? You have both
9:25
static and dynamic stabilizers working together.
9:28
The static stabilizers are primarily the ligaments,
9:31
the joint capsule, and the labrum, that cartilaginous
9:33
rim around the socket. The interior gliohumeral
9:37
ligament complex, or IGHLC, is absolutely critical
9:40
for stability. The IGHLC, OK. Within this complex,
9:44
the anterior band of the IGHL is considered the
9:46
most important static restraint against anterior
9:49
instability, the shoulder sliding forward, especially
9:51
when the arm is abducted and externally rotated
9:54
to 90 degrees. Which is exactly the position
9:56
of peak stress and late cocking, right? Exactly.
9:59
In that position, the anterior band is tight.
10:02
Conversely, the posterior band of the IGHL is
10:05
tight in abduction and internal rotation, providing
10:08
posterior stability. And the axillary pouch,
10:11
the sort of hammock -like portion at the bottom,
10:13
also contributes to stability, particularly against
10:16
inferior translation. Can these ligaments get
10:18
stretched out or damaged just from repeated throwing?
10:21
Not necessarily a single big traumatic event
10:24
like a dislocation? Yes, absolutely. That's a
10:27
key point experts make. With a recurrent instability,
10:30
even if it's just micro instability or repeated
10:32
subluxations, that repetitive microtrauma and
10:35
cyclic overloading can cause plastic deformation
10:38
in the IGHL. Plastic deformation, meaning it
10:40
stretches and doesn't fully snap back? Precisely.
10:43
The ligament stretches slightly. and doesn't
10:45
fully return to its original length. Now, the
10:48
reported permanent stretch might sound small
10:50
in some studies, maybe less than a millimeter,
10:53
but even these seemingly minor changes in ligament
10:56
length and tension can significantly impact the
10:58
joint stability in kinematics over time. Research
11:00
has actually shown a direct positive linear correlation.
11:04
The longer the anterior band of the IGHL becomes,
11:08
the more external rotation is possible at the
11:10
shoulder, and importantly, the greater the anterior
11:13
translation, or forward sliding, of the humeral
11:15
head on the glenoid. So a little stretch leads
11:17
to a little more wobble, which can add up. What
11:19
about the dynamic stabilizers, the muscles? The
11:22
rotator cuff muscles are your primary dynamic
11:24
stabilizers. They do much more than just move
11:27
the arm. They work synergistically to actively
11:29
center the humeral head on the relatively small
11:31
and shallow glenoid socket. This crucial mechanism
11:35
is called concavity compression. Concavity compression?
11:38
Yes, by compressing the ball, humeral head, into
11:40
the concave socket, glenoid, and maintaining
11:42
a balanced force couple between the anterior
11:45
subscapularis and posterior infraspinatus teres
11:47
minor cuff muscles. The rotator cuff provides
11:50
dynamic stability throughout the entire range
11:52
of motion, preventing excessive translation or
11:55
shearing of the humeral head, especially during
11:57
high velocity movements. And we can't forget
12:00
the scapulothoracic muscles, the ones controlling
12:02
the shoulders. blade. They are absolutely essential
12:06
dynamic stabilizers too. If they are weak or
12:09
not firing correctly, leading to that scapular
12:12
dyskinesis we mentioned. The platform is unstable.
12:14
Exactly. The glenohumeral mechanics are compromised.
12:17
The rotator cuff has to work harder to compensate,
12:20
increasing its own risk of fatigue and injury.
12:22
Given these extreme forces and all this repetitive
12:25
motion, it's no wonder certain specific overuse
12:28
patterns develop, often described under the umbrella
12:30
of impingement. Right. And one key pattern specifically
12:33
seen in overhead athletes is internal impingement.
12:37
This is distinct from the classic subacromial
12:39
impingement you might hear about more often in,
12:40
say, older individuals with bone spurs. Internal
12:44
impingement happens within the joint itself.
12:46
OK. Inside the joint. How? Specifically, it occurs
12:49
when the undersurface, the articular side of
12:51
the posterior rotator cuff tendons, typically
12:54
the supraspinatus and infraspinatus, makes physical
12:57
contact with the posterior rim of the labrum
13:00
and the edge of the glenoid socket. When does
13:02
this contact happen? It happens during that position
13:05
of maximal abduction and external rotation, the
13:08
late cocking phase of throwing. So the rotator
13:11
cuff is literally getting pinched between the
13:13
humeral head and the back. top part of the socket
13:16
rim. Precisely. But it's the underside of the
13:18
cuff hitting the back top of the socket and labrum
13:21
in that extreme end range throwing position.
13:25
This repetitive contact, this microtrauma, can
13:28
lead to irritation, fraying, inflammation, and
13:31
eventually partial thickness tears developing
13:33
on the articular side of the rotator cuff. Oh,
13:36
OK. It can also cause damage to the posterior
13:38
superior labrum itself, often contributing to
13:41
or occurring alongside SLAP lesions, which we'll
13:43
get to. Internal impingement is strongly associated
13:46
with other factors like posterior capsule tightness
13:48
and some degree of anterior laxity, often linking
13:51
back to that GRD phenomenon. And the symptom
13:54
an athlete might feel from this? A classic symptom
13:56
is posterior shoulder pain. Pain felt deep in
14:00
the back of the shoulder, specifically reproduced
14:02
when the athlete's arm is placed in that late
14:04
cocking or early acceleration position. Experts
14:08
also note that muscle fatigue maybe later in
14:10
a game or practice, can lead to slight changes
14:13
in throwing mechanics and potentially increase
14:15
angular velocity, which could exacerbate the
14:18
severity of this impingement. No, there's also
14:20
a specific impingement pattern that happens down
14:22
at the elbow in throwers caused by those same
14:26
valgus forces we mentioned earlier. Yes, that's
14:29
valgus extension overload, or VEO. The repetitive
14:32
valgus stress of throwing that force, pushing
14:34
the forearm outward relative to the upper arm,
14:37
can over time lead to laxity or stretching of
14:39
the ligaments on the inside, the medial side
14:41
of the elbow, primarily the UCL. Now, as the
14:45
elbow straightens out rapidly during the throwing
14:46
motion, this increased valgus laxity allows the
14:50
back part of the ulna bone, the ulacranon process,
14:52
to repeatedly impact against the humerus bone
14:55
in the post remedial aspect of the joint. So
14:57
bone hitting bone in the back inside part of
15:00
the elbow. Exactly. This causes chronic irritation
15:03
and often leads to the formation of bone spurs,
15:06
or osteophytes, on the ulacranon. This post -permedial
15:09
older crannon impingement is noted in the sources
15:12
as being a very common surgical diagnosis in
15:14
baseball players. It causes pain, clicking, and
15:18
sometimes locking in the elbow. Another phenomenon
15:20
that seems strongly linked to all these throwing
15:22
mechanics is GRD, glenohumeral internal rotation
15:26
deficit. You see this talked about a lot with
15:27
throwers. Yes, GRD is almost an expected adaptation
15:30
you could say in many high level overhead athletes,
15:33
but it can definitely become pathological and
15:35
contribute to injury. It's generally defined
15:37
as a loss of internal rotation range of motion
15:40
in the throwing shoulder compared to the non
15:43
-throwing side. The cutoff varies slightly, but
15:46
it's usually considered significant if it's greater
15:48
than say 20 or 25 degrees difference. What's
15:50
the underlying cause? Why does the internal rotation
15:53
decrease? The primary cause experts point to
15:55
is tightness or contracture, developing in the
15:58
posterior capsule of the shoulder joint and potentially
16:01
the posterior band of the IGHL. Basically, the
16:04
tissues at the back of the shoulder get tight
16:06
and shortened from the repetitive stress of deceleration.
16:09
Okay, so the back of the shoulder gets stiff
16:11
or shortened. How does that actually affect the
16:14
movement, the kinematics? This posterior tightness
16:18
acts like a tether, and disrupts the normal mechanics,
16:21
especially during that critical leg cocking phase
16:23
where the arm needs to achieve maximal external
16:25
rotation. Because the back is tight, it restricts
16:28
the normal posterior glide of the humeral head.
16:31
So to compensate and still achieve the required
16:33
layback or external rotation, the humeral head
16:36
can be forced to shift abnormally, often posteriorly,
16:40
that's backwards and slightly upwards on the
16:42
glenoid socket. Okay, so it shifts into a slightly
16:45
different spot on the socket. Correct. And this
16:47
abnormal shift then puts increased strain and
16:50
stretching forces on the anterior capsule and
16:52
ligaments, particularly the anterior band of
16:54
the IGHL. Ah, so tightness in the back actually
16:57
leads to stretching and potentially laxity in
17:00
the front. That's counterintuitive. It is, but
17:02
that's exactly the mechanism proposed. And this
17:05
postural superior shift also has consequences
17:07
for the superior labrum and the biceps anchor
17:10
attachment right at the top of the socket. How
17:12
so? As the arm moves into maximal external rotation
17:15
with the humeral head shifted backwards and upwards
17:18
due to the posterior tightness, it can cause
17:20
the superior labrum, along with its biceps tendon
17:22
attachment, to literally peel away or lift off
17:26
the underlying glenoid bone. Okay. Experts call
17:30
this the peel back progression mechanism. This
17:33
specific mechanism is strongly implicated in
17:35
the development of those articular -sided rotator
17:37
cuff tears we talked about as the shifted head
17:40
impinges differently and critically in the formation
17:43
of SLAP lesions. Wow. So GRD isn't just a simple
17:47
lack of internal rotation. It actually sets off
17:49
this whole cascade, this chain reaction that
17:52
can damage multiple structures within the shoulder.
17:54
Precisely. It's a really key insight from the
17:57
biomechanics research. An adaptation, the posterior
18:00
tightness that allows for increased external
18:02
rotation needed for throwing, can become a pathological
18:05
mechanism that directly leads to injury, like
18:08
anterior stretching, the peel -back effect causing
18:11
SLAP tears, and altered contact patterns contributing
18:14
to cuff tears. That's fascinating. It's also
18:17
worth noting, as the sources point out, that
18:19
even with decreased internal rotation and the
18:22
commonly seen increased external rotation in
18:24
the dominant arm, the total arc of motion adding
18:27
IR and ER together, might actually remain the
18:30
same as the non -dominant side. So it represents
18:32
a complex adaptation, a shifting of the motion
18:35
arc, rather than just a simple loss of motion.
18:38
That's a great insight into how the body adapts,
18:40
but sometimes that adaptation clearly has negative
18:42
consequences down the line. This whole biomechanical
18:45
understanding really helps explain why certain
18:47
injury patterns are so common in these athletes.
18:50
Let's dive deeper into those specific injuries
18:52
now, starting with the rotator cuff itself. Right.
18:55
Rotator cuff problems in overhead athletes really
18:58
cover a spectrum from simple tendonitis and those
19:02
impingement symptoms we discussed all the way
19:04
to partial thickness and sometimes full thickness
19:07
tears of the tendons. Okay. A key point experts
19:10
make though is that the type of rotator cuff
19:12
tear often seen in throwers is distinct from
19:14
what you might typically see in say older less
19:17
active individuals with degenerative tears. How
19:20
so? Because of the repetitive tensile overload
19:23
during deceleration and that internal impingement
19:25
mechanism we just discussed, the most common
19:28
tears found in throwing athletes are partial
19:30
thickness tears located on the articular side.
