Latest / Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast. / Advanced Shoulder Instability

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Advanced Shoulder Instability · Deep Dive Ortho — Orthopaedic Surgery, AI & Digital Health Podcast.

0:00
Did you know that even after just one shoulder
0:02
dislocation, a really significant number of patients
0:05
already show signs of bone loss? That's right.
0:08
There's a study by Griffith and colleagues. Quite
0:12
striking, really. They found galenoid bone loss
0:14
that's on the socket in 41 % of cases after a
0:17
first time dislocation. 41%. Wow. And presumably,
0:21
it gets worse if it happens again. Oh, dramatically
0:24
worse. That same study found the rate jumped
0:26
to 86 % in patients with recurrent dislocations.
0:30
And other research backs this up, showing significant
0:32
bone defects on both sides of the joint, the
0:35
socket and the ball, becoming almost the norm
0:37
in those chronic cases. And for younger active
0:40
people, that risk of it happening again, it's
0:43
incredibly high, isn't it? Disturbingly high.
0:45
Rates up to 96 % recurrence been reported for
0:49
young patients after a first traumatic dislocation.
0:52
It sets the stage for a cycle of instability.
0:54
So it begs the question, what happens when this
0:57
common painful injury just keeps coming back?
0:59
When it becomes this recurring nightmare causing
1:02
complex problems that the usual straightforward
1:05
fixes just can't seem to handle? That's the crux
1:07
of the issue we're exploring today. Welcome to
1:10
the deep dive. We're the show that aims to cut
1:12
through the jargon and extract the really crucial
1:15
insights from dense source material. Today, we
1:18
are digging into the complexities of shoulder
1:20
instability. And we're drawing heavily on some
1:23
very detailed clinical perspectives, particularly
1:26
from the book Complex and Revision Problems in
1:29
Shoulder Instability. Exactly. Our focus isn't
1:32
on a simple strain or first -time injury that
1:35
gets better easily. We're navigating the much
1:37
tougher terrain. Think significant bone damage,
1:41
specific patient factors making things trickier,
1:44
or situations where previous surgeries haven't
1:46
quite worked out. These are the scenarios that
1:48
demand more advanced thinking, more sophisticated
1:51
techniques. We want to understand why those standard
1:53
approaches sometimes fail and what the next level
1:56
of solutions actually involves. And exploring
1:59
that intricate landscape requires a clear view
2:01
of the evidence and the practicalities. Which
2:03
is why I'm delighted you're here to guide us.
2:06
Your expertise in synthesizing this complex medical
2:08
knowledge, connecting the dots between diagnosis,
2:11
treatment, and importantly, long -term patient
2:13
outcomes is exactly what we need. Happy to be
2:16
here and delve into it. Right. Let's kick off
2:18
with a quick rapid fire round just to set the
2:21
scene for our deep dive. Three quick questions.
2:24
Fire away. OK, first one. When a shoulder keeps,
2:27
you know, popping out, what's the fundamental
2:30
problem we need to consider beyond just tearing
2:33
ligaments? Well, while the ligaments in the capsule
2:36
are definitely injured initially, the critical
2:38
issue, especially with repeated instability,
2:41
is often damage to the bone. Specifically, bone
2:44
loss. Bone loss. Yes. Either from the glenoid,
2:47
the socket, or the humeral head, the ball. Losing
2:50
that bone fundamentally changes the joint shape
2:53
and its mechanics. It makes it inherently less
2:55
stable, irrespective of the soft tissues. OK,
2:57
so bone loss is absolutely central. Second question.
3:01
Why might an initial soft tissue repair, something
3:04
like a bank art repair, not be enough, especially
3:07
for certain people? The main reason they fail,
3:09
quite often, is that the underlying bone loss
3:12
wasn't fully appreciated or adequately addressed.
3:15
If you're missing a significant chunk of bone
3:17
from either side, just stitching the labrum back
3:19
on doesn't restore the joint's structural integrity.
3:22
Makes sense. And we know the risk factors for
3:24
failure pretty well, now being young, playing
3:26
high -demand contact sports, and critically having
3:29
pre -existing bone defects, even seemingly small
3:32
ones sometimes. These patients are much more
3:35
likely to fail a simple soft tissue fix. Right,
3:37
those factors really flag who might need a more
3:40
robust solution from the start. And final, rapid
3:42
fire. In orthopedic terms, what makes a shoulder
3:46
problem complex or needing revision? Okay, so
3:50
complex generally means your standard straightforward
3:52
treatments probably won't work. This could be
3:54
due to major bone loss, maybe the patient has
3:56
other conditions like epilepsy or connective
3:58
tissue disorder, or perhaps it's just a very
4:00
unusual injury pattern. And revision? Revision
4:03
means exactly what it sounds like. A previous
4:05
surgery to stabilize the shoulder has failed.
4:08
So now you're going back in. Operating on a joint
4:11
that's already been surgically altered likely
4:13
still has underlying problems, perhaps scar tissue.
4:16
It makes the second or even third attempt significantly
4:20
more challenging. That really clarifies the scope.
4:23
Complex and revision. It's not the simple stuff.
4:26
Yeah. Okay, let's settle in now for our first
4:29
proper segment. Let's really unpack the anatomy
4:31
first. Before anything goes wrong, how does a
4:35
healthy shoulder stay stable? It has such incredible
4:38
movement. How does it manage it? It's a fascinating
4:40
bit of biological engineering, actually. The
4:43
shoulder cleverly uses different mechanisms depending
4:45
on where the arm is. OK. So in the mid -range
4:48
of motion, think arm by your side, maybe slightly
4:50
out in front, but not at the extremes. Stability
4:53
mostly comes from non -ligamentous factors. Like
4:55
what? Two main things. One is the negative intra
4:58
-articular pressure. Basically, a suction or
5:00
vacuum effect within the joint capsule helps
5:02
hold the ball centered in the socket. A vacuum
5:04
seal, almost. Kind of, yes. And the other is
5:08
the concavity compression effect. This is where
5:10
the rotator cuff muscles actively pull the humeral
5:13
head, the ball, firmly into the concave glenoid
5:16
socket. Like pressing a ball into a perfectly
5:19
matched cup, the muscles provide the compression
5:22
force. Okay, so suction and muscle compression
5:25
keep it centered during everyday movements. What
5:27
about when you reach right up high or throw something?
5:30
The extremes of motion. That's when the passive
5:33
structures take over, primarily the capsule ligamentous
5:36
structures. The joint capsule itself and the
5:39
thickened bands within it called the glenohumeral
5:41
ligaments become taut. They tighten up. Exactly.
5:44
They act like check reins, physically stopping
5:46
the humeral head from sliding too far forward,
5:48
backward, or downward on the glenoid through
5:50
the end -range stabilizers. It's quite elegant,
5:52
really. Different systems for different jobs.
5:55
Now, let's bring it back to the injury. What
5:57
actually happens to these structures during a
5:59
traumatic anterior dislocation? It sounds quite
6:01
violent. Often is. A forceful anterior dislocation
6:05
typically tears the structures at the front and
6:07
bottom of the joint, the anteroinferior capsulutamentus
6:10
complex. So ripping the capsule and ligaments
6:12
there? Yes, and when this involved the labrum
6:15
tearing off the glenoid rim, that's what we commonly
6:17
call a bankart lesion. But, and this is a crucial
6:20
point from our source material, this event frequently
6:23
causes significant bone damage at the same time.
