Imagine a tiny bone in your wrist, no bigger
than a sugar cube, suddenly losing its lifeline,
its blood supply. Hmm. What happens then isn't
just a simple sprain or a minor ache. It's a
journey into chronic pain, progressive stiffness,
and actually a surprisingly complex medical condition
we're diving deep into today. Indeed. We're talking
about Kinvox disease, a condition that, at its
core, involves the vascular necrosis, or you
might hear osteonecrosis, of the lunate bone
in the wrist. Lunatomalacia is another term you
might come across. Right, lunatomalacia. It's
a rare condition, often quite insidious, initially
mimicking far less serious problems, which must
make diagnosing it a significant challenge. Exactly.
And our exploration today isn't just a general
overview, it's a deep dive, specifically tailored
to the source materials you provided, a stack
of articles, research papers, excerpts from various
medical resources like StatPearls, OrthoBullets,
the Hand Society, and others, all focusing on
this specific condition. OK, so our mission,
leveraging these resources, is to extract the
most important, insightful information. We want
to understand precisely what Kinbach's disease
is, maybe unravel the mystery of why it happens,
given there seems to be no single cause. That's
a key point. It's multifactorial. Right. And
identify who it typically affects, delve into
how medical professionals diagnose and stage
its progression using different imaging techniques.
Which is crucial for treatment. Absolutely. and
explore the range of treatment options available,
from non -surgical approaches right through to
quite complex procedures, and critically understand
what the long -term outlook and potential future
holds for someone living with this condition.
It's really about turning dense medical information
into clear, actionable understanding for you
listening. Think of it as your essential guide
to becoming well -informed about Kinbach's disease,
extracting the core knowledge and key considerations
directly from the expert literature we've looked
at. OK, let's unpack this. Let's start with the
anatomy and the star of our deep dive. That tiny
bone, the lunate. The lunate, yes. So this whole
condition revolves around the lunate bone. Where
exactly is it located, and why is it such a crucial
player in the wrist's mechanics? Well, the lunate
holds a really central and critical position
in the wrist structure. It sits squarely in the
middle of the proximal purple row. That's the
first line of eight small carpal bones in your
wrist, the ones closest to your forearm. OK.
Its neighbors are the scaphoid on the thumb side
and the trichotrum on the pinky side, with the
pisiform sort of sitting on the trichotrum. More
importantly, it articulates or connects directly
with the two long bones of your forearm, the
radius and the ulna. How does it connect to both?
It connects specifically through the radial side
and then via the triangular fibrocartilage complex
or TFCC on the ulnar side. So it's literally
right there bridging the forearm and the hand.
What does that central position mean for its
function? It means it's absolutely fundamental
to wrist movement and load bearing. The lunidate
acts as a key intermediary. You know, facilitating
the complex range of motion we have in our wrists,
flexion, bending down, extension, bending back,
and to some extent, that side -to -side deviation
as well. And the load -bearing aspect. Yes. Perhaps
its most significant role, and one that's highly
relevant to Kinbach's disease, is its function
in absorbing and transmitting the forces that
travel through your hand and wrist. particularly
during activities like gripping, lifting, or
bearing weight on your hands. Right. That makes
sense. Our sources actually provide some fascinating
statistics on this load transmission. Approximately
35 % of the axial load that goes through your
wrist during these activities is transmitted
directly through the articulation between the
radius and the radial -lunate joint. 25%. And
another 10 % goes through the TSCC to the ulna.
So yeah, a significant portion of force, about
a third, is concentrated right on this one small
bone. 35 % of the source going through your wrist
on a bone no bigger than a sugar cube. That sounds
like an awful lot of stress for such a small
structure. It is. It's no wonder that if something
goes wrong here, the consequences can be significant.
Precisely. And the history of understanding problems
with this bone goes back further than you might
think. While there were earlier observations,
figures like Peste back in the 19th century,
the specific condition we call Keenbok's disease
was formally described by Robert Keenbok, an
Austrian radiologist, in 1910. 1910. So we've
been piecing together the puzzle of this lunate
failure for well over a century. We have indeed.
Who is typically affected by this condition.
Is there a pattern in the patients diagnosed?
The data from the sources does show a typical
demographic profile, although it's not exclusive,
of course. It predominantly affects males, generally
within a relatively specific age range, most
commonly between 20 and 40 years old. Younger
men, mostly. Yes. And while it's considered a
rare condition overall, within the category of
a vascular necrosis affecting the carpal bones,
it's the second most common type after AVN of
the scaphoid bone. OK, second only to the scaphoid.