19:33
That's the side facing inside the joint, the
19:35
underside of the tendon. Right from that pinching
19:37
during late cocking. Exactly. These are often
19:40
associated with internal impingement symptoms
19:42
and sometimes underlying instability. In contrast,
19:46
degenerative tears in older populations are more
19:48
often full thickness and tend to start on the
19:50
bursal side, the top side of the tendon. Another
19:53
key difference is that rotator cuff tears in
19:55
athletes can sometimes be secondary to underlying
19:58
shoulder instability, which isn't usually the
20:01
case in older degenerative tears. And the symptoms
20:03
an athlete might report if they have a rotator
20:05
cuff issue. Typically, it's diffuse shoulder
20:07
pain, often poorly localized, but particularly
20:11
bothersome during or after their overhead activity.
20:14
They might notice weakness, especially with movements
20:16
involving rotation or lifting the arm. And crucially
20:19
for a thrower, a common complaint is a noticeable
20:22
decrease in throwing velocity, or maybe a loss
20:25
of control or endurance. You mentioned SLAP pairs
20:27
being linked to that peel -back mechanism related
20:30
to GRD. Let's talk a bit more about those specifically.
20:33
Okay, so SLAP stands for Superior Labral -Anterior
20:37
-Posterior. These are tears that occur in the
20:40
top portion of the labrum, that fibrous ring
20:42
around the glenoid socket, that helps deepen
20:44
it and serves as an attachment site for ligaments
20:46
and the biceps tendon. Right, the rim cartilage.
20:49
Exactly. The superior labrum is precisely where
20:51
the long head of the biceps tendon attaches,
20:54
making this area particularly vulnerable to forces
20:56
transmitted through the biceps, especially peeling
20:59
or twisting forces during overhead motions like
21:01
throwing. The incidence figures for SLAT tiers
21:05
reported in the literature vary quite a bit,
21:07
maybe anywhere from 6 % up to 26 % in various
21:10
surgical series looking at shoulder problems.
21:12
Is diagnosing SLIP tear usually straightforward?
21:16
Actually, it can be quite challenging. One reason
21:18
is that the anatomy of the superior labrum and
21:20
exactly how the biceps anchor attaches to it
21:22
is highly variable from person to person. There
21:25
are normal variations like sublaboral recesses
21:27
or holes that can sometimes mimic a tear on imaging.
21:30
Okay, so MRI might be tricky. It can be. This
21:34
anatomical variability can make interpreting
21:36
imaging like MRI or MRA difficult. Sometimes
21:40
what looks like a tear might actually be a normal
21:42
anatomical variant like a sublaboral foramen
21:45
or the Buford complex. This is why arthroscopy
21:48
actually looking inside the joint with a camera
21:50
during surgery is often considered the gold standard
21:53
for definitively diagnosing and classifying SLA
21:57
tears. So you can see it directly. Exactly. During
22:00
arthroscopy the surgeon can visually inspect
22:02
the labrum, and importantly, use a probe to physically
22:05
assess the stability of the labrum and the biceps
22:07
anchor. They can even reproduce that peel -back
22:10
sign by positioning the arm in abduction and
22:12
external rotation to see if the labrum actually
22:15
lifts off the underlying bone, confirming instability.
22:17
So if the labrum peels away during that specific
22:20
test inside the joint, that confirms the instability.
22:23
Yes. Essentially, it verifies that the labrum
22:25
is detached and unstable in that critical throwing
22:28
position. And as we discussed, SLAP tears don't
22:32
usually happen in isolation. They are often associated
22:34
with other issues like internal impingement,
22:37
those partial articular -sided rotator cuff tears,
22:40
sometimes underlying shoulder hyperlaxity, and
22:42
that posterior capsule contracture related to
22:44
GRD, often via that peel -back progression mechanism.
22:48
Okay. Beyond just tears in the labrum or the
22:51
cuffed tendons, overall shoulder instability
22:53
is a major concern, particularly in young athletes,
22:55
isn't it? Absolutely. Shoulder instability exists
22:58
on a spectrum. At one end, you have a frank dislocation
23:02
where the humeral head completely separates from
23:04
the glenoid socket and usually needs to be put
23:06
back in place. Right. Less severe is subluxation,
23:09
which is a symptomatic partial translation of
23:11
the humeral head on the glenoid. Maybe shifts
23:13
part way out, but then pops back in spontaneously.
23:15
Yeah. Athletes might feel a clunk or a a sudden
23:18
sense of their shoulder giving out. Then there's
23:21
apprehension, which is more of a feeling or fear
23:23
of impending dislocation, often triggered when
23:26
the arm is put in the specific position where
23:28
they previously dislocated or subluxed classically.
23:31
that 90 degrees abduction combined with 90 degrees
23:35
external rotation position. The throwing position
23:37
again. Exactly. And finally, clinicians sometimes
23:40
describe the unstable, painful shoulder where
23:43
the main complaint might be pain during certain
23:45
movements, particularly when tested for apprehension,
23:49
but underlying that pain is evidence of instability
23:52
or associated pathology like a labral tear causing
23:55
the symptoms. And instability can be primary,
23:59
the first time it happens, or very commonly in
24:01
athletes, recurrent. Recurrent instability sounds
24:04
like it's just setting the stage for more and
24:06
more problems down the road. It definitely is.
24:08
Recurrent anterior instability, the shoulder
24:10
slipping forward, is particularly common in young
24:12
athletes, especially those involved in contact
24:15
sports like football, rugby, or wrestling. And
24:18
it has a notoriously high rate of happening again
24:20
after the initial event, especially if treated
24:23
non -operatively in that young, high -risk group.
24:26
it happens, it causes more damage. Exactly. Each
24:29
time the shoulder subluxes are fully dislocated,
24:32
it can cause progressive damage to both the bone
24:33
and the soft tissues. This includes bony damage.
24:37
A bankart lesion, which is essentially a fracture
24:39
or wearing away of the bone on the front lower
24:42
part of the glenoid rim where the labrum and
24:44
capsule pull off. Okay. And a hill -sax lesion.
24:47
which is an impaction fracture or dent created
24:50
on the back, outer part of the humeral head caused
24:52
when it impacts against the front edge of the
24:54
glenoid during the dislocation event. How is
24:57
the severity of that bone loss, say, on the glenoid
24:59
measured? Is there a threshold where it becomes
25:01
really problematic? Yes. Experts use imaging
25:04
like specialized X -rays, like the Brnagov view,
25:07
or more accurately CT scans to assess the size
25:10
and morphology of the bain -carte lesion or the
25:12
amount of glenoid bone loss. Significant glenoid
25:16
bone loss is often considered when it's greater
25:18
than about six millimeters wide, or represents
25:20
more than 20 -25 % of the total articular surface
25:23
width of the glenoid, which is typically only
25:25
about 24 millimeters wide to begin with. So losing
25:27
25 % is a big deal. It's a very big deal for
25:30
stability. Visually, during surgery, severe bone
25:34
loss can make the normally oval -shaped glenoid
25:36
look like an inverted pair, with the bottom front
25:39
portion missing. For Hillsac's lesions on the
25:42
humeral head, surgeons assess not just the size
25:44
but critically whether the defect is engaging
25:47
or off track. Engaging, meaning it catches. Yes.
25:51
It means that as the arm rotates externally,
25:53
the Hillsac's defect lines up with and actually
25:56
catches or drops over the front edge of the glenoid,
25:59
which dramatically increases the risk of future
26:01
instability and often necessitates addressing
26:03
the bone defect surgically. And is there a way
26:06
to predict the risk of the instability coming
26:08
back even after surgery, say, after a standard
26:11
bank heart repair? Yes. For anterior instability
26:13
treated with an arthroscopic bank heart repair,
26:15
which primarily fixes the soft tissues back to
26:17
the bones, experts use scoring systems like the
26:20
ISA score. That stands for the Instability Severity
26:23
Index score. ISA score. It's a 10 -point scale
26:25
that incorporates several predictive factors.
26:28
The athlete's age, being under 20, scores higher
26:31
risk points. whether they participate in competitive
26:34
contact sports or sports involving forced overhead
26:37
movements, if they have signs of generalized
26:39
joint hyperlaxity, if they have a visible hill
26:42
-sax lesion on their pre -op x -rays, and if
26:45
there's evidence of glenoid bone loss or erosion
26:47
of the glenoid contour. And a higher score means
26:50
higher risk of it failing. Exactly. A total score
26:53
greater than 6 points on the ISA scale is associated
26:56
with a significantly higher risk, potentially
26:58
around 70%, according to some studies of recurrent
27:01
instability after an isolated soft tissue bankart
27:04
repair. This score is really valuable because
27:06
it helps surgeons identify patients who might
27:08
benefit from a more robust procedure, perhaps
27:11
one that addresses bone loss up front, rather
27:14
than just a soft tissue repair alone. Makes sense.
27:16
What about instability that's not just in one
27:18
direction, like forward? Sometimes you hear about
27:20
shoulders being loose all over. Right, that's
27:22
generally termed multi -directional instability,
27:25
or MDI. It's often described by patients, quite
27:28
simply, as loose shoulder. It means the shoulder
27:32
is symptomatically unstable, feeling like it
27:34
slips or shifts in more than one direction, commonly
27:37
anteriorly forward, inferiorly downward, and
27:40
sometimes posteriorly backward as well. MDI is
27:44
usually linked to underlying factors like generalized
27:46
capsule or redundancy, meaning the joint capsule
27:49
is naturally looser or more voluminous than average,
27:52
or it could be part of a picture of constitutional
27:54
hyperlaxity throughout the body. Okay. Now, moving
27:57
slightly away from the main ball and socket joint,
27:59
what about problems up at the AC joint where
28:01
the collarbone meets the top of the shoulder
28:04
blade? Yes, the AC or acromioclavicular joint.
28:07
Injuries here are extremely common, particularly
28:09
in contact sports or activities where falls directly
28:11
under the point of the shoulder are frequent
28:13
football tackles, hockey checks, or falling off
28:16
a bike. The usual mechanism is a direct force
28:19
applied to the point of the shoulder, the acroman,
28:22
while the arm is tucked into the side, adducted.
28:24
This drives the acromion downwards and inwards
28:27
relative to the clavicle collarbone, which is
28:30
relatively stabilized by muscles and its connection
28:32
to the sternum. This force causes tearing of
28:36
the ligaments that support the AC joint, leading
28:38
to varying degrees of separation. And separate
28:40
from those traumatic AC joint sprains, there's
28:43
a specific bone issue that can affect the end
28:46
of the clavicle in some athletes, particularly
28:48
weightlifters. Yes, that's distal clavicular
28:50
osteolysis, or DCO. Experts in the sources particularly
28:55
note the atraumatic form, ADCO, meaning it occurs
28:58
gradually from overuse rather than a single traumatic
29:01
event. It's reported as being surprisingly prevalent
29:04
in dedicated weightlifters, with one study cited
29:06
showing a 27 % prevalence in that specific group.
29:09
Wow, over a quarter of them. What's happened
29:11
to the bone? It's characterized by chronic inflammation,
29:14
stress reaction, and eventually degeneration
29:17
or resorption of the bone at the very end of
29:19
the collarbone, right where it articulates with
29:21
the acromion. Imaging often shows changes like
29:24
bone erosion, cystic changes, and inflammation.