6:26
It's not just soft tissue. And that's where those
6:29
startling statistics you mentioned right at the
6:31
beginning come into play. It's not a rare thing
6:33
for the bone to be damaged. Not at all. The numbers
6:35
really drive it home. Griffith study again. 41
6:39
% glenoid bone loss after just a first dislocation.
6:42
It's happening right from the start in many cases.
6:44
Not just after years of problem. Precisely. And
6:47
after recurrent dislocations, that figure jumps
6:49
to 86%. Other studies, like Piasecki's, found
6:53
similarly high rates, 49 % to 89 % with glenoid
6:56
loss and an incredible 70 % to 100 % incidence
7:00
of damage to the humeral head, the ball, in recurring
7:02
cases. 100%. Almost everyone with recurrent dislocations
7:05
has damage on the ball side. in that specific
7:08
cohort. Yes. And with Jajan and colleagues added
7:12
another layer. They found that damage on both
7:15
the glenoid and the humeral head occurred simultaneously
7:18
in 54 % of patients after just one traumatic
7:22
anterior dislocation. So bipolar bone loss damage
7:25
on both sides is common even after the first
7:28
time. Yes. It forces us to think differently.
7:30
This isn't just an occasional complication. Bone
7:33
loss is a frequent almost expected consequence
7:36
of shoulder dislocation, especially if it happens
7:39
more than once. Those figures really do shift
7:41
the perspective. It's not just about stitching
7:42
up torn ligaments. You have to account for the
7:44
missing bone. How does this bone loss actually
7:47
look on the bones themselves? What forms does
7:49
it take? Good question. On the glenoid, the socket,
7:52
you typically see two main patterns. One is erosion
7:55
type loss. which is more common in chronic instability,
7:58
the bone gradually wears away over time. It gets
8:00
ground down? Essentially, yes. The other is a
8:02
fragment type loss, often from the initial trauma,
8:05
where the front rim of the glenoid actually fractures
8:07
off. We often call this a bony bankart lesion.
8:10
OK, so wearing away or breaking off on the socket
8:13
side, what about the humeral head, the ball?
8:15
When the humeral head is forced forwards out
8:17
of the socket, the relatively sharp anterior
8:20
rim of the glenoid impacts the softer bone on
8:23
the back outer aspect of the humeral head. This
8:26
creates a compression fracture, basically a dent
8:28
or divot. That's the classic Hill Sachs lesion.
8:31
or HSL. The hill -sax lesion, right? Right. And
8:33
when you have both the glenoid bone loss, whether
8:36
it's erosion or a bony bankart, and the hill
8:39
-sax lesion on the humeral head, what's that
8:41
called? That combination is termed bipolar bone
8:43
loss. It signifies that you have these coupled
8:46
bony problems on both the socket and the ball.
8:49
And that inherently makes the instability problem
8:51
much more complex to manage because you've lost
8:53
structural support on both articulating surfaces.
8:56
OK. Bipolar bone loss. Socket potentially chipped
9:00
or worn down, ball with a dent. Now there's a
9:03
really key insight, particularly from researchers
9:05
like DiGiacomo, that challenges how we used to
9:08
think about the Hill Sachs lesion. It suggests
9:10
the size of that dent alone isn't the main issue.
9:12
Is that right? Absolutely. That was a pivotal
9:15
shift in understanding. For years, we focused
9:18
heavily on just measuring the depth and width
9:20
of the Hill Sachs lesion. Bigger lesion must
9:23
be worse, right? Seems logical. But it turns
9:26
out it's more nuanced. The real question isn't
9:28
just how big is the dent, but will that dent
9:32
physically engage or lock onto the front edge
9:35
of the remaining glenoid during movement? Ah,
9:37
so it's about contact. Does the dent catch on
9:40
the socket rim? Exactly. If the hill -sax lesion
9:43
engages the rim, it levers the humeral head out
9:46
of place, causing instability or apprehension.
9:48
If it doesn't engage, even quite a large hillsax
9:51
might not be the primary driver of the instability
9:53
in that particular patient. Okay, so engagement
9:55
is key. How do we figure out if a particular
9:58
hillsax lesion is likely to engage? This is where
10:01
the concept of the glenoid track comes in. It's
10:04
a brilliant way to conceptualize and, importantly,
10:07
quantify the contact zone between the humeral
10:09
head and the glenoid doing functional movements,
10:12
especially those abduction and external rotation
10:14
movements where dislocations often happen. The
10:16
track, like a pathway on the socket. Precisely.
10:19
DJ Komo and his team proposed a method to calculate
10:22
the width of this safe contact zone, this track,
10:26
and Critically, the calculation accounts for
10:29
any anterior glenoid bone loss. How do they calculate
10:31
it? The formula they developed is 0 .83 times
10:35
the intact glenoid diameter minus the amount
10:38
of the anterior glenoid bone defect. Okay, so
10:41
0 .83 times the socket width minus the bit that's
10:44
missing. That gives you a number representing
10:47
the track width. What do you do with that number?
10:49
You then measure the Hill Sachs lesion on imaging.
10:51
usually a CT scan, you look at where the medial
10:54
edge, the inner edge of the hill sacs lesion
10:56
lies relative to that calculated glenoid track
10:58
width. Right. If the medial edge of the hill
11:01
sacs falls medial to the glenoid track, meaning
11:03
it's further toward the center of the joint than
11:05
the track extends, then that lesion is considered
11:07
off track. Off track. And that means? It means
11:10
it will engage the anterior glenoid rim during
11:12
end range motion. It's a definite risk factor
11:14
for instability. If the medial edge of the hill
11:17
sacs lies lateral to the calculated track, it's
11:20
considered on track. And theoretically, it shouldn't
11:22
engage. OK. Off -track equals engagement. Definite
11:26
problem. On -track means it should stay clear.
11:30
Is it always that simple, or are on -track lesions
11:33
completely safe? Ah, well, it's rarely that simple
11:36
in biology. There are definitely nuances. And
11:39
the source material highlights this. Even on
11:41
-track lesions aren't always benign. they can
11:43
still contribute to instability and lead to worse
11:46
outcomes after a simple soft tissue repair if
11:49
they are very large or very close to the edge
11:51
of the track. So location matters, even if it's
11:53
technically on. Yes. Yamamoto and colleagues
11:56
introduced the idea of peripheral track lesions.
12:00
These are on track, but they take up a large
12:02
portion, maybe 75 % or more, of the humeral head's
12:05
circumference where the track lies. Yang found
12:08
a similar high occupancy ratio of predicted recurrence.
12:11
Others talk about near -track lesions maybe within
12:13
eight millimeters of the track edge. These are
12:15
also considered higher risk. So the on -track
12:17
off -track distinction is the foundation, but
12:19
you still need to look at the size and proximity
12:21
to the edge for those on -track ones. Exactly.