Correct. Interestingly, the sources also note
that it's quite rare to see keen box disease
affecting both wrists at the same time. It's
usually unilateral, just one side. So younger
to middle aged men are the most common demographic,
though certainly not the only ones affected.
Now, the big question and one the sources emphasize
is still not fully answered. Why does this happen?
Given the central role of blood supply loss,
you'd think there'd be a clear cause. You would,
wouldn't you? But the sources are clear there
isn't one single consensus reason. It's described
as multi -factorial. That's right. The mystery
of Keenbox is that it seems to arise from a confluence
of factors rather than a single event or deficiency.
The sources detail several key proposed mechanisms
that likely interact to lead to the disease.
Okay, what are the main contenders? One of the
most compelling and frequently cited is biomechanical
imbalance. Specifically, variations in the lengths
and angles of the bones in the forearm and wrist.
The most prominent example is ulnar negative
variance, often called ulna minuses. Okay, let's
break that down. Ulnar negative variance, what
does that actually look like in the wrist? Simply
put, it means the ulna bone that's the forearm
bone on the pinky side is congenitally shorter
relative to the radius bone, the one on the thumb
side. OK, shorter ulna. Because the radius is
relatively longer. The load that should ideally
be shared between the radius and the ulna. gets
disproportionately shifted towards the radial
side of the wrist. Ah, so the lunate, sitting
mostly under the radius, ends up taking on an
even greater share of that load than it normally
would, more than that 35%. Exactly. That 35 %
load transmission through the radial -lunate
joint gets magnified. The sources cite studies
showing a remarkably high correlation between
Keenbach's disease and ulnar -negative variants,
up to 78 % in some patient populations. 78%,
that's huge. It is. that even a small anatomical
difference in bone length can have a profound
biomechanical consequence over time. Another
related factor mentioned is a decreased radial
inclination angle, which is the angle formed
by the end of the radius bone. A lower angle
here also seems to direct more force onto the
lunate. It's fascinating how such subtle variations
can predispose someone to this serious condition.
What else contributes? Well, repetitive microtrauma
and compression loading are also strongly implicated.
While a single traumatic event can sometimes
play a role, the sources emphasize that cumulative
stress from repeated wrist movements, perhaps
hyperextension, flexion, or significant axial
loading. Like from certain jobs or sports? Precisely.
Like from certain sports, manual trades, or even
just repetitive heavy gripping. This can cause
micro -damage to the lunate. Now, if this micro
-damage outpaces the bone's ability to repair
itself, it can compromise the local blood supply.
So constant low -level stress, not necessarily
a single big injury, could be part of the problem.
You mentioned blood supply earlier. That seems
absolutely fundamental to a vascular necrosis.
It absolutely is. And the specific anatomy of
the lunates' blood supply makes it particularly
vulnerable. It receives blood from a network
of small arteries that penetrate the bone from
the dorsal, the back, and volar, the palm. sides
of the wrist. These form anastomosis connections
outside the bone. OK. But the crucial point highlighted
in the sources is that the lunate has relatively
sparse intraosseous collaterals. Meaning? Meaning
there aren't many backup blood vessels running
within the bone itself to provide alternative
routes for blood flow if one of the main penetrating
arteries gets compromised. So if a main supply
line is blocked or damaged, there aren't many
internal detours to keep the bone alive. That
sounds like a significant point of vulnerability.
It really is. And the sources specifically note
that a lower number of these penetrating arteries,
especially the vulgar branches coming from the
palmar radiocarpal arch, is associated with an
increased risk of developing kin box. Fewer entry
points, more risk. Exactly. Different patterns
of arterial supply have even been identified
described as Y, X, or I patterns. The eye pattern,
where there are fewer connections and less redundancy,
is found in a significant proportion of patients,
around 31%, and is postulated to be the most
precarious in terms of blood supply. So the eye
pattern might put those individuals at higher
risk? Potentially, yes. The source has also mentioned
the possibility of disruption to venous outflow,
getting blood out of the bone. If that's impaired,
it could lead to increased pressure within the
bone, further compromising blood flow. Ah, so
it's not just getting blood in, but also getting
it out. Precisely. Venous outflow is part of
the puzzle. So the lunid's blood supply is naturally
a bit precarious, and if you have fewer main
entry points or struggle to get blood out, it's
a setup for potential failure. What about the
bone's own structure or shape? Does that play
a role? Yes. Lunate morphology is another piece
of the puzzle. The size and shape of the lunate
itself matter. Logically, a smaller lunate will
experience higher stress per unit area under
the same load. More significantly, perhaps, the
shape plays a role. Lunates are often described
as either more triangular, type 1, which lacks
a medial, articular facet, or more square rectangular,
type 3, which has that facet. The type I lunate
is considered a risk factor because it seems
to have a weaker internal trabecular pattern,
making it potentially less resilient to stress.