29:28
Sometimes there's even a direct communication
29:30
scene between the distal clavicle changes and
29:33
the AC joint itself. Importantly, it frequently
29:37
occurs alongside other shoulder problems like
29:39
instability or impingement, kind of adding insult
29:42
to injury and contributing to overall shoulder
29:44
dysfunction and pain, especially with pressing
29:46
movements. Okay. And finally, one more structure
29:49
around the biceps tendon, the long head specifically,
29:52
which originates near the top of the shoulder
29:54
socket. That can cause issues too. Correct. The
29:57
long head of the biceps tendon, or LHBT, runs
30:00
in a groove. the occipital groove, at the front
30:03
of the humerus bone. Its stability within that
30:05
groove relies on a complex sling -like arrangement
30:07
of ligaments and tendon fibers, often referred
30:10
to collectively as the biceps pulley system.
30:13
The pulley system, okay. This system is primarily
30:15
formed by parts of the superior glenohumeral
30:18
ligament, SGHL, the coracohumeral ligament, CHL,
30:22
and also contributions from fibers of the uppermost
30:25
subscapularis tendon and the anterior edge of
30:28
the supraspinatus tendon. If this pulley system
30:30
is injured, often due to trauma or associated
30:33
with rotator cuff tears, the biceps tendon can
30:36
become unstable. It can sublux, meaning partially
30:39
slip out of the groove, or even fully dislocate
30:41
from the groove. Does the direction the biceps
30:43
tendon moves, like forward or sideways, tell
30:46
you something about which specific parts of that
30:48
pulley system might be damaged? Yes, it can provide
30:51
important diagnostic clues. Experts describe
30:54
different patterns of LHBT instability. It might
30:57
sublux predominantly anteromedially, forward
30:59
and towards the body, or maybe post -trolaterally,
31:02
or even just shift back and forth and or posterior.
31:04
The direction of instability can correlate with
31:06
which specific components of the pulley system,
31:09
or which adjacent rotator cuff tendons, like
31:11
the supraspinatus or subscapularis, are torn.
31:13
For instance, an anteromedial dislocation of
31:17
the biceps tendon is often strongly linked to
31:20
a full thickness tear of the supraspinatus tendon.
31:23
and sometimes what are called hidden lesions
31:25
involving tears of the deep fibers of the corco
31:28
humeral and superior glenohumeral ligaments along
31:31
with the very top part of the subscapularis tendon
31:34
which form that medial wall of the pulley. Understanding
31:37
these specific patterns helps surgeons pinpoint
31:40
the full extent of the damage during diagnosis
31:42
and ensure all injured structures are addressed
31:44
during surgery. Okay, so from the extreme forces
31:47
to the kinetic chain, the interplay of stabilizers,
31:50
and these specific impingement patterns like
31:52
GRD and internal impingement, we can really see
31:55
how the shoulder is uniquely vulnerable in overhead
31:57
athletes. But as you mentioned, the elbow also
32:00
takes a tremendous beating in these sports. Let's
32:03
shift our focus down the arm a bit. What are
32:05
the most common elbow injuries we see highlighted
32:08
in the sources for these athletes? Well, one
32:10
condition that's quite specific to the throwing
32:12
elbow, particularly in younger athletes, adolescents
32:14
maybe, is osteochondritis diskin or OCD of the
32:18
capitolum. OCD of the capitellum. OK, what's
32:21
the capitellum? The capitellum is that rounded
32:24
bony knob at the end of the humerus, the upper
32:26
arm bone, specifically on the outer or lateral
32:29
side of the elbow. It's the part that articulates
32:31
or forms a joint with the head of the radius
32:34
bone in the forearm. Got it. And what causes
32:37
OCD there? Is it trauma? The suspected mechanism
32:41
in throwers isn't usually a single trauma, but
32:43
rather chronic repetitive direct loading or compressive
32:46
forces acting on the capitellum bone and its
32:49
overlying articular cartilage. As the elbow goes
32:52
through the throwing motion, particularly into
32:54
extension and maybe some pronation, the radial
32:57
head bone compresses up against the capitellum.
32:59
Okay. Because this compressive force is applied
33:01
repeatedly, at high velocity, and often with
33:04
some valgus stress as well, specifically in the
33:06
dominant throwing arm, it's thought to disrupt
33:08
the delicate blood supply to the subchondral
33:11
bone, the bone just underneath the cartilage
33:13
surface. This can lead to a segment of bone and
33:16
the overlying cartilage losing its blood supply,
33:18
potentially softening, becoming unstable, and
33:21
in some cases eventually loosening or even breaking
33:23
off as a fragment. And it's mostly just in the
33:26
throwing arm. Exactly. It's telling that this
33:28
condition is reported as being very rare on the
33:30
non -throwing side, strongly implicating those
33:32
repetitive throwing mechanics. What would someone
33:35
actually see on imaging, like an x -ray or MRI
33:38
for OCD? The findings on imaging vary a lot depending
33:42
on the stage of the condition. Early on, it might
33:45
just be a subtle area of decreased bone density
33:48
or a small area of haziness. a translucency seen
33:52
on x -ray. As it progresses, you might see a
33:54
more clearly defined fragment of bone, which
33:57
could still be attached but unstable, non -displaced,
34:00
or it might become completely detached and form
34:02
a loose body floating within the elbow joint.
34:05
Imaging, especially MRI, or sometimes CT orthography,
34:09
is really critical not just for making the diagnosis,
34:11
but also for staging the severity, looking at
34:13
the integrity and health of the overlying articular
34:16
cartilage, assessing whether the bone fragment
34:18
is stable or unstable, and identifying any associated
34:21
loose bodies. This dating is crucial for guiding
34:24
treatment decisions. Okay, now probably the most
34:27
A well -known elbow injury in throwing athletes,
34:31
largely because of the surgery named after the
34:33
baseball player, is the ulnar collateral ligament
34:37
tear, the UCL tear. Absolutely. The medial ulnar
34:40
collateral ligament, or MUCL as it's often abbreviated,
34:44
located on the inner side of the elbow, is the
34:46
primary victim here. As we discussed when talking
34:49
about valgus extension overload, the repetitive
34:51
high -force valgus stress generated during the
34:54
throwing motion puts tremendous tension specifically
34:57
on this ligament complex, particularly its anterior
35:00
bundle. Right, that outward force on the forearm.
35:03
Exactly. Injuries to the UCL can happen acutely,
35:06
maybe from a single, particularly forceful throw
35:08
where the athlete feels a pop in immediate pain,
35:11
indicating a sudden rupture of the ligament.
35:12
But perhaps more often, these injuries occur
35:14
on a background of chronic microtrauma. gradual
35:17
wear and tear again? Sort of. The ligament is
35:20
progressively overloaded with each throw, sustaining
35:23
multiple microscopic injuries over months or
35:25
years. This leads to gradual attenuation, stretching
35:29
and degeneration of the ligament tissue. Eventually
35:32
this chronic damage can culminate in a partial
35:35
or complete tear, sometimes with an acute event,
35:37
like one bad throw, being the final straw that
35:40
causes the already weakened ligament to fail
35:42
completely. What makes the MUCL so important
35:45
biomechanically for the elbow? Why is it so critical
35:48
for throwers? It's the primary static stabilizer
35:50
against valgus stress, particularly when the
35:53
elbow is moving through the range of motion between
35:55
about 30 and 120 degrees of flexion, which is
35:58
exactly the range used during throwing. Without
36:00
an intact and functional MUCL, the elbow joint
36:03
would essentially be unstable and tend to gap
36:06
open on the inside under the immense valgus forces
36:08
of throwing. But it's not the only thing providing
36:10
stability on that side. No, that's a very important
36:13
point. It's not the only thing. The flexor pronator
36:15
muscle group, which originates from the medial
36:17
epicondyle right near the UCL attachment muscles
36:20
like the flexor carpe ulnaris, FCU, and the flexor
36:23
agitorum superficialis, act as critical dynamic
36:26
stabilizers. Dynamic, meaning the muscles help
36:29
actively? Yes. They contract powerfully, especially
36:33
during the late cocking and acceleration phases
36:34
of throwing, helping to actively resist that
36:37
valgus force and thereby protect the passive
36:40
ligamentous structure, the UCL. If these dynamics
36:43
stabilizing muscles to teague or are weak, then
36:46
the static UCL structure has to take on even
36:49
more of that valgus load, increasing its risk
36:51
of injury. OK. Elbow dislocations, I assume,
36:53
are usually more sudden and traumatic events
36:55
compared to overuse UCL tears. Yes. Typically,
36:58
elbow dislocations are the result of a significant
37:00
trauma, most often a fall onto an outstretched
37:03
hand, what we often call a foosh injury. The
37:05
mechanism usually involves some combination of
37:08
axial load coming up the arm, a valgus force
37:10
pushing the elbow inward, and often some degree
37:13
of supination or palm up twisting of the forearm.
37:16
And are there different types? Yes. They can
37:18
be classified as simple. meaning only the ligaments
37:20
around the elbow are injured or complex, which
37:23
means there are associated fractures involved
37:25
as well. Common fractures seen with complex elbow
37:28
dislocations include fractures of the coronoid
37:30
process of the ulna or the radial head. What's
37:33
the most critical thing to assess right after
37:36
an elbow dislocation is put back in place, reduced?
37:40
Assessing the stability of the elbow joint after
37:42
the reduction is absolutely crucial. the clinician
37:45
will carefully move the elbow through a range
37:47
of motion, often under fluoroscopy, live x -ray,
37:50
to check for any signs of instability or resubluxation.
37:54
A key finding, according to the sources, is if
37:56
the elbow remains unstable and tends to sublux
37:58
or even re -dislocate when it's flexed between
38:01
approximately 45 and 60 degrees. Why is that
38:03
45 -60 degree range so important? Because instability
38:07
in that mid -range of flexion typically indicates
38:09
severe ligamentous damage, often involving not
38:12
just the medial side, UCL, but also disruption
38:15
of the lateral collateral ligament complex, UCL,
38:18
on the outside, which is critical for preventing
38:20
post -relateral rotatory instability. This level
38:24
of instability usually requires surgical intervention
38:27
to repair the damaged ligaments and restore stability.
38:29
Without adequate stability, you simply can't
38:33
start the necessary early range of motion exercises
38:35
needed to prevent debilitating long -term stiffness,
38:38
which is a major risk after elbow dislocations.
38:41
Right. Stiffness is a big problem for elbows.
38:43
And just revisiting VEO syndrome quickly, we
38:45
talked about the post remedial impingement aspect,
38:47
the bone spurs, but it's also considered a syndrome
38:50
of overuse itself, separate from an acute UCL
38:53
tear. Right. While the underlying mechanism involves
38:56
those same valgus overload forces, VEO syndrome
38:59
is really conceptualized as the chronic condition
39:01
that develops over time from repetitive throwing.
39:03
It manifests not just as potential medial elbow
39:07
laxity due to stretching or micro -damage of
39:09
the emusial over time, but also, very commonly,
39:12
involves that painful post -romedial impingement.
39:15
That's caused by the repeated forceful contact
39:18
between the oligacranone process of the ulna
39:20
and the humerus during full extension, leading
39:22
to inflammation and eventually the formation
39:25
of those characteristic osteophytes, or bone
39:27
spurs, in the back, inside part of the elbow.
39:30
And as noted earlier, the symptoms from this
39:33
post -trimedial older cranial impingement related
39:35
to VEO are reported as being a very common reason
39:38
for elbow surgery in professional baseball players.
39:40
OK, so we've covered the demanding mechanics
39:42
and the resulting catalog of potential injuries
39:44
in both the shoulder and the elbow. Now, how
39:47
do clinicians actually piece all this together?