12:24
The key takeaway is that assessing a hill -sax
12:26
lesion requires more than just measuring its
12:29
size. You absolutely have to consider its relationship
12:33
to the glenoid, particularly any bone loss there.
12:36
this glenoid tract concept and its refinements.
12:39
That relationship is what truly determines the
12:41
risk it poses. That makes complete sense. It's
12:44
about the interaction between the two damaged
12:46
surfaces. And this deeper understanding directly
12:49
explains why just fixing the soft tissues, like
12:52
a standard bankart repair, isn't always going
12:54
to be enough. Precisely. An arthroscopic bankart
12:57
repair works well when you have a simple labral
12:59
tear and minimal or no significant bone loss.
13:03
But if you've got, say, more than 15 -20 % glenoid
13:06
bone loss or an engaging off -track Hillsax lesion,
13:09
just reattaching the labrum doesn't address the
13:12
fundamental bony instability. The foundation
13:13
is still compromised. Correct. And that's why
13:16
the reported failure rates for bank art repair
13:18
alone can be quite high in some studies. Figures
13:20
ranging from under 10 % up to over 35 % are cited.
13:24
And significant bone loss is consistently identified
13:26
as a major reason for those failures. Which naturally
13:29
led people to try and figure out before surgery
13:32
who is likely to fail that standard repair, right?
13:35
To identify those who need something more substantial.
13:38
Yes, exactly. This spurred the development of
13:41
scoring systems, the most well -known probably
13:43
being the Instability Severity Index Score, or
13:46
ISIS score. ISIS score? What does that measure?
13:49
It combines several known risk factors for failure
13:52
after a bank art repair. Things like the patient's
13:55
age younger is higher risk, their activity level
13:58
collision sports are higher risk, whether they
14:00
had generalized ligament laxity or hyper laxity,
14:03
and crucially, the presence and extent of bone
14:06
defects seen on imaging both glenoid and humeral
14:09
head. So it quantifies the overall risk profile.
14:12
Precisely. The original recommendation based
14:14
on the score was that if you scored above six
14:16
points, you were considered high risk for bank
14:17
art failure and a bony procedure like the latar
14:20
jet should be strongly considered instead. Has
14:22
that threshold changed? There's been discussion
14:25
and some studies suggesting that for certain
14:27
very high risk groups, perhaps even a lower threshold,
14:30
maybe four points or even three points, might
14:33
be more appropriate for recommending a bony procedure.
14:35
It reflects a growing awareness that even combinations
14:38
of seemingly moderate risk factors can lead to
14:41
failure. The point is, we now have tools to help
14:44
stratify patients and tailor the treatment, rather
14:48
than just doing a bank card on everyone with
14:50
instability. So the ISIS score and the glenoid
14:53
tract concept are guiding lights here, helping
14:55
surgeons decide who needs more than just soft
14:58
tissue work. And as you said, if you identify
15:00
an off -track hill -sax lesion, a bankart repair
15:03
alone is basically off the table. That's the
15:06
current thinking, yes. If you know that lesion
15:08
is going to engage the rim, performing only a
15:11
bankart repair doesn't solve the mechanical problem.
15:13
You need a procedure that either directly addresses
15:15
the hill -sax defect itself or alters the glenoid
15:19
geometry to prevent that engagement. A bank card
15:21
doesn't do either of those things. Okay, so this
15:24
sets the stage perfectly. If that simple soft
15:27
tissue fix isn't appropriate, particularly with
15:30
bone loss or these engaging lesions, what are
15:32
the surgical options? Let's move into our next
15:35
segment and really explore these more advanced
15:38
procedures. Sounds good. There are several approaches
15:40
depending on the specific problem. Let's start
15:43
with the Hill Sachs lesion. If that's deemed
15:45
the main issue needing direct attention, perhaps
15:48
alongside a bank heart repair for the labrum,
15:51
how can surgeons deal with that dent on the ball?
15:53
A common and effective technique is called remplassage.
15:56
It's a French term, roughly meaning to fill.
15:59
Remplassage. Filling the defect. How does that
16:01
work mechanically? It's usually done arthroscopically
16:04
at the same time as the bank heart repair. The
16:06
surgeon identifies the hillsack's defect on the
16:08
back of the humeral head. Then they take the
16:11
infraspinatus tendon, which is one of the rotator
16:13
cuff tendons, and the underlying posterior capsule,
16:16
and they suture, or tendities, that tissue directly
16:19
into the bony defect. Stitching the tendon into
16:22
the dent. Essentially, yes. The idea is that
16:24
this soft tissue fills the hole. So when the
16:27
arm moves into that vulnerable position of abduction
16:29
and external rotation, where the hill sacs would
16:32
normally engage the glenoid rim, now this plug
16:35
defect with the soft tissue makes contact instead.
16:38
It prevents the bony locking mechanism. It effectively
16:41
makes the defect extra -articular. Ah, I see.
16:44
So it acts like a soft bumper, preventing the
16:46
bone -on -bone clash. What do the results look
16:48
like when remplassage is added? Does it actually
16:51
reduce the risk of dislocation? Yes. The data
16:54
is quite compelling. Adding remplassage to a
16:56
bank card repair has been shown to significantly
16:58
lower recurrence rates compared to doing the
17:00
bank card alone, particularly in patients selected
17:02
appropriately. How much lower? Well... Overall,
17:05
recurrence rates with the combined procedure
17:06
are reported as low as 4 % in some series. But
17:09
looking at studies that directly compared, the
17:11
differences are stark. Our source material cites
17:13
comparisons like 2 .1 % recurrence with remplasage
17:17
versus 9 .3 % without, 1 .8 % versus 11%, 5 %
17:21
versus 30%, even 13 % versus 47 % in another
17:25
group. The pattern is consistent. It provides
17:27
a clear protective benefit against repeat instability.
17:30
Those are really significant reductions in recurrence.
17:33
Does the stitched -in tissue actually heal well
17:35
into the bone defect? Yes. Healing rates appear
17:38
to be very good. Studies using MRI or second
17:41
-look arthroscopy have shown integration of the
17:44
Tenedes tissue into the Hill Sachs defect in
17:46
the range of 85 % to 100 % at follow -up. And
17:50
encouragingly, longer -term studies haven't shown
17:53
major concerning changes in that tissue, suggesting
17:55
it's biologically well tolerated. It sounds effective.
17:59
Who is it typically recommended for now? Have
18:01
the indications changed over time? They certainly
18:03
have broadened. Initially, Remplisage was mainly
18:06
reserved for those definite off -track hillsax
18:08
lesions, the ones clearly engaging. However,
18:11
its use has expanded quite a bit. In what way?
18:13
It's now often considered even for on -track
18:15
lesions. If other factors put the patient at
18:17
high risk of recurrence, young age, collision
18:20
sports, maybe borderline bone loss. And importantly,
18:23
it's being used increasingly for patients with
18:25
what's termed subcritical glenoid bone loss,
18:28
usually defined as between maybe 15 % and 25%.
