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