39:49
How do they figure out exactly what's wrong with
39:51
a specific athlete presenting with shoulder or
39:53
elbow pain? What tools are in their diagnostic
39:56
toolkit? Well, the absolute foundation. the real
39:59
cornerstone of diagnosis, is always starting
40:01
with a thorough history and a comprehensive physical
40:04
examination. You simply have to talk to the athlete
40:07
and examine them carefully. What kind of things
40:09
in the history are most important? You need to
40:11
understand how the injury occurred. Was there
40:13
a specific event, a pop, a fall, or did it come
40:17
on gradually over time? What position was the
40:19
arm in when it started hurting? Has this happened
40:22
before? And then really drilling down on the
40:25
exact nature and timing of their symptoms? When
40:28
does it hurt? What makes it worse? What makes
40:31
it better? Is the primary symptom pain? Is it
40:34
instability, a feeling of looseness or giving
40:36
way? Is it weakness? Is it stiffness? Where exactly
40:40
is the pain located? Does it hurt during late
40:42
cocking? During acceleration? During follow through?
40:45
After activity? All these details from the athlete's
40:48
story are critical clues. Then comes the physical
40:50
exam, where the clinician systematically looks
40:53
at the shoulder and elbow, comparing it to the
40:55
uninjured side. They'll assess active and passive
40:58
range of motion, measure muscle strength, palpate
41:01
carefully for specific areas of tenderness, and
41:03
then perform a whole battery of specific clinical
41:06
tests designed to stress or evaluate the integrity
41:09
and function of different structures, ligaments,
41:12
tendons, the labrum, joint stability. They'll
41:15
also look for things like muscle atrophy, or
41:17
wasting, or any visible asymmetry. And experts
41:20
also stress the importance of evaluating the
41:22
cervical spine, the neck, early on, especially
41:25
if the pain is radiating, as pain from neck problems
41:27
can sometimes be referred down to the shoulder
41:29
or arm and mimic shoulder pathology. Right, rule
41:32
out the neck first. And there are dozens, maybe
41:35
hundreds, of specific physical exam tests described
41:37
for the shoulder, right? It seems quite complex.
41:40
There are many. and each is designed ideally
41:42
to try and isolate or stress a particular structure
41:45
or test a specific function. For example, the
41:49
scapular pinch test assesses the strength and
41:51
endurance of the scapular tractor muscles that
41:53
control the shoulder blade. The sulcus test checks
41:56
for inferior laxity or downward instability by
42:00
pulling down on the arm and looking for a gap
42:02
below the acromion. The clunk test, often performed
42:05
with the arm overhead and being rotated, is one
42:08
test used to try and detect certain types of
42:10
labral tears or instability. The load and shift
42:13
test is where the examiner manually tries to
42:15
slide the humeral head forward and backward on
42:17
the glenoid socket to assess the amount of anterior
42:19
and posterior laxity or translation. And the
42:22
apprehension test. The apprehension test. where
42:25
the arm is passively moved into that provocative
42:27
90 degrees abduction in external rotation position,
42:30
is key for assessing anterior instability. Does
42:33
it reproduce the patient's feeling of instability
42:35
or fear of dislocation? And the relocation test
42:38
follows that, where the examiner applies a posterior
42:40
force to the humeral head while in the apprehension
42:43
position. If this pressure relieves the apprehension
42:46
or pain, it further supports anterior instability
42:49
as the cause. What about testing the rotator
42:52
cuff? For the rotator cuff, tests like the liftoff
42:54
test or the belly press test specifically assess
42:58
the subscapularis tendon at the front. Resistant
43:01
external rotation tests, the infospinatus and
43:03
teres minor at the back, and tests like the empty
43:06
can or full can test evaluate the supraspinatus
43:09
tendon at the top. Although the specificity of
43:11
some of these tests is debated, manual muscle
43:14
testing quantifies strength in different planes.
43:16
And impingement tests? Impingement tests, like
43:18
the nearest sign, passively forcing the arm into
43:21
forward elevation, and the Hawkins test, passively
43:24
forcing the arm into internal rotation while
43:26
elevated, aim to provoke pain by mechanically
43:29
narrowing the subacromial space. The Yoakum test
43:33
is another variation, and that hyperexternal
43:35
rotation test we mentioned earlier specifically
43:38
helps assess for posterior superior labral issues
43:42
and internal impingement by stressing that extreme
43:45
late cocking position. You mentioned watching
43:47
the scapula move earlier as being important.
43:49
Is that formally part of the physical exam? Oh,
43:52
absolutely. Observational assessment of scapular
43:54
kinematics, how the shoulder blade moves during
43:56
arm elevation and lowering, is considered crucial.
43:59
Clinicians look specifically for signs of scapular
44:01
dyskinesis abnormal movement patterns like excessive
44:04
winging of the medial border or perhaps decreased
44:07
upward rotation or maybe excessive shrugging
44:09
during arm elevation. And can you test if correcting
44:11
the scapular motion helps? Yes, a key diagnostic
44:15
technique mentioned in the sources is using dynamic
44:17
corrective maneuvers. This involves having the
44:20
athlete perform the painful movement, like raising
44:22
their arm, while the examiner manually assists
44:25
in stabilizing or positioning the scapula correctly,
44:28
for example, manually assisting upward rotation
44:31
or preventing winging, like the sternal lift
44:33
technique described. If the athlete's pain or
44:36
symptoms significantly improve with this manual
44:39
correction of the scapular motion, it strongly
44:41
suggests that the abnormal scapular mechanics
44:43
are a major contributing factor to their problem,
44:47
which then directly guides the focus of rehabilitation.
44:49
That makes a lot of sense. And are there specific
44:52
physical tests for the elbow that are highlighted?
44:55
Yes. For the elbow, careful palpation along the
44:58
medial side for tenderness over the UCL attachment
45:00
or over the post remedial ocarina for VEO spurs
45:04
is important. Palpating along the occipital groove
45:06
at the front of the shoulder down towards the
45:08
elbow can sometimes reveal tenderness if there's
45:11
biceps tendon involvement extending down, though
45:14
as mentioned, it's not highly specific. What
45:16
about tests for the biceps or labrum originating
45:19
near the shoulder but causing elbow symptoms?
45:21
Tests like O 'Brien's test, resisted forward
45:24
flexion with the arm internally rotated, Speed's
45:26
test, resisted forward flexion with the palm
45:28
up, and your Gaston's test, resisted supination
45:31
with the elbow flexed, are traditionally used
45:33
to try and identify pathology involving the proximal
45:36
biceps tendon or the superior labrum. SLAP tears.
45:41
However, the sources note that these tests often
45:43
have variable sensitivity and specificity and
45:46
can be difficult to interpret reliably in isolation.
45:49
Some experts suggest that combining tests, like
45:51
performing the speeds test along with an uppercut
45:53
motion, resistant flexion with the fist moving
45:55
towards the chin, might be somewhat better at
45:57
differentiating true biceps pathology from SLAP
46:00
tears, but it remains challenging clinically.
46:02
And testing the UCL, the Tommy John ligament.
46:05
For assessing the integrity of the critical ulnar
46:08
collateral ligament. The primary test is the
46:11
valgus stress test. This is performed with the
46:14
elbow slightly flexed, usually around 20 -30
46:16
degrees, to unlock the bony stability and the
46:20
examiner applies an outward directed valgus force
46:22
to the forearm while stabilizing the upper arm.
46:26
They feel for any excessive gapping or laxity
46:28
on the medial side compared to the uninjured
46:30
elbow. The moving valgus stress test is another
46:33
dynamic test where a valgus stress is applied
46:36
while the examiner moves the elbow through an
46:38
arc of flexion and extension, looking to reproduce
46:40
the athlete's specific pain or sense of instability,
46:43
often felt in a particular part of the range.
46:46
Okay, so beyond the crucial hands -on history
46:49
and exam, imaging is usually the next step, providing
46:51
that visual look inside. But as you hinted, different
46:54
types of aging are best suited for looking at
46:56
different things, right? That's exactly right.
46:58
You usually start with basic radiographs, standard
47:01
x -rays. These are essential as a baseline for
47:03
identifying any obvious bony abnormalities like
47:06
fractures, including subtle bankart rim fractures
47:09
or hill -sax impaction fractures, assessing the
47:12
overall joint alignment, looking for signs of
47:14
arthritis or degenerative changes, evaluating
47:17
the AC joint for separation or arthritis. The
47:20
Zanka view is specifically good for the AC joint.
47:22
Looking for loose bodies. bone chips floating
47:24
in the joint, identifying osteophytes or bone
47:27
spurs, like in VEO, and helping to stage OCD
47:30
lesions in the capitalum based on bony changes.
47:33
X -rays are also crucial, of course, for confirming
47:35
that an elbow dislocation has been properly reduced.
47:38
What if you need more detail on the bone, say,
47:40
to measure the exact amount of glenoid bone loss
47:42
after dislocations or to get a better look at
47:45
a complex fracture? That's where CT scans, computed
47:48
tomography, particularly with 3D reconstructions,
47:51
become invaluable. CT provides the most detailed
47:54
assessment of bony anatomy and is considered
47:56
the gold standard for accurately quantifying
47:58
the extent and morphology of glenoid bone loss
48:01
and hill sacs lesions. This information is critical
48:04
for surgical planning, especially when considering
48:06
bone augmentation procedures like the Littarjet.
48:10
CT is also excellent for visualizing AC joint
48:12
displacement in multiple planes and for assessing
48:15
the changes seen in distal clavicular osteolysis.
48:19
And 3DCT reconstructions are very helpful for
48:21
planning surgery for complex OCD lesions, allowing
48:24
the surgeon to really understand the shape and
48:26
extent of the defect. Okay, so CT for bone detail.
48:29
What about the soft tissues, the ligaments, tendons,
48:31
the labrum, the cartilage? What's the best imaging
48:34
modality for those? For soft tissues, MRI magnetic
48:37
resonance imaging is generally the go -to modality.
48:40
It provides excellent visualization of the rotator
48:42
cuff tendons, showing tendinosis, partial tears,
48:44
full tears, the labrum around the glenoid, the
48:47
glenohumeral ligaments within the capsule, the
48:49
joint capsule itself, and the articular cartilage
48:51
covering the bone surfaces. Is standard MRI always
48:55
enough, or are there variations? For detecting
48:57
more subtle tears, especially the labrum or the
49:01
ligaments, or small partial tears of the rotator
49:03
cuff, MRA magnetic resonance orthography is often
49:07
preferred. This involves injecting gadolinium
49:10
contrast dye directly into the joint before the
49:12
MRI scan. The contrast fluid fills the joint
49:15
space and, importantly, seeps into any tears
49:18
or defects in the labrum, ligaments, or cuff
49:20
tendons, making them much easier to see. The
49:24
dye highlights the tears. Exactly. Experts and
49:27
the sources often recommend direct MRA, injecting
49:29
into the joint, as the diagnostic tool of choice
49:32
for evaluating the rotator cuff and particularly
49:34
the labrum in young athletic populations, as
49:36
it significantly increases the sensitivity and
49:39
diagnostic accuracy for these often subtle injuries
49:41
compared to non -contrasted MRI. MRA is also
49:44
very useful for assessing the integrity of the
49:46
UCL in the elbow and for visualizing the status
49:49
of the cartilage and detecting loose bodies in
49:51
cases of OCD of the capitalum. But even with
49:54
MRA, you mentioned earlier that diagnosing SLAP
49:57
specifically can still be tricky because of those
49:59
normal anatomical variations. Yes, that's a known
50:02
limitation and a common challenge. Even with
50:05
state -of -the -art MRI or MRA, it can sometimes
50:08
be difficult for radiologists to definitively
50:10
differentiate certain normal variations in the
50:12
superior labrum and biceps anchor attachment,
50:14
like a sublaboral foramen or Buford complex,
50:17
from a true pathological SLAP tear. This inherent
50:21
ambiguity on imaging is one of the main reasons
50:23
why arthroscopy, the minimally invasive surgical
50:26
procedure where a small camera is inserted directly
50:28
into the joint, is often still considered the
50:30
gold standard for definitively diagnosing and
50:32
classifying certain lesions, particularly SLA
50:35
tears, and also for evaluating the cartilage
50:37
surface and OCD of the capital. So seeing is
50:40
believing, essentially. Pretty much. Arthroscopy
50:43
allows the surgeon to directly visualize the
50:46
structures in question, magnify them, and use
50:48
a small probe to physically palpate them, assessing
50:51
their stability and tissue quality. They can
50:54
perform dynamic testing, like reproducing the
50:57
peel -back sign for acessilabed hair, and directly
51:00
assess the condition of the articular cartilage.