18:31
Why in that group specifically? Because studies
18:33
show that in this subcritical bone loss group,
18:36
doing a bank heart plus rumpusage significantly
18:39
reduced the failure rate compared to just doing
18:41
a bank heart alone. It seems to add stability
18:44
even when the primary issue isn't necessarily
18:46
an engaging HSL, but rather borderline glenoid
18:50
deficiency. So it's becoming a tool for managing
18:52
moderate risks. To some extent, yes. Some surgeons
18:56
referenced in our source material now advocate
18:58
considering Bancart plus remplasage for nearly
19:01
all young active patients with less than, say,
19:04
15, 20 percent glenoid bone loss, almost irrespective
19:07
of the glenoid tract calculation. They might
19:10
reserve an isolated bank heart repair primarily
19:12
for perhaps older, 25, lower demand patients
19:15
experiencing their first dislocation with minimal
19:17
bone loss. So the trend is definitely towards
19:20
using RemplaSage more broadly in high -risk patients.
19:22
That's a really interesting evolution in practice.
19:24
OK, so RemplaSage deals with the humeral head
19:26
side, the HSL, or helps bolster stability and
19:29
borderline glenoid loss. But what if the glenoid
19:32
bone loss is more substantial, say clearly over
19:34
20 % or 25 %? Is filling the HSL enough then?
19:37
No, probably not. Once you get into significant
19:41
anterior glenoid bone deficiency, simply addressing
19:44
the humeral head defect or the labrum usually
19:46
isn't sufficient. The socket itself is too shallow
19:49
to unstable. In these cases, you need to physically
19:52
reconstruct the missing part of the glenoid using
19:54
a bone graft. Right, replacing the lost bone.
19:57
Has the threshold for deciding you need a bone
19:59
graft changed? Yes, it has tended to decrease
20:02
over time, especially for high -risk individuals.
20:05
Historically, the threshold might have been cited
20:07
as 20 % or 25 % glenoid bone loss. Now, many
20:11
surgeons will consider a bony reconstruction
20:13
for defects over 15 -20 % and sometimes even
20:16
lower, perhaps around 13 .5 -15 % if the patient
20:19
is very high -risk, young collision athlete,
20:22
or if it's a revision surgery after a failed
20:24
bank art. Subcritical bone loss itself is now
20:26
recognized as a significant risk factor. Okay,
20:29
so the bar for needing a bony fix is getting
20:31
lower. Where does the actual bone for the graft
20:34
come from? There are two main sources, autograft
20:36
and allograft. Autograft means using the patient's
20:39
own bone. The most common place to take it from
20:41
for glenoid reconstruction is the iliac crest,
20:43
the top part of the hip bone. Taking it from
20:45
the hip. Are there other spots? Yes. Sometimes
20:48
bone can be harvested from the distal clavicle,
20:50
the end of the collarbone, or parts of the scapula
20:53
itself, like the scapular spine. The alternative
20:56
is allograft. Allograft meaning donor bone. Exactly.
21:00
Bone from a tissue bank, which has been processed
21:03
and sterilized. Common allograft sources used
21:06
for the glenoid include the distal tibia, the
21:09
lower end of the shin bone, parts of the femoral
21:11
head, the ball of the hip joint, or even a donor
21:15
humeral head. Is any particular type of graft
21:18
highlighted as being especially suitable for
21:21
rebuilding the glenoid? The distal tibial osteoarticular
21:25
allograft gets mentioned quite positively in
21:27
the source material. Why that one specifically?
21:29
Several reasons. Its natural shape often matches
21:31
the curvature of the glenoid quite well. It's
21:34
known to be dense, strong bone, which is good
21:36
for holding screws securely, but perhaps most
21:39
importantly, it comes with its own layer of articular
21:41
cartilage intact. Ah, so it rebuilds not just
21:43
the bone but the smooth joint surface too. Precisely.
21:47
That allows for a more anatomical reconstruction.
21:50
which theoretically might lead to better long
21:53
-term joint health and potentially less arthritis
21:55
down the line compared to using a graft that's
21:58
just bare bone. Clinical results reported are
22:00
generally good. with high healing rates around
22:02
89 % sighted and relatively low rates of the
22:06
graft shrinking or resorbing over time, maybe
22:09
around 3%. That cartilage surface does sound
22:11
like a big advantage. What are the general pros
22:14
and cons of using donor bone, the allograft,
22:16
versus the patient's own bone, the autograft?
22:19
The main advantage of allograft is avoiding donor
22:21
site morbidity. You don't have to make a separate
22:23
incision and take bone from the patient's hip
22:25
or elsewhere, which avoids the pain, potential
22:27
nerve issues or other complications associated
22:29
with that harvest site. Makes sense. And specifically
22:32
for the distal tibial allograft, you get that
22:34
cartilage surface, good bone stock, and it can
22:37
often be shaped to fill quite large defects.
22:41
The disadvantages. Well, allografts are more
22:44
expensive. There can sometimes be issues with
22:46
availability. There's an extremely small theoretical
22:49
risk of disease transmission, though screening
22:51
and processing methods are very rigorous now.
22:54
And the surgical technique for implanting an
22:56
allograft, especially an osteoarticular one,
22:58
can be technically quite demanding. Right. Technical
23:01
complexity is a factor. Okay, moving on from
23:04
free bone grafts, perhaps the most famous bony
23:06
procedure for shoulder instability is the latarget.
23:09
It seems like a real workhorse for these complex
23:12
cases. Can you break down what the latarget procedure
23:14
actually involves? Certainly. The latarget procedure
23:18
is named after Michel Latourge. the French surgeon
23:20
who described it. It involves taking a specific
23:23
piece of bone from the patient's own shoulder
23:25
blade, the scapula called the coracoid process,
23:28
along with the tendons that attach to it, and
23:30
transferring this whole unit to the front lower
23:32
edge of the glenoid socket. So moving a piece
23:35
of bone from one part of the shoulder blade to
23:38
the rim of the socket. Why that specific piece?
23:42
How does it stabilize the shoulder? It provides
23:45
stability through what's famously known as the
23:47
triple blocking effect. It's quite clever. Triple
23:49
effect. What are the three parts? Okay, first,
23:51
the bone block itself. Transferring the coracoid
23:55
bone physically extends the glenoid surface area,
23:58
replacing the missing bone and deepening the
24:00
socket at the front. That's the direct bony block.
24:02
Right, just making the socket bigger. Second,
24:04
the tendons attached to the coracoid, the conjoint
24:07
tendon, which is formed by the short head of
24:09
the biceps and the coracobrachialis muscle, are
24:12
transferred along with the bone. they end up
24:14
lying across the front of the shoulder joint.
24:16
When the arm is moved into vulnerable positions
24:19
like abduction and external rotation, these muscles
24:21
contract, and the tendon acts like a dynamic
24:24
sling, actively resisting the humeral head from
24:27
sliding forward. A dynamic sling. Active muscle
24:30
support. That's clever. It is. And third, the
24:33
procedure also has a tenodesis effect. Transferring
24:36
the coracoid and its tendon effectively reinforces
24:40
the often stretched out or damaged antero -inferior
24:43
joint capsule. So you get bony augmentation,
24:46
a dynamic muscular sling, and capsule reinforcement
24:48
all in one. It's a powerful combination. That
24:51
triple effect makes sense why it's so effective.