51:02
It removes much of the ambiguity that can sometimes
51:05
exist with imaging alone, although care must
51:08
still be taken by the surgeon to distinguish
51:10
true pathology from normal variants even during
51:13
arthroscopy. Are there any other imaging techniques
51:16
commonly used? Ultrasound is also mentioned as
51:19
being used, particularly for certain applications.
51:22
It has advantages like being relatively inexpensive,
51:24
portable, can be done in the clinic, non -invasive,
51:27
no radiation, and generally well tolerated by
51:29
patients. Musculoskeletal ultrasound is particularly
51:32
useful for evaluating rotator cuff tendon pathology,
51:35
looking for tendonitis, calcifications, partial
51:38
tears, or full tears. It's also very good for
51:40
assessing fluid collections, like in the subacromial
51:43
bursa. Can it be used for treatment, too? Yes,
51:45
it's excellent for guiding injections accurately
51:47
into specific locations like the subacromial
51:50
space, the biceps tendon sheath, or the AC joint.
51:53
It's also used by some clinicians to monitor
51:55
the healing of rotator cuff repairs after surgery
51:58
by visualizing the tendon integrity over time.
52:02
And the source has also mentioned it can be helpful
52:03
in assessing the superficial aspects of OCD lesions,
52:07
although MRI is generally better for overall
52:09
staging. And you mentioned earlier incorporating
52:11
the athlete's own perspective in the assessment
52:13
process. How is that done? Absolutely. Using
52:16
patient -reported outcome measures, or PROMs,
52:19
is increasingly recognized as being very important.
52:22
The source has mentioned tools like the Senane
52:24
score, that's the single -assessment numeric
52:26
evaluation. It's very simple. The patient is
52:28
just asked to rate their affected shoulder or
52:30
elbow function on a scale from 0%, worst possible,
52:33
cannot use the limb, to 100%, completely normal,
52:36
pre -injury level. OK, just one number. Just
52:39
one number. Giving a global sense of their perceived
52:41
function. Another tool mentioned is the PSFS,
52:45
the patient -specific functional scale. This
52:48
one is more individualized. The athlete identifies
52:51
up to three specific activities that are most
52:53
important to them but are currently difficult
52:55
due to their injury. Maybe it's throwing a baseball
52:58
at full speed, swimming a specific stroke without
53:01
pain, or lifting a certain amount of weight overhead.
53:03
Right, things relevant to them. Exactly. Then
53:06
they rate their current ability to perform each
53:08
of those specific activities on a scale of zero.
53:11
unable to perform the activity at all, to 10,
53:15
able to perform the activity at their pre -injury
53:17
level without any difficulty. These tools are
53:19
valuable because they directly capture the patient's
53:22
subjective experience and their perceived functional
53:24
limitations, which are vital pieces of the puzzle,
53:27
especially early in the diagnostic process and
53:29
for tracking progress over time. Okay, so putting
53:32
it all together, the detailed history, the thorough
53:34
physical exam with all those specific tests,
53:37
the targeted imaging like x -ray, CT, MRI, or
53:41
MRA, maybe ultrasound, and getting the athlete's
53:44
own functional rating clinicians can usually
53:46
arrive at a pretty accurate diagnosis. What are
53:49
the next steps then? Treatment. When is trying
53:52
non -operative management without surgery, the
53:55
right path to start on. Non -operative treatment
53:57
is typically the first line of management attempted
53:59
for many, if not most, shoulder and elbow conditions
54:02
in athletes, especially those that seem to be
54:04
related to chronic overuse or involve less severe
54:07
structural damage that doesn't necessarily require
54:09
surgical repair to heal or become stable. This
54:13
would include conditions like rotator cuff tendonitis,
54:16
milder forms of shoulder impingement, both subacromial
54:18
and internal, chronic distal clavicular osteolysis,
54:21
DCO, lateral epicompylitis, tennis elbow in the
54:25
elbow, and critically, as we mentioned, most
54:27
initial cases of multi -directional instability,
54:29
MDI, or general shoulder looseness. What does
54:32
that conservative non -operative treatment usually
54:34
involve? The core components generally include
54:36
a period of relative rest and significant activity
54:39
modification. This means substantially reducing
54:43
or temporarily stopping the specific activity
54:45
or movements that provoke the pain, like throwing,
54:48
swimming, or heavy lifting. Okay, stop irritating
54:51
it. Exactly. NSAID's nonsteroidal anti -inflammatory
54:55
drugs like ibuprofen or naproxen are often used
54:58
for a short course to help manage pain and reduce
55:00
inflammation, although their long -term use is
55:03
generally discouraged. Injections can sometimes
55:05
play a role in providing temporary relief and
55:08
aiding rehabilitation. Corticosteroid combined
55:10
with local anesthetic injections can be targeted
55:13
to specific areas like the subacromial space
55:15
for impingement, the AC joint, or around inflamed
55:18
tendons to calm down inflammation and break the
55:21
pain cycle. What about other types of injections
55:23
like PRP? The sources mention other types of
55:26
injections like hyaluronic acid, fisco supplementation,
55:29
or platelet -rich plasma PRP, but they also note
55:32
that the evidence supporting their effectiveness,
55:34
particularly for many shoulder and elbow conditions,
55:37
is still somewhat debated or evolving, and they
55:39
aren't universally recommended as first -line
55:42
treatments based on the material presented. For
55:45
certain elbow issues, like MUCL sprains or during
55:48
recovery from VEO, bracing might be used for
55:51
instance. A hinged elbow brace that limits full
55:53
extension might be employed to provide support
55:56
and protect the healing tissues during activities.
55:58
And physical therapy, I assume, is absolutely
56:00
central to any non -operative approach. Absolutely.
56:03
Physical therapy or physiotherapy is paramount.
56:06
It's really the cornerstone of effective non
56:09
-operative management. The specific goals are
56:12
always tailored to the individual athlete and
56:14
their specific injury. But broadly speaking,
56:16
PT focuses on several key areas. Restoring normal,
56:20
pain -free range of motion is often a primary
56:22
goal. Improving flexibility is crucial. especially
56:26
addressing any specific tightness identified,
56:29
like that posterior capsule contracture contributing
56:31
to GRD enthrowers, strengthening the key muscle
56:34
groups responsible for stability and controlled
56:36
motion is vital. This includes the rotator cuff
56:39
muscles, the scapular stabilizing muscles like
56:42
the serratus anterior, rhomboids, trapezius,
56:44
and importantly, strengthening the core and lower
56:46
body musculature to improve the efficiency of
56:49
that entire kinetic chain. Right, fix the chain.
56:52
Exactly. And enhancing neuromuscular control
56:54
and coordination, essentially retraining the
56:56
brain and muscles to work together smoothly and
56:58
efficiently, is also a major focus. Specific
57:02
stretching techniques mentioned in the sources
57:04
include the cross -body stretch, the sleeper
57:06
stretch, lying on the side and internally rotating
57:09
the arm, and other internal rotation or horizontal
57:12
adduction stretches, all designed to target that
57:14
posterior shoulder tightness associated with
57:16
GRD. For elbow conditions like lateral epicondylitis,
57:20
kinase elbow, eccentric training protocols, which
57:23
focus specifically on the muscle's ability to
57:25
lengthen under load, have demonstrated particularly
57:27
good results in research. Can you get a sense
57:30
during that initial assessment phase if someone
57:32
is likely to respond well to just physical therapy
57:35
and conservative care or if they're probably
57:37
heading towards surgery eventually? For certain
57:39
conditions, yes, there might be some predictive
57:41
factors. For instance, experts note that for
57:44
internal impingement of the shoulder, certain
57:46
findings during the physical examination can
57:49
help predict the likelihood of success with non
57:51
-operative management. These might include the
57:54
specific pattern of pain reproduction with resisted
57:56
arm movements like abduction or forward flexion,
58:00
the athlete's baseline scapular position and
58:02
their ability to control it during arm motion,
58:04
and perhaps their ability to sustain rotator
58:07
cuff strength, particularly at 90 degrees of
58:09
abduction. If these factors look favorable, the
58:12
prognosis with rehab might be better. And for
58:15
MDI, that generalized loose shoulder. You mentioned
58:17
earlier that therapy is strongly recommended
58:19
as the primary approach there. Yes, absolutely.
58:22
For multidirectional instability, the sources
58:24
emphasize that non -operative treatment, focusing
58:27
intensely on strengthening the dynamic stabilizers,
58:30
the rotator cuff and the scapular muscles, and
58:33
improving neuromuscular control and proprioception
58:35
is strongly recommended as the primary treatment
58:37
strategy. The goal is to improve the muscular
58:40
control and stability around the joint to compensate
58:43
for the underlying capsular laxity. Experts explicitly
58:47
state in the material that thermal capsulorophy,
58:49
an older surgical technique that used radio frequency
58:52
heat to try and shrink the redundant joint capsule,
58:55
is not recommended for MDI due to unacceptably
58:58
high rates of failure, recurrence of instability,
59:01
and potential complications like nerve injury
59:03
or cartilage damage. So PT is really the mainstay
59:06
for MDI. So non -operative treatment is often
59:08
the starting point, especially for overuse issues
59:11
or less severe injuries. When does surgery become
59:14
the necessary or recommended option? Surgery
59:16
is typically considered when a well -structured
59:18
and compliant non -operative treatment program
59:20
fails to adequately relieve the athlete's symptoms
59:23
and restore their desired level of function after
59:27
a reasonable period, usually at least three to
59:29
six months. or surgery might be indicated more
59:32
acutely if the injury involves significant structural
59:35
damage that is unlikely to heal on its own and
59:38
poses a clear risk of ongoing instability, progressive
59:40
damage, or functional limitation. This would
59:44
include things like symptomatic large partial
59:46
thickness, greater than 50 % thickness, or full
59:50
thickness tears of the rotator cuff tendons,
59:52
especially in younger active individuals. It
59:55
includes significant shoulder instability, particularly
59:58
traumatic interior dislocations in young, high
1:00:01
-risk athletes that keep recurring despite attempts
1:00:04
at rehabilitation. Symptomatic bony lesions that
1:00:08
cause mechanical problems, like large, engaging
1:00:10
hillsacks defects or significant glenoid bone
1:00:13
loss, often require surgical correction. Unstable
1:00:17
OCD lesions in the elbow with loose fragments
1:00:19
usually need surgery. And complete tears of critical
1:00:22
ligaments, like the elbow, UCL, that result in
1:00:25
functional instability and don't respond adequately
1:00:27
to conservative care are also common surgical
1:00:30
indications in athletes. Let's go through some
1:00:32
of the specific surgical procedures mentioned
1:00:34
for the shoulder, starting again with the rotator
1:00:36
cuff tears in athletes. What are the typical
1:00:38
options there? The surgical options really depend
1:00:40
on the specific characteristics of the tear,
1:00:42
its size, thickness, location, and the quality
1:00:45
of the tendon tissue. For smaller partial thickness
1:00:48
tears, say less than 50 % of the tendon's thickness,
1:00:52
particularly if they're causing impingement symptoms,
1:00:55
an arthroscopic debridement might be performed.