24:54
When is Letarge at the go -to procedure, and
24:56
when might it not be suitable? The primary indication
25:00
is significant anterior glenoid bone loss, typically
25:03
over that 15 -20 percent threshold we discussed,
25:06
depending on the patient. It's also very commonly
25:08
used for revision surgery after a failed bankart
25:10
repair, especially if bone loss was the reason
25:13
for failure or has developed since. And contraindications?
25:16
Well, if the bone loss is absolutely massive,
25:18
perhaps beyond what the coracoid can reasonably
25:21
reconstruct, although there are technical modifications
25:24
like the congruent arc technique for larger defects,
25:27
these might carry slightly higher risks. Significant
25:30
instability in other directions, like posterior
25:32
instability, might also be a relative contraindication
25:35
or require additional procedures. You mentioned
25:37
techniques. Can this be done arthroscopically,
25:40
minimally, invasively, or is it typically an
25:43
open operation? It can be done both ways. Traditionally,
25:46
it was an open procedure requiring a larger incision.
25:49
But over the last couple of decades, techniques
25:51
for performing the latarjet arthroscopically
25:54
through keyhole surgery have become well established.
26:00
Both approaches have demonstrated excellent results
26:03
in terms of restoring stability and function,
26:05
with low rates of recurrent dislocation when
26:08
performed well. The reported recurrence rates
26:10
after Latorgiat are generally low figures like
26:13
4 % at 5 years, maybe up to 11 % at 10 years
26:16
are cited. One large series even reported just
26:19
1 % recurrence. That's impressively stable. It
26:22
is. And while overall complication rates reported
26:24
in the literature can seem broad, ranging from
26:27
6 % up to nearly 24%, in the hands of surgeons
26:30
who do a lot of these procedures, the rates tend
26:32
to be much lower, often in the 4 -7 % range.
26:36
It's technically demanding either way. You mentioned
26:38
recurrence is low, but when it does happen after
26:40
a latarjet, is there a typical time frame? Yes.
26:43
Interestingly, most recurrences following a latarjet
26:47
procedure tend to happen relatively early, usually
26:50
within the first year or two after surgery. Compared
26:53
to bank heart repair, though, latarjet generally
26:56
provides superior long -term stability, especially
26:59
in those high -risk patients. And for athletes,
27:02
that's often the key group needing this. What
27:04
about getting back to sport after a latarjet?
27:07
Return to sport rates are consistently high,
27:09
which is a major advantage and why it's often
27:11
favored for athletes, particularly those in contact
27:14
or collision sports. The source material suggests
27:17
overall return rates up to 88%, with around 72
27:21
% managing to get back to their pre -injury level
27:23
of competition. That's very encouraging for athletes
27:26
facing this. Absolutely. That combination of
27:28
high stability and high return to sport rates
27:30
makes it a very appealing option for that population,
27:33
even though it's a more complex operation than
27:35
a simple bank car. Okay, so excellent stability,
27:39
good return to sport, but it is more complex.
27:42
What are the potential downsides or complications
27:44
specific to the Letarjet procedure? Well, the
27:47
main conceptual disadvantage is that it's inherently
27:49
non -anatomical. You're changing the shoulder's
27:52
natural structure by adding bone and moving tendons.
27:55
This can potentially make any future surgery,
27:58
should it be needed, more difficult. Right, operating
28:00
on altered anatomy. Exactly. Also, The bone graft
28:04
itself, the coracoid, doesn't have articular
28:07
cartilage on the surface that faces the humeral
28:09
head. There's a theoretical concern, though it's
28:13
debated, that this bone -on -cartilage articulation
28:16
could potentially increase the risk of developing
28:18
osteoarthritis over the very long term. And other
28:21
complications. Specific complications can include
28:24
problems with the graft itself, putting it in
28:26
the wrong position, it not healing to the glenoid,
28:29
non -union, or shrinking over time, resorption.
28:32
The screws used for fixation can cause issues
28:34
if they're too long, too short, break, or irritate
28:37
tissues. Persistent instability can still occur
28:39
if the underlying issues weren't fully addressed.
28:42
Infection is a risk, as with any surgery. And
28:45
nerve injuries, while uncommon, are a known potential
28:47
complication due to the location of the dissection.
28:50
Let's pause on those specific challenges for
28:52
a moment. Our source material delves into certain
28:55
patient groups where instability is particularly
28:58
complex. You mentioned patients with seizure
29:00
disorders earlier. How do seizures complicate
29:03
shorter instability? It seems like a difficult
29:05
combination. It really is, and it's a crucial
29:07
group to consider. Patients with epilepsy, or
29:10
PWE, can have incredibly forceful, uncontrolled
29:14
muscle contractions during seizures. These contractions
29:17
can be strong enough to actually dislocate the
29:19
shoulder or even cause fractures around the joint.
29:22
So the seizure itself causes the dislocation.
29:25
Yes, it can be the primary mechanism of injury
29:27
or re -injury. Historically, posterior dislocations
29:31
were often associated with seizures, perhaps
29:33
due to typical arm positioning, but actually
29:36
both anterior and posterior dislocations are
29:38
well documented. The forces are just overwhelming.
29:41
Furthermore, repeated seizures, especially if
29:44
poorly controlled and perhaps in younger patients
29:46
whose bones are still developing, might lead
29:48
to gradual bony changes over time, like increased
29:51
retroversion, backward tilt, of the glenoid socket,
29:54
further predisposing to instability. Wow. So
29:57
the underlying condition directly impacts the
29:59
gaint mechanics and risk. How does this change
30:02
the treatment approach? It adds significant complexity.
30:06
Trying non -operative management is often less
30:08
successful if seizure control isn't optimal.
30:11
When considering surgery, achieving good control
30:13
of the seizure disorder first is absolutely paramount.
30:16
That's so critical. Because having a major seizure
30:19
soon after surgery could easily disrupt the repair
30:22
or reconstruction. Many recommend aiming for
30:24
a seizure -free period, perhaps at least six
30:26
months, before undertaking elective stabilization
30:29
surgery to minimize this risk. And the type of
30:31
surgery. Does it influence that, too? Yes, strongly.
30:35
Given the potential for massive uncontrolled
30:37
forces during a seizure, relying solely on a
30:40
soft tissue repair is often considered too risky.
30:43
Bony stabilization procedures, like the Laffer
30:45
jet for anterior instability, or perhaps bone
30:48
grafting for posterior defects, are frequently
30:51
favored. They provide more robust structural
30:54
stability that's less likely to be overcome by
30:56
muscle contraction. The absolute key, though,
30:59
is multidisciplinary care. Close collaboration
31:02
between the orthopedic surgeon and the neurologist
31:05
managing the epilepsy is essential. That integrated
31:08
approach sounds vital. What about the other challenging
31:10
group mentioned patients with hyperlaxity, maybe
31:12
conditions like Ehlers -Danlos syndrome where
31:14
ligaments are naturally loose? Yes. Managing
31:17
instability and generalized hyperlaxity is a
31:19
different kind of challenge. Here, the core problem
31:22
isn't usually a single traumatic tear, but rather
31:25
the inherent stretchiness of all the connective
31:27
tissues. So surgery might not be the first step.