1:00:58
This essentially involves shaving or cleaning
1:01:00
up the frayed edges of the tear without actually
1:01:02
repairing it. Okay. For larger partial thickness
1:01:05
tears, generally considered more than 50 % thickness,
1:01:08
or for full thickness tears where the tendon
1:01:10
is completely torn through, surgical repair is
1:01:13
usually indicated, especially in active individuals.
1:01:16
This typically involves reattaching the torn
1:01:18
tendon back down to its bony insertion site on
1:01:21
the humerus, the greater tuberosity. This can
1:01:24
usually be done arthroscopically using suture
1:01:26
anchors placed into the bone. Occasionally, for
1:01:29
very large or complex tears, a mini -open technique
1:01:32
might be used. Is anything else done at the same
1:01:35
time, like addressing impingement? Sometimes
1:01:36
an acromioplasty, which involves shaving down
1:01:39
some bone from the underside of the acromion,
1:01:41
the bone forming the roof of the shoulder, might
1:01:43
be performed concurrently, particularly if there
1:01:46
are clear signs of subacromial impingement, like
1:01:49
a bone spur or associated changes in the corco
1:01:52
-chromial ligament contributing to the problem.
1:01:55
However, The routine use of a chromioplasty,
1:01:57
especially in the context of tears primarily
1:02:00
caused by internal impingement or instability
1:02:02
in athletes, is somewhat debated among surgeons.
1:02:05
Are there specific repair techniques mentioned
1:02:07
for larger tears? Yes. Experts mentioned advanced
1:02:11
arthroscopic techniques like the MPTOE repair,
1:02:14
which stands for medial portal, transoceous equivalent.
1:02:17
This is often used for full thickness tears that
1:02:19
are larger than about 10 millimeters in size.
1:02:21
The goal of this technique is to create a stronger
1:02:24
and more anatomical hair interface by using suture
1:02:27
anchors placed both medially closer to the joint
1:02:30
surface and laterally on the bone footprint,
1:02:33
creating a broader area of tendon to bone compression
1:02:35
that better mimics the natural tendon insertion
1:02:38
and potentially improves biomechanical load sharing.
1:02:41
Sounds complex, are there downsides? Like any
1:02:43
technique, it has potential pitfalls. The source
1:02:46
has mentioned concerns like potential failure
1:02:48
of the medial row anchors, if not placed securely,
1:02:51
or a possible purse string effect where overtightening
1:02:54
the sutures could constrict blood flow to the
1:02:56
tendon edge. But regardless of the specific repair
1:02:59
technique used, a critical point that experts
1:03:01
emphasize repeatedly is that athlete noncompliance
1:03:05
with the lengthy and strict post -operative rehabilitation
1:03:08
protocol is a major risk factor for surgical
1:03:11
failure and re -tear. even if the initial repair
1:03:14
was technically perfect. Rehab is key. Now what
1:03:17
about surgery for those tricky SLA peers we discussed?
1:03:20
When is that done and how? Surgery for SLAP tears
1:03:22
is generally considered for symptomatic unstable
1:03:25
tears, typically those classified as type 2,
1:03:28
where the superior labrum and biceps anchor are
1:03:30
detached from the glenoid rim, or more complex
1:03:32
types, especially in athletes who haven't improved
1:03:34
sufficiently with a course of physical therapy
1:03:36
focused on addressing associated issues like
1:03:38
GRRD or scapular dyskinesis. And what does the
1:03:41
surgery involve? The standard procedure involves
1:03:44
arthroscopically repairing the torn labrum back
1:03:46
to the bone. The surgeon will first abride, or
1:03:49
clean up, the frayed edges of the torn labrum
1:03:52
and then prepare the bony surface of the glenoid
1:03:54
rim underneath it to create a bleeding surface
1:03:56
that promotes healing. Then, small suture anchors
1:04:00
loaded with strong sutures are placed into the
1:04:02
bone along the glenoid rim. These sutures are
1:04:05
then passed through the torn labrum and the base
1:04:07
of the biceps anchor and tied down securely,
1:04:10
compressing the labrum back onto the prepared
1:04:12
bone bed. Are there any nuances in how the repair
1:04:15
is done? Yes, surgeons often prefer using multiple
1:04:19
smaller anchors rather than fewer larger ones
1:04:21
to create a broader area of fixation. They are
1:04:24
also typically careful about anchor placement,
1:04:27
particularly avoiding placing anchors too far
1:04:29
anteriorly and superiorly as this could potentially
1:04:32
over -constrained the biceps tendon or alter
1:04:34
its normal excursion, leading to post -operative
1:04:37
stiffness or pain. And critically, if there are
1:04:39
any other associated injuries found during the
1:04:41
arthroscopy, like other labelled tears elsewhere
1:04:43
around the rim or concurrent rotator cuff tears,
1:04:46
those are usually repaired during the same surgical
1:04:48
procedure. Is repair always the answer for SLAP
1:04:52
tears? What about that biceps tenodesis you mentioned?
1:04:55
biceps tenodesis, which involves detaching the
1:04:57
long head of the biceps tendon from its origin
1:04:59
on the superior labrum and reattaching it surgically
1:05:03
to the humerus bone lower down, outside the joint
1:05:05
is presented as a viable alternative option in
1:05:08
certain situations. It might be considered for
1:05:10
failed SLAP repairs, for SLAP tears that extend
1:05:13
significantly into the biceps tendon itself,
1:05:16
classified as type 40 tears, or often in older
1:05:18
athletes, say over 40, where the SLAP tear might
1:05:21
be more degenerative in nature and the primary
1:05:23
pain generator might be the biceps tendon itself
1:05:26
rather than just the labral instability. Okay.
1:05:28
And for contact athletes with both instability
1:05:30
and a SLAP tear. For contact athletes presenting
1:05:33
specifically with anterior shoulder instability
1:05:35
and a concomitant SLAP tear, some experts mentioned
1:05:39
in the sources advocate for earlier arthroscopic
1:05:41
intervention to repair both the anterior labrum,
1:05:44
bank cart lesion, and the SLAP lesion simultaneously,
1:05:47
along with addressing any other associated injuries
1:05:49
found, aiming for a quicker and more stable return
1:05:52
to their high -demand sport. Makes sense. Now,
1:05:55
how about the surgical approaches for shoulder
1:05:57
instability itself? Especially when there's that
1:06:00
significant bone loss we talked about. A simple
1:06:03
bankart repair isn't always enough, then. That's
1:06:05
correct. For anterior shoulder instability, that
1:06:08
is primarily due to soft tissue damage, a tear
1:06:11
of the anterior labrum and stretching of the
1:06:13
capsule, a bankart lesion, and where there is
1:06:15
minimal or no significant glenoid bone loss,
1:06:18
generally considered less than 20 -25%. A standard
1:06:21
arthroscopic bank heart repair is often the procedure
1:06:23
of choice. This involves using suture anchors,
1:06:26
similar to SLAP repair, to reattach the torn
1:06:29
labrum and tighten the stretched anterior capsule
1:06:31
back to the front rim of the glenoid. But when
1:06:34
there is significant bone loss? When there is
1:06:36
significant glenoid bone loss, more than 20 -25%.
1:06:40
Or a large, engaging hill sacs lesion on the
1:06:42
humeral head, performing just a soft tissue percent.
1:06:46
Bancart repair alone has been shown to have a
1:06:48
very high failure rate, with recurrent dislocations
1:06:51
being common, particularly in young active athletes
1:06:54
playing contact or collision sports. In these
1:06:57
situations, osseous reconstruction procedures,
1:07:00
surgeries that address the bone deficiency are
1:07:02
often necessary to restore stability. What kind
1:07:05
of procedures? The latarjet procedure is perhaps
1:07:07
the most well -known and commonly performed for
1:07:09
significant anterior glenoid bone loss. It involves
1:07:12
surgically transferring the coracoid process,
1:07:14
which is a bony projection from the front of
1:07:17
the scapula that has strong muscles attached
1:07:18
to it and fixing it onto the deficient anterior
1:07:21
glenoid rim. This does two things. It creates
1:07:24
a bony buttress that physically blocks the humeral
1:07:26
head from dislocating forward. And the transferred
1:07:29
muscles also provide a dynamic sling effect when
1:07:31
the arm is abducted and externally rotated, further
1:07:34
enhancing stability. Okay, the Letarjet for glenoid
1:07:37
bone loss. What about the Hill -Sachs lesion
1:07:39
on the humeral head? For large hill -sax lesions
1:07:42
that are deemed to be engaging but maybe occur
1:07:44
in the setting of less severe glenoid bone loss,
1:07:46
a procedure called Rimpel -Sage might be performed,
1:07:49
often in conjunction with an arthroscopic bankart
1:07:52
repair. Rimpel -Sage involves arthroscopically
1:07:55
suturing the posterior rotator cuff tendon, infus
1:07:58
minatus, and the posterior capsule into the hill
1:08:00
-sax dinafect on the back of the humeral head.
1:08:03
This effectively fills the defect and prevents
1:08:05
it from catching or engaging on the front edge
1:08:07
of the glenoid during external rotation. For
1:08:10
cases with severe bone loss on both the glenoid
1:08:12
and humeral head, more complex bone grafting
1:08:15
procedures using bone taken from the patient's
1:08:18
iliac crest, hip bone, or allograft donor bone
1:08:20
might be required. These osseous reconstructions
1:08:23
generally require a different, often more cautious
1:08:26
rehabilitation approach compared to simple soft
1:08:28
tissue repairs. Okay. And quickly, what about
1:08:30
surgery for severe GRD or DCO if conservative
1:08:33
treatment fails? Yes. For significant GRD that
1:08:36
remain symptomatic and restrictive despite dedicated
1:08:39
stretching and physical therapy, a surgical posterior
1:08:42
capsular release can be performed arthroscopically.
1:08:45
This involves carefully cutting or releasing
1:08:47
the thickened posterior capsule to restore more
1:08:50
normal internal rotation range of motion. Studies
1:08:53
cited have recorded significant increases in
1:08:56
internal rotation gained after this procedure.
1:08:59
And for distal clavicular osteolysis, at DCO,
1:09:02
that continues to be painful and limit function
1:09:04
despite rest, activity modification, and other
1:09:07
conservative measures, surgical resection of
1:09:09
the very distal end of the clavicle, usually
1:09:11
the outer 5 -10mm, is performed to remove the
1:09:14
damaged inflamed bone and decompress the AC joint.
1:09:18
An arthroscopic approach, often done through
1:09:19
the subacromial space, is frequently pursued
1:09:22
by surgeons for this, allowing for quicker recovery
1:09:24
compared to an open approach. Alright, now shifting
1:09:27
down to elbow surgery. What are the surgical
1:09:29
options outlined for OCD of the capitellum, that
1:09:32
bone and cartilage issue? Surgical treatment
1:09:34
for OCD of the capitellum is really dependent
1:09:37
on the stage of the lesion, particularly its
1:09:40
stability and the condition of the overlying
1:09:42
cartilage. For very early, stable lesions where
1:09:46
the cartilage is intact, continued non -operative
1:09:49
management might still be attempted, sometimes
1:09:51
with adjuncts like lipis. low -intensity pulsed
1:09:54
ultrasound, which some research mentioned in
1:09:56
the sources suggests might potentially help shorten
1:09:59
the natural healing or repair period, although
1:10:02
evidence is limited. But if it's unstable or
1:10:04
loose? For unstable lesions, or those with detached
1:10:07
or loose fragments, or lesions that have failed
1:10:09
to heal with non -operative care, surgery is
1:10:12
usually necessary. Several options exist. Arthroscopic
1:10:15
drilling or microfracture involves creating small
1:10:18
holes in the underlying bone within the defect
1:10:20
to stimulate bleeding and hopefully promote some
1:10:22
fiber cartilage healing. However, the sources
1:10:24
suggest this has limited indications, maybe only
1:10:27
for very small, contained, early -stage lesions.
1:10:30
What about filling the defect? Bone peg graphs
1:10:32
are a technique described where small cylindrical
1:10:35
plugs of bone often harvested arthroscopically
1:10:38
or through a small incision from the patient's
1:10:40
own olochranon process, the bony point at the
1:10:42
back of the elbow, are used to fill the bony
1:10:45
defect beneath the unstable cartilage lesion,
1:10:48
providing structural support. The harvest site
1:10:51
in the olochranon typically regenerates bone
1:10:53
over time. Osteochondral mosaicplasty is another
1:10:56
option, particularly for slightly larger defects,
1:10:59
where plugs of healthy bone and its overlying
1:11:01
cartilage are harvested from a less critical
1:11:03
non -weight -bearing part of the patient's knee.
1:11:05
or sometimes the elbow itself, and transplanted
1:11:07
into the capitolar defect, like laying mosaic
1:11:09
tiles. What if the lesion is really large? For
1:11:12
large, extensive OCD lesions, especially if there's
1:11:15
significant cartilage damage or perhaps early
1:11:18
secondary osteoarthritis developing, more complex
1:11:21
reconstructive procedures like costal osteochondral
1:11:24
grafts might be considered. This involves harvesting
1:11:27
a larger piece of cartilage and underlying bone
1:11:29
from one of the patient's ribs and shaping it
1:11:31
to fit the defect. The sources mention a case
1:11:34
example where delayed treatment of a large OCD
1:11:36
lesion led to significant osteoarthritis, highlighting
1:11:39
the importance of timely intervention for better
1:11:41
outcomes. Okay. And the famous Tommy John surgery
1:11:45
for the UCL tear in the elbow, what does that
1:11:47
involve? Right. Ulnar collateral ligament reconstruction,
1:11:50
often called Tommy John surgery, is performed
1:11:52
for athletes, most famously baseball pitchers,
1:11:55
who have significant medial elbow instability
1:11:57
due to a complete or high grade partial tear
1:11:59
of the MUCL that has not responded adequately
1:12:03
to non -operative management and prevents them
1:12:05
from throwing effectively. The indication is
1:12:07
usually based on clinical exam findings. laxity
1:12:10
with valgus stress, especially between 45 -60
1:12:12
degrees, and confirmed by imaging like MRA. How
1:12:16
is the ligament reconstructed? The goal is to
1:12:18
reconstruct the torn ligament using a tendon
1:12:21
graft to replace it. The most commonly used graft
1:12:24
source is the palmaris lungus tendon, a small
1:12:27
tendon in the patient's own forearm, which is
1:12:30
functionally redundant for most people. If that's
1:12:33
not available or suitable, Other options include
1:12:35
using a portion of a hamstring tendon from the
1:12:38
leg, or sometimes using an allograft tendon from
1:12:40
a cadaver donor, like the Achilles tendon. Various
1:12:44
surgical techniques exist to secure the graft
1:12:46
tendon across the medial elbow joint, drilling
1:12:49
tunnels in the humerus and ulna bones in the
1:12:51
location of the original UCL attachment points.
1:12:54
Common techniques mentioned include the original
1:12:56
job technique, often using a figure of eight
1:12:58
graft passage, or newer techniques like the Dane
1:13:01
TJ which use interference screws for fixation
1:13:03
in the bone tunnels. What about the ulnar nerve
1:13:05
which runs right near there? That's a critical
1:13:07
consideration. The ulnar nerve runs in a groove
1:13:10
just behind the medial epicondyle, very close
1:13:12
to the UCL. Historically, the ulnar nerve was
1:13:16
often routinely transposed. surgically moved
1:13:19
to a different position, usually more anteriorly
1:13:22
during Tommy John surgery, to prevent potential
1:13:24
irritation or scarring around the nerve from
1:13:27
the surgery itself. However, experts in the sources
1:13:30
now generally recommend selective ulnar nerve
1:13:33
transposition. This means the nerve is only moved
1:13:35
if it was already symptomatic before surgery,
1:13:38
if it shows signs of instability, subluxing out
1:13:40
of its groove, or if it seems clearly at risk
1:13:43
during the ligament reconstruction. This selective
1:13:46
approach aims to avoid the potential complications
1:13:48
associated with nerve transposition itself, such
1:13:51
as neuropraxia, nerve bruising or temporary dysfunction,
1:13:54
or persistent nerve symptoms. Okay. And for those
1:13:57
unstable elbow dislocations after they've been
1:13:59
reduced, what's the surgical approach? If the
1:14:01
elbow remains significantly unstable, particularly
1:14:04
in that 45 -60 degree flexion range, after closed
1:14:07
reduction, surgical repair of the disrupted ligaments
1:14:10
is usually indicated. In the common posterolateral
1:14:13
dislocation pattern, the lateral -collateral
1:14:15
ligament, LCL complex, is often the primary structure
1:14:18
injured and requires repair back to its attachment
1:14:21
on the humerus to restore stability against gravity
1:14:23
and prevent recurrent sublixation. The medial
1:14:26
-collateral ligament, MUCL, may also be injured
1:14:28
and require repair, especially if there is significant
1:14:31
valgus instability as well. The goal of surgical
1:14:34
repair is to restore enough static stability
1:14:36
to allow for early controlled range of motion
1:14:38
exercises to begin shortly after surgery. Why
1:14:41
is early motion so important? Because the elbow
1:14:43
joint is notoriously prone to developing severe
1:14:46
stiffness and contracture if it's immobilized
1:14:48
for too long after an injury or surgery. Achieving
1:14:51
stability that permits early motion is absolutely
1:14:53
critical for preventing long -term functional
1:14:56
deficits. In rare cases of severe instability
1:14:59
where even ligament repair doesn't provide adequate
1:15:01
stability, temporary external fixation using
1:15:04
a frame outside the arm connected by pins drilled
1:15:07
into the humerus and ulna might be used for a
1:15:09
few weeks to hold the joint in a reduced position
1:15:12
while the soft tissues begin to heal, allowing
1:15:14
for some controlled motion through the fixator
1:15:16
hinge if possible. And finally, surgery for VEO
1:15:19
syndrome, those bone spurs causing impingement.
1:15:21
Surgical treatment for symptomatic valgus extension
1:15:24
overload syndrome typically involves arthroscopic
1:15:26
debridement. The surgeon uses minimally invasive
1:15:29
techniques to go into the back of the elbow joint
1:15:31
and remove the problematic osteophytes, bone
1:15:34
spurs, from the post remedial aspect of the olacranon
1:15:37
process and also remove any loose bodies within
1:15:40
the joint that might be causing mechanical symptoms
1:15:42
like clicking or locking. The goal is to relieve
1:15:44
the impingement. Importantly, if the chronic
1:15:47
valgus stress that led to the VEO has also resulted
1:15:50
in a significant symptomatic tear or insufficiency
1:15:53
of the MUCL, then UCL reconstruction is often
1:15:56
performed at the same time as the spur removal
1:15:58
to address the underlying instability component
1:16:01
as well. Okay, so that covers the main surgical
1:16:03
options. Now, whether an athlete has had surgery
1:16:06
or has been managed non -operatively, the recovery
1:16:08
process, the rehabilitation phase seems like
1:16:10
it's absolutely crucial for getting back to sport.
1:16:13
It cannot be stressed enough. Rehabilitation
1:16:15
is not just some passive part of the treatment.
1:16:18
It is arguably the most critical phase for determining
1:16:20
the ultimate success of the intervention. Experts
1:16:23
in the sources consistently highlight that athlete
1:16:26
noncompliance with the prescribed rehab program
1:16:29
or trying to rush the process is a major risk
1:16:32
factor for failure, re -injury, or a suboptimal
1:16:35
outcome, regardless of whether the initial treatment
1:16:38
was surgical or non -surgical. What are the general
1:16:40
principles guiding that rehab process? It must
1:16:43
be carefully structured. Yes. Rehabilitation
1:16:47
almost always follows a structured, phased approach,
1:16:50
with progression based on meeting specific criteria
1:16:52
related to healing time, pain levels, range of
1:16:55
motion, strength, and functionability, rather
1:16:57
than just following a strict calendar timeline.
1:17:00
Typically, it's divided into phases like the
1:17:02
acute early protection phase, the intermediate
1:17:05
strengthening and neuromuscular control phase,
1:17:07
and the advanced or return to play phase. What
1:17:09
happens in that early acute phase? The primary
1:17:12
goals in the acute phase are to protect the injured
1:17:14
or surgically repaired structures, control pain
1:17:17
and swelling using things like ice compression
1:17:19
elevation, and initiate gentle controlled range
1:17:22
of motion exercises to prevent stiffness and
1:17:25
maintain joint health. Early range of motion
1:17:28
is particularly critical for the elbow after
1:17:30
dislocation or surgery to try and prevent the
1:17:33
development of debilitating stiffness. Slings
1:17:35
are commonly used for support and protection
1:17:37
after shoulder injuries or surgery. Sometimes
1:17:40
specific types like external rotation slings
1:17:42
are used after certain rotator cuff or instability
1:17:45
repairs to offload the repaired tissues. Hinged
1:17:48
elbow braces are frequently used after elbow
1:17:50
surgery, like UCL reconstruction, or complex
1:17:53
dislocations to allow controlled motion within
1:17:55
a safe range while protecting the healing ligaments.
1:17:58
What kind of exercises are typically involved
1:18:00
in these different phases? In the acute phase,
1:18:03
basic exercises might include simple passive
1:18:05
pendulum swings for the shoulder to encourage
1:18:08
joint fluid movement without muscle activation,
1:18:11
gentle passive or active assisted range of motion
1:18:13
exercises within protected limits, and maybe
1:18:16
isometric exercises, muscle contractions without
1:18:18
joint movement. Specific stretching techniques
1:18:21
might be introduced early on to regain lost motion
1:18:24
or address identified tightness, like those sleeper
1:18:27
stretches or internal rotation stretches for
1:18:29
posterior capsule tightness in the shoulder.
1:18:31
And as they progress. As the athlete progresses
1:18:33
to the intermediate phase, the focus shifts towards
1:18:36
gradually restoring full range of motion and
1:18:38
initiating strengthening exercises. This usually
1:18:41
starts with low resistance using elastic bands
1:18:44
or light pulleys, targeting the rotator cuff
1:18:46
muscles, internal external rotation, abduction,
1:18:50
the deltoid, and critically, the scapular stabilizing
1:18:54
muscles, exercises like rows, protraction, retraction.