31:30
Absolutely not. The initial approach, and often
31:33
the mainstay of treatment, is intensive non -operative
31:37
management. This means a prolonged course of
31:39
dedicated physical therapy, often lasting three
31:42
to six months or even longer. What's the focus
31:45
of the physio? It's all about building dynamic
31:47
stability, strengthening the muscles around the
31:50
shoulder, the rotator cuff, the muscles that
31:52
control the scapula, and improving proprioception,
31:56
which is the joint sense of its position in space.
31:59
The aim is to use active muscle control to compensate
32:02
for the loose passive ligaments and capsule.
32:05
Trying to make the muscles do the stabilizing
32:07
work the ligaments can't. Exactly. And if that
32:10
extensive physio still isn't enough, what are
32:12
the surgical options then? If surgery becomes
32:14
necessary, it's usually focused on tightening
32:16
the overly loose joint capsule. For patients
32:19
with true multi -directional instability, where
32:22
the shoulder feels loose in all directions, the
32:24
typical procedure is an arthroscopic pen capsule
32:26
application. Pen capsule application. Tightening
32:30
the whole capsule. Yes, essentially gathering
32:32
up and suturing the redundant capsule from all
32:35
sides to reduce the joint volume and improve
32:37
stability. If the hyperlaxity is present, but
32:41
the main problem is still primarily anterior
32:44
instability, sometimes surgeons might perform
32:47
a bank heart repair, combined with a procedure
32:49
to augment or tighten the subscapularis tendon
32:52
at the front. What's the big challenge when operating
32:55
on hyperlax patients? The challenge is finding
32:58
the sweet spot. You need to tighten things enough
33:00
to provide stability, but because their tissues
33:03
are inherently stretchy, it's easy to over tighten
33:06
and leave them with significant functionally
33:08
limiting stiffness. It's a very delicate balancing
33:11
act. Right, so we've journeyed from the basic
33:13
mechanics through to advanced procedures like
33:15
remplasage and letarget, tackled bone loss, and
33:19
considered these specific patient complexities.
33:21
But as we know, surgery isn't always the final
33:23
chapter and things can go wrong. Let's pivot
33:26
now to look at complications, the challenges
33:28
of revision surgery, and the longer term outlook
33:30
for these shoulders. Indeed, understanding potential
33:33
failures and complications is crucial. You mentioned
33:35
earlier that failure after a standard bankart
33:38
repair often links back to unaddressed bone loss.
33:42
Is there a characteristic way the glenoid bone
33:44
fails after that kind of repair, especially with
33:47
modern anchor techniques? Yes. There's a specific
33:50
pattern that's been described, particularly following
33:52
arthroscopic bankart repairs using suture anchors
33:55
drilled into the bone. It's sometimes called
33:58
the postage stamp fracture. Postage stamp fracture.
34:01
Why that name? Because if the shoulder redislocates
34:04
after such a repair, especially if there was
34:06
already some bone loss, the anterior rim of the
34:09
glenoid can fracture right through the holes
34:11
where the anchors were placed. It creates this
34:13
fragmented, almost perforated look along the
34:16
rim, like the edge of a sheet of postage stamps.
34:19
Ah, I see. The ankle holes become weak points.
34:22
Exactly. It suggests the bone quality wasn't
34:24
sufficient to withstand the forces. Potentially
34:27
exacerbated by the underlying bone loss, and
34:30
maybe even related to the stress concentration
34:32
caused by the anchors themselves, their placement,
34:34
size, or material might play a role. That sounds
34:37
like it would make going back in for revision
34:39
surgery even trickier. When a bankart does fail,
34:43
how do surgeons decide what to do next? Try another
34:45
bankart or switch to something like a latarjet?
34:49
That's a really critical decision. If the primary
34:52
bankart failed clearly because of significant
34:55
bone loss that wasn't addressed initially, or
34:57
if the patient has multiple high -risk factors
34:59
like being a young collision athlete, then simply
35:02
repeating the bankart repair is very unlikely
35:05
to succeed. It's often considered contraindicated
35:08
in those situations. So, letarget becomes the
35:10
main option? In most cases of failed bankart
35:12
repair, yes, especially if there's documented
35:14
bone loss either initially missed or developed
35:17
over time or the patient falls into that high
35:19
-risk category. A bony procedure like the letarget
35:22
or sometimes a bone grafting technique is generally
35:25
the preferred revision strategy. How do the outcomes
35:27
compare revising with another bankart versus
35:30
revising with a letarget? The source material
35:32
suggests that Generally, revising a failed bank
35:36
card with a Letarget leads to better functional
35:39
scores, better stability, and higher rates of
35:41
return to sport compared to attempting a revision
35:44
bank card. However... There's always a however.
35:47
There is. Revisional latargette doing a latargette
35:51
after a previous failed surgery can be technically
35:53
more demanding than doing a latargette as the
35:55
first operation. It might be associated with
35:57
slightly higher complication rates, potentially
36:00
more post -operative pain, and sometimes greater
36:02
loss of external rotation compared to a primary
36:05
latargette. So while it's often the better option
36:08
for stability, it's not without its own challenges.
36:11
Revision surgery is just inherently more complex.
36:14
What about failures of the bony procedures themselves?
36:16
Can letarget or bone grafts fail too? Oh, absolutely.
36:19
They can fail for various reasons. Yeah. Technical
36:21
issues during the initial surgery are one cause.
36:24
Maybe the graft wasn't sized correctly, or it
36:26
was put in the wrong position, or the screws
36:29
used for fixation weren't quite right, leading
36:31
to instability or non -healing. So surgical technique
36:34
is paramount. Hugely important. Other causes
36:37
can include failing to address other problems
36:39
at the same time. like significant soft tissue
36:42
damage elsewhere, or a large hillsax lesion that
36:45
also needed attention. Infection is always a
36:48
risk. Hardware can fail or break. And specific
36:51
to bone grafts, they can sometimes fail to heal
36:54
to the patient's bone, non -union, or they can
36:57
gradually resorb or shrink over time. The bone
37:01
graft actually disappearing. That sounds like
37:03
a major problem for long -term stability. How
37:05
often does that happen? It is a concern, particularly
37:08
perhaps more with allografts than autografts,
37:10
although it can occur with both. The reported
37:12
rates vary quite a bit in the literature, but
37:14
significant resorptions say losing more than
37:17
25 % of the graft volumes definitely described.
37:20
It seems less common now with modern techniques
37:22
and fixation, but it's a known potential long
37:25
-term complication. What causes the graft to
37:27
resorb? It's often thought to be related to mechanical
37:29
factors. If the graft isn't positioned perfectly
37:32
flush or isn't held absolutely rigidly with a
37:34
fixation, any tiny movement or micromotion at
37:38
the graft -host interface can hinder proper bone
37:41
healing and potentially trigger resorption. The
37:43
biological properties of the graft type might
37:45
also play a role, with some suggesting living
37:48
autograft cells might make it less prone to resorption
37:51
than processed allograft. Really meticulous surgical
37:54
technique and achieving solid fixation are key
37:57
to minimizing the risk. Beyond the surgery just
38:00
not working to stabilize the shoulder, what other
38:02
common complications can pop up after these complex
38:05
instability procedures? Well, nerve injury is
38:07
one that always needs careful consideration.