1:18:57
More advanced strengthening in the later intermediate
1:19:00
and advanced phases involves progressively increasing
1:19:02
resistance and complexity, incorporating exercises
1:19:05
like seated cable rows, various push -up progressions,
1:19:09
starting against a wall, then incline, then floor,
1:19:12
dumbbell exercises like flies or presses carefully
1:19:14
introduced, and more challenging tubing or cable
1:19:17
exercises targeting different muscle groups and
1:19:19
movement patterns. What about the rest of the
1:19:20
body? Crucially, Throughout all phases, rehabilitation
1:19:24
should incorporate core strengthening exercises
1:19:26
and lower body exercises like squats, lunges,
1:19:30
and gluteus activation exercises. Remembering
1:19:33
that kinetic chain concepts, a strong and stable
1:19:35
core and lower body are essential for efficient
1:19:37
energy transfer and reducing stress on the throwing
1:19:40
arm. Addressing specific muscle imbalances identified
1:19:43
during the assessment, like tightness in the
1:19:45
pectoralis minor muscle, which can pull the scapula
1:19:47
forward and contribute to altered mechanics,
1:19:49
is also an important part of comprehensive rehab.
1:19:52
And specifically for the throwing athlete who
1:19:54
wants to get back on the mound or the tennis
1:19:56
court or into the pool, the rehab must become
1:19:59
very sport -specific towards the end. Absolutely.
1:20:02
The final phases of rehabilitation must become
1:20:05
progressively more sports specific to prepare
1:20:08
the athlete for the unique demands of their activity.
1:20:11
Key principles reiterated by the experts for
1:20:14
throwing athletes include maintaining the necessary
1:20:16
functional range of motion, which might even
1:20:18
include preserving some of that adapted GRD pattern,
1:20:22
increased ER, decreased IR, seen in their dominant
1:20:24
arm, as long as the total arc of motion is symmetrical
1:20:27
to the non -dominant side and they have good
1:20:29
control. ensuring excellent muscle balance, strength
1:20:32
and endurance throughout the entire kinetic chain
1:20:34
is paramount. At achieving high levels of neuromuscular
1:20:37
control and proprioception, the joint sense of
1:20:40
position is critical for coordinated efficient
1:20:42
movement. What does that look like in terms of
1:20:44
exercises? The intermediate phase often involves
1:20:47
building strength and power through both open
1:20:50
chain hand -foot free and closed chain hand -foot
1:20:53
fixed exercises and starting to introduce basic
1:20:56
plyometric exercises like medicine ball throws,
1:20:59
rebounder work, to retrain explosive power and
1:21:02
reactive muscle firing. The advanced phase is
1:21:05
where the athlete truly prepares for a return
1:21:07
to their sport. This involves progressing from
1:21:09
light activity to increasingly intense sport
1:21:11
-specific drills, like initiating an interval
1:21:14
throwing program for baseball players or specific
1:21:17
stroke drills for swimmers. And scapula control
1:21:19
remains important throughout. Yes. Experts emphasize
1:21:22
that optimizing scapular control and ensuring
1:21:25
proper scapulohumeral rhythm, the coordinated
1:21:27
movement of the scapula and humerus, should be
1:21:30
a key determinant for deciding when an athlete
1:21:32
is ready and safe to begin a return to play throwing
1:21:35
or overhead activity program. The goals for clearing
1:21:38
an athlete to return to sport typically include
1:21:40
achieving full pain -free range of motion, demonstrating
1:21:44
strength and endurance that's close to their
1:21:45
baseline, or the uninjured side. often measured
1:21:48
ithokinetically, having static stability on clinical
1:21:52
testing, and exhibiting smooth, well -controlled
1:21:54
movement patterns during functional activities
1:21:56
and sport -specific movements. OK. So after going
1:22:00
through potentially months of this entire process
1:22:02
diagnosis, maybe surgery, definitely lengthy
1:22:04
rehab, The ultimate question for the athlete
1:22:07
is, when can I actually get back to competing?
1:22:09
And maybe more importantly, what are the chances
1:22:11
of me returning to the same level I was at before
1:22:13
the injury? Yeah, that's a million dollar question
1:22:16
for every injured athlete. And the answer is
1:22:18
that return to play timelines vary significantly
1:22:20
based on a lot of factors. The specific injury,
1:22:24
the type of treatment they had, surgical versus
1:22:26
non -surgical and which specific procedure, the
1:22:28
demands of their particular sport, their level
1:22:30
of competition, professional versus recreational,
1:22:33
and individual factors like age, adherence to
1:22:36
rehab, and biological healing response. It's
1:22:40
rarely a quick process, particularly after major
1:22:42
surgery for significant structural injuries.
1:22:45
Are there some typical timelines mentioned in
1:22:47
the sources for common procedures that give us
1:22:49
a ballpark idea? Yes, they do provide some examples,
1:22:52
but these should be seen as general guidelines.
1:22:54
For instance, after a SLAP repair surgery, return
1:22:58
to contact sports might be possible around the
1:23:00
three month mark. But for repetitive overhead
1:23:02
athletes like pitchers or swimmers, returning
1:23:04
to full sport activity typically takes much longer,
1:23:07
often cited as being over six months. And the
1:23:10
sources note that patient satisfaction rates
1:23:12
after SLAP repair can sometimes be lower for
1:23:15
chronic tears compared to acute traumatic tears.
1:23:18
What about rotator cuff repairs? For rotator
1:23:20
cuff repairs, especially in elite athletes like
1:23:23
professional baseball pitchers, the outlook can
1:23:25
be more guarded. Experts point out that reported
1:23:28
return to play rates back to their pre -injury
1:23:31
elite performance level have historically been
1:23:33
somewhat poor, although surgical techniques and
1:23:35
rehab protocols are continually improving. Osseous
1:23:39
shoulder reconstructions, like the latarget for
1:23:41
bone loss, might allow a return to some activities
1:23:44
around 2 -3 months, but returning fully to contact
1:23:47
sports likely takes longer. maybe six months
1:23:49
or more. Similarly, posterior shoulder instability
1:23:52
repair aiming for return -to -contact sports
1:23:54
is often targeted around the six -month mark.
1:23:58
Limited surgical resection for distal clavicular
1:24:00
osteolysis is one of the procedures with a potentially
1:24:04
faster return, with athletes possibly resuming
1:24:06
training within just one to two weeks if symptoms
1:24:08
allow. UCL reconstruction, the Tommy John surgery,
1:24:12
generally reports high rates of return to play
1:24:14
overall, but the time frame is notoriously lengthy,
1:24:18
often taking 12 months or even longer for pitchers
1:24:20
to get back to competitive pitching. Arthroscopic
1:24:23
treatment of VEO syndrome, removing those bone
1:24:25
spurs, also shows generally satisfactory results
1:24:28
in high return rates mentioned in the sources,
1:24:30
perhaps around 4 -6 months on average. Are there
1:24:33
factors that help predict who will do better
1:24:35
or worse in terms of returning to play? Yes.
1:24:38
Some prognostic factors are mentioned. For SLIP
1:24:41
tears, having other simultaneous injuries identified
1:24:44
during surgery, like a concurrent rotator cuff
1:24:47
tear or additional labral damage elsewhere, are
1:24:50
generally considered negative prognostic factors
1:24:52
associated with potentially less successful outcomes
1:24:55
or a more difficult return. For anterior shoulder
1:24:58
instability treated with a standard bankart repair,
1:25:01
that ISA score we discussed earlier is a valuable
1:25:03
tool for predicting the risk of redislocation,
1:25:06
which obviously impacts the ability to return
1:25:07
safely to high -risk activities. A higher ISA
1:25:11
score predicts a higher chance of failure and
1:25:13
may influence the initial surgical choice or
1:25:15
counseling about return to sport. It sounds like
1:25:18
while the science on the surgical techniques
1:25:20
and the rehab protocols are incredibly advanced,
1:25:22
the road back to peak elite performance can still
1:25:25
be a really significant challenge for some athletes,
1:25:27
depending on the specific injury and the demands
1:25:29
of their sport. It absolutely can be. Managing
1:25:32
the cumulative effects of chronic microtrauma
1:25:34
versus a single acute injury, dealing with the
1:25:37
complexities of certain surgical procedures,
1:25:39
and avoiding potential complications like...
1:25:42
nerve issues after some elbow surgeries, or stiffness,
1:25:44
or hardware problems after certain shoulder bone
1:25:46
procedures, and simply regaining the highly fine
1:25:50
-tuned neuromuscular control, confidence, and
1:25:53
power required at the elite level after a major
1:25:56
structural injury are all ongoing challenges
1:25:59
in sports medicine. It's not always straightforward.
1:26:02
This deep dive has really highlighted the incredible,
1:26:04
almost violent demands placed on the shoulder
1:26:06
and elbow in overhead sports, showing us exactly
1:26:09
why these specific and often complex injury patterns
1:26:11
occur. We've navigated through the diverse ways
1:26:14
these injuries are diagnosed, explored the wide
1:26:16
range of non -operative and surgical treatment
1:26:18
strategies available, and underscored the absolutely
1:26:21
non -negotiable importance of a dedicated, structured,
1:26:24
and highly tailored rehabilitation program to
1:26:27
even have a chance at successfully getting back
1:26:28
on the field. court or in the pool. It really
1:26:31
gives you a profound appreciation for the remarkable
1:26:34
engineering of the human body, capable of generating
1:26:37
such forces and velocities, but also its inherent
1:26:40
limitations when pushed consistently to its absolute
1:26:43
physical edges. And it highlights the constant
1:26:46
evolution of the science and medicine dedicated
1:26:48
to understanding these limits, helping athletes
1:26:50
recover, and hopefully finding better ways to
1:26:54
prevent these injuries from happening in the
1:26:55
first place. And thinking about the sheer magnitude
1:26:58
of those forces, the way chronic microtrauma
1:27:00
seems to inevitably build up over time in many
1:27:03
athletes, the way the body sometimes adapts in
1:27:06
ways that seem helpful but actually become harmful,
1:27:09
like GRD leading to peelback, and the fact that
1:27:12
even with the very best treatment available today,
1:27:15
returning to that pre -injury elite performance
1:27:17
level isn't always a guarantee. It definitely
1:27:20
leaves you with a provocative thought, doesn't
1:27:21
it? It certainly makes you wonder. in this relentless
1:27:24
pursuit of maximizing athletic performance pushing
1:27:28
boundaries harder, faster, stronger. Are these
1:27:31
kinds of debilitating joint injuries simply an
1:27:34
inevitable trade -off, the unfortunate but accepted
1:27:36
cost of competing at the highest levels in these
1:27:39
overhead sports? Or is it possible that a truly
1:27:41
perfected understanding of individual biomechanics,
1:27:44
maybe combined with predictive analytics, personalized
1:27:47
prevention strategies, and even more advanced
1:27:49
biological treatments in the future could one
1:27:52
day fundamentally shift that balance? Could we
1:27:54
reach a point where athletes can achieve these
1:27:56
incredible feats of power and precision without
1:27:58
necessarily paying such a long -term physical
1:28:01
toll on their shoulders and elbows. It's a fascinating
1:28:04
and critical question for the future of sports
1:28:06
and the long -term health of these dedicated
1:28:08
athletes.