38:10
Fortunately, permanent nerve damage is rare,
38:12
but transient injuries or irritation can happen.
38:15
Which nerves are most at risk? It depends a bit
38:17
on the procedure. With the latar jet, because
38:21
the dissection is near the coracoid process,
38:23
the muscular cutaneous nerve is most commonly
38:25
cited as being at risk. Some reports mention
38:28
it in up to 30 % of nerve complications, though
38:31
actual lasting weakness is much less frequent.
38:35
The axillary nerve, which runs around the back
38:37
and side of the shoulder, is also vulnerable,
38:40
especially during screw placement, or if extensive
38:42
dissection is needed, maybe around 13 % of nerve
38:45
issues involve the axillary nerve. The superscapular
38:48
nerve can also be at risk during certain arthroscopic
38:51
approaches. So careful nerve monitoring is needed.
38:54
Careful technique during surgery and a thorough
38:56
neurological exam after surgery are crucial.
38:59
If a nerve deficit is found, especially if there's
39:01
suspicion it might be due to misplaced hardware
39:03
compressing the nerve, then urgent further investigation
39:06
like a CT scan and potentially revision surgery
39:09
to reposition or remove the hardware might be
39:11
necessary. Okay, nerves are one thing. What about
39:13
stiffness? We touched on it with hyperlaxity,
39:15
but is it a general risk? Yes, stiffness, particularly
39:19
loss of external rotation, is a well -recognized
39:22
potential downside. It's that constant trade
39:25
-off. Surgeons are trying to make the shoulder
39:27
stable, which often involves tightening structures,
39:30
but overdo it, and you sacrifice motion. Which
39:33
procedures are most likely to cause stiffness?
39:36
Some older open techniques that involved splitting
39:38
or significantly tightening the subscapularis
39:41
muscle were known for causing external rotation
39:43
loss. Modern arthroscopic capsule replication
39:47
used for laxity intentionally tightens the capsule
39:49
and can limit motion if not done judiciously.
39:53
And the literature jet procedure, due to the
39:55
anterior bone block and potential scarring, can
39:57
also lead to some loss of external rotation.
40:00
While small loss might be acceptable for improved
40:02
stability, significant stiffness can be very
40:04
disabling, so rehabilitation is key to manage
40:07
this. And infection. How common and serious is
40:10
that? Thankfully, deep infection after shoulder
40:12
instability surgery is rare, probably less than
40:15
1 % in most series, but when it happens, it's
40:18
serious. Superficial wound infections might just
40:21
need antibiotics, but a deep joint infection
40:24
requires urgent surgical washout and debridement,
40:27
plus a long course of antibiotics. Does the hardware,
40:31
like screws or anchors, complicate infection
40:33
treatment? It certainly can. If the infection
40:37
involves the implants, particularly those holding
40:39
a critical bone graft in place, you face a real
40:42
dilemma. Removing the hardware might be necessary
40:44
to clear the infection, but doing so could compromise
40:47
the stability the surgery aimed to achieve. It
40:50
requires very careful management. Thinking even
40:52
longer term now, we've mentioned osteoarthritis.
40:55
Is there a specific link between having shoulder
40:57
instability and developing arthritis later in
40:59
life? Yes, absolutely. The term used is dislocation
41:02
arthropathy. This describes the osteoarthritis,
41:05
the cartilage wear, joint space narrowing, bone
41:08
spur formation that develops as a consequence
41:10
of having had chronic or recurrent shoulder instability.
41:13
And importantly, this can happen whether or not
41:15
the shoulder was surgically stabilized. So the
41:17
instability itself damages the joint over time.
41:20
Precisely. The repeated episodes of the joint
41:22
sliding partially or fully out of place, the
41:25
abnormal forces across the cartilage, the damage
41:28
from the initial injury and subsequent events,
41:30
potentially subtle joint incongruity from bone
41:33
loss. All these factors contribute to wearing
41:36
down the joint surfaces over years. even if surgery
41:39
successfully stops the dislocations. Even then,
41:41
the joint has already suffered insults. The surgery
41:44
itself, while necessary, might also slightly
41:46
alter joint mechanics. So while stabilization
41:49
surgery is crucial to prevent further damage
41:51
and improve function, it doesn't necessarily
41:54
erase the increased long -term risk of developing
41:56
arthropathy that comes with having had significant
41:59
instability in the first place. What does dislocation
42:01
arthropathy mean for the patient? Over time,
42:04
it typically leads to increasing pain and stiffness.
42:07
Ironically, the joint often becomes more stable
42:10
as the arthritis progresses, but it's a stiff,
42:12
painful stability. It can significantly limit
42:15
function. And the data shows this isn't just
42:17
theoretical studies looking at patients years
42:19
after bankart repairs, for example, show a clear
42:22
increase in osteoarthritis rates compared to
42:25
their preoperative state. Figures cited show
42:27
rises from maybe 9 % pre -op to nearly 20 % at
42:30
6 .5 years, or from 10 % pre -op up to 60 % in
42:34
one study looking out over 13 years. It's a real
42:37
long -term consequence. That really hammers home
42:39
the importance of managing instability effectively,
42:42
and perhaps early, to protect the joint long
42:44
term. Are there specific strategies recommended
42:47
to try and prevent or at least minimize this
42:49
risk of dislocation arthropathy? Yes, the International
42:52
Society of Arthroscopy, Knee Surgery, and Orthopedic
42:54
Sports Medicine, ISACOS, has put forward recommendations.
42:57
A key one is trying to reduce the number of dislocations
43:00
the patient experiences before surgery. This
43:02
implies that earlier surgical intervention, rather
43:05
than letting someone have multiple dislocations
43:07
over years, might be protective for long -term
43:09
joint health. So don't wait too long if dislocations
43:12
keep happening. That's the suggestion. Other
43:14
recommendations include meticulously assessing
43:17
all the existing damage, bone loss, cartilage
43:19
damage, pre -existing arthritis, before deciding
43:22
on and performing the surgery, as this informs
43:25
the best procedure and prognosis. And for soft
43:28
tissue repairs, ensuring really accurate anchor
43:31
placement right on the glenoid rim and secure
43:34
fixation is emphasized to minimize the chance
43:36
of early failure, recurrence, and the subsequent
43:39
joint damage that follows. The underlying theme
43:42
is controlling the instability effectively and
43:44
managing the bony architecture properly. Makes
43:46
sense. Okay, one last area before we wrap up
43:49
getting back to activity, especially for athletes.
43:52
What's the typical journey after these surgeries?
43:55
The rehabilitation and return to sport discussion
43:57
is often complex, particularly for athletes.
44:00
There's that fundamental trade -off we touched
44:01
on earlier. Non -operative versus operative.
44:04
Yes. Trying non -operative management, mainly
44:06
physio, might allow a quicker return to play,
44:09
possibly even within the same season for some.
44:12
But it comes with a significantly higher risk
44:15
of the shoulder dislocating again. Where is surgery?
44:17
Surgery almost always means the athlete is out
44:20
for the remainder of that season. Recovery typically
44:23
takes a minimum of five, six months, sometimes
44:26
longer depending on the procedure in the sport.
44:28
However, the major benefit is a much, much lower
44:31
rate of recurrence in the long run and therefore
44:33
a higher chance of a durable return to sport.
44:35
That must be an incredibly difficult conversation
44:38
and decision for a young athlete focused on their
44:40
current season or scholarship prospects. It is
44:43
one of the toughest decisions in sports medicine.
44:45
The discussion has to be very comprehensive.
44:48
You need to consider the athlete's specific history.
44:51
How many times has it dislocated? What level
44:53
do they play at? Then the physical exam findings,
44:56
detailed imaging like CT and MRI to see the extent
44:58
of the damage, especially bone loss, and then
45:01
layer on the timing factors. Where are they in
45:03
their season? Are championships coming up? Are
45:05
they trying to get recruited? Attempting to push
45:07
through a season non -operatively is often seen
45:10
as a very high -risk gamble. Once the decision
45:13
for surgery is made, what does the rehab process
45:16
generally involve? Is it similar for different
45:18
procedures? The underlying principles of rehab
45:20
are similar, whether it was non -operative or
45:23
post -operative treatment you need to restore
45:25
range of motion, rebuild strength, improve neuromuscular
45:28
control and proprioception, and then gradually
45:31
reintroduce sport -specific movements. However,
45:34
the timeline and specific restrictions vary hugely
45:37
depending on the surgery performed. How so? Bony
45:41
procedures like latarjet or significant bone
45:44
grafting usually require longer periods of protection,
45:47
perhaps limited weight bearing or stricter range
45:50
of motion restrictions initially to allow the
45:52
bone to heal properly compared to a standard
45:54
soft tissue bank heart repair. Adhering to the
45:57
specific protocol for the procedure done is critical.
46:00
And deciding when someone is actually ready to
46:02
go back to playing their sport, is it just based
46:04
on time? Time -based criteria, like saying, okay,
46:07
it's been six months, are still commonly used
46:09
as a general guideline. But there's a strong
46:11
shift towards incorporating more objective functional
46:14
testing alongside clinical assessment. Objective
46:16
tests, like what? Things like measuring strength
46:19
using isokinetic machines, assessing upper body
46:22
endurance and stability with tests like the closed
46:25
kinetic chain, upper extremity stability, CKC
46:28
-UES test, or evaluating balance and proprioception
46:31
using something like the Y balance test. These
46:34
provide measurable data points. So moving beyond
46:37
just how does it feel to what can it actually
46:40
do? Exactly. These objective tests help the medical
46:44
team, the athlete, and the coach make a more
46:46
informed, evidence -based decision about whether
46:49
the shoulder is truly ready to withstand the
46:51
demands of their sport without an unacceptably
46:53
high risk of re -injury. It helps take some of
46:56
the guesswork out of that crucial return to play
46:58
decision. That makes so much sense. Right, wow,
47:01
we have covered an enormous amount of detail
47:03
there. We started with basic stability, explored
47:05
the huge impact of bone loss, dived into advanced
47:08
surgeries like rimplassage, grafting, latarjet,
47:11
looked at tricky patient groups, faced complications
47:14
and revision surgery, and considered the long
47:16
-term health of the joint right through to recovery.
47:19
Let's try and crystallize some of that with a
47:20
quick lightning round. Ready? Let's do it. OK,
47:23
question one. In a healthy shoulder, what are
47:26
the two main ways it stays stable in the mid
47:28
-range of motion? Negative intra -articular pressure
47:32
and the concavity compression effect from the
47:34
muscles. Spot on. Question two. What concept
47:38
is key to understanding if a hill -sax lesion
47:40
is problematic, looking beyond just its physical
47:43
size? The glenoid tract concept, whether the
47:46
lesion engages the glenoid rim. Perfect. Question
47:49
three. If there is significant bone loss from
47:52
the glenoid socket, what are the two main surgical
47:54
strategies used to replace that missing bone?
47:57
Bone grafting using either autograft or allograft
47:59
and the latarjet procedure. Excellent. And final
48:02
lightning question, what's the potential long
48:05
-term consequence for the joint surfaces resulting
48:07
from recurrent shoulder instability, even if
48:10
it's treated? That would be dislocation or arthropathy,
48:12
which is essentially progressive osteoarthritis.
48:14
Fantastic. Great summary points. So let's try
48:17
and pull together maybe five key actionable takeaways
48:20
from this really in -depth discussion on complex
48:22
shoulder instability. One. Remember that recurrent
48:25
shoulder instability is very often more than
48:27
just a ligament tear. Bone loss on both the socket
48:31
and the ball is incredibly common and absolutely
48:34
critical to assess properly. Couldn't agree more.
48:37
Assessment is key. Two. When looking at a hill
48:40
-sax lesion, don't just measure its size. Use
48:42
the glenoid tract concept to determine if it's
48:45
likely to engage the glenoid rim. That's what
48:48
really drives instability risk from the HSL.
48:50
Engagement is the crucial factor. Three. If significant
48:54
bone loss or specific patient risk factors mean
48:57
a simple soft tissue repair isn't enough or is
49:00
likely to fail, then advanced techniques like
49:02
remplasage, bone grafting, or the Letarjet procedure
49:05
become necessary. Each has specific indications,
49:09
benefits, and potential drawbacks. Matching the
49:11
procedure to the specific pathology and patient
49:13
is vital. 4. Patient -specific factors matter
49:16
hugely. age, activity level, especially collision
49:19
sports, the number of previous dislocations,
49:21
and any underlying conditions like epilepsy or
49:24
hyperlaxity significantly influence the risk
49:26
and the boost treatment plan. It cannot be a
49:28
one -size -fits -all approach. Absolutely. Personalized
49:31
medicine is essential here. And five, while modern
49:33
surgery can do a fantastic job of improving stability
49:36
and getting people back to activity, it's not
49:39
without risks like stiffness, nerve issues, or
49:42
infection. And critically, the history of instability
49:45
itself carries a long -term risk of joint degeneration
49:48
dislocation arthropathy. This really underscores
49:52
the importance of timely, effective treatment
49:55
and thorough rehabilitation. The goal is stability
49:59
now, but also preserving joint health for the
50:02
future. Precisely. Now, if you listening found
50:04
these insights as valuable as I did, perhaps
50:07
consider rating and sharing this deep dive on
50:09
your professional networks, maybe LinkedIn or
50:11
X. It genuinely helps others find and benefit
50:14
from these important conversations. Hearing different
50:16
perspectives is always useful. Absolutely. And
50:19
that leaves us with a final thought to mull over.
50:22
Given the potential for serious long -term joint
50:24
damage and the complex trade -offs involved in
50:27
treatment, especially for young, very active
50:29
people, how do we truly strike the right balance?
50:32
How do we best weigh that immediate, often intense
50:35
desire for a rapid return to sport against the
50:38
arguably more important goal of preserving the
50:40
long -term health and function of the shoulder
50:41
joint? How can surgeons, patients, families,
50:44
coaches all collaborate effectively to navigate
50:46
those potential competing priorities. That is
50:48
the million dollar question, isn't it? A challenge
50:50
we face every day.