So, a combination of biomechanical stress from
potentially misaligned forearm bones, repetitive
microtrauma, a naturally fragile blood supply
pattern, and maybe even a smaller or weaker shaped
lunate bone. It really does sound like multiple
risk factors converging to overwhelm this small
bone. It's precisely that sort of perfect storm
scenario that the sources point towards. And
while a history of a single significant trauma
is sometimes reported and can contribute, the
sources emphasize that in a surprising number
of cases, there's no clear traumatic event in
the patient's history. The onset is often more
gradual, more insidious. And are there any other
medical conditions that seem to increase the
risk? Any systemic links? Yes. The sources list
several systemic conditions that are associated
with Keenbox disease. These include conditions
that might affect blood clotting or circulation,
like sickle cell anemia, or inflammatory conditions
like gout and lupus. Okay. Cerebral palsy is
also mentioned, though the mechanism there might
be related more to abnormal muscle forces affecting
wrist mechanics. Osteoporosis, a condition causing
weakened bones, particularly in older women,
is also noted as a potential factor, though Keenbox
is generally less common in that demographic
compared to younger males. So these conditions
might predispose someone by affecting the health
of blood vessels or the bone tissue itself. That
seems to be the thinking, yes. They add another
layer of potential vulnerability. It's quite
remarkable how seemingly unrelated systemic health
issues can connect back to this problem in a
tiny wrist bone. You touched on it briefly, but
I've often heard Keenbox mentioned in the context
of occupational hazards, like using vibrating
tools. Does the research and the sources strongly
support that link? That's a common association,
certainly. And historically, occupational exposure,
particularly to hand -arm vibration, was strongly
suspected. However, the sources specifically
highlight a systematic review which found, perhaps
surprisingly, only weak evidence to definitively
link Keenbox disease directly to occupational
hand -arm vibration exposure. Oh really? Weak
evidence? Yes. So while the idea of repetitive
stress contributing is still very valid, the
specific link to occupational vibration tools
appears less strongly supported by current reviews
than the sources than perhaps previously thought.
This is a key point to note, as it does challenge
a common assumption. Okay, so to sum up this
complex etiology, it's rarely one single thing.
It's more likely a combination of subtle individual
anatomical variations, the mechanical demands
placed on the wrist, a predisposed vascular architecture
of the lunet, and potentially contributing systemic
health issues. It's a fascinating interplay of
factors. It truly is a multifactorial puzzle,
and getting a handle on these potential contributors
is crucial for diagnosis and deciding on treatment.
even though the exact cause in any individual
case can still be difficult to pinpoint definitively.
And that difficulty brings us neatly to our next
segment, experiencing this disease and the process
of figuring out what's actually going on. Diagnosis
and evaluation, yes. So someone is starting to
feel pain in their wrist. How does Keenbox typically
manifest from the patient's perspective? What
are the common symptoms? Well, the sources describe
a typical presentation that unfortunately often
starts quite subtly. The most common initial
symptom is pain, usually felt on the dorsal or
back side of the wrist, right over where the
lunate bone sits. Okay, dorsal wrist pain. Initially,
this pain might be mild, intermittent, perhaps
just feeling like a nagging ache after certain
activities. It's very often dismissed as just
a sprain or a minor strain, which contributes
to that delay in diagnosis we mentioned earlier.
So it's not usually a sudden, acute pain at the
very beginning, like a fracture might be. Not
typically, no. It's more often a gradual onset.
The pain characteristically worsens with activities
that put stress through the wrist, especially
those involving wrist extension, bending it backwards,
or significant axial loading. Like push -ups
or lifting. Exactly. Things like push -ups, lifting
heavy objects, or any task requiring strong gripping
or leaning on the wrist. As the disease progresses
and the bone degenerates, this activity -related
discomfort can become more constant and debilitating,
significantly impacting daily function. What
else might someone experience? Beyond pain, other
symptoms tend to emerge. On physical examination,
a doctor might find localized swelling over the
lunate area. There's almost always significant
tenderness when pressing directly over the limate
bone on the back of the wrist. Sinnovitis, which
is inflammation of the joint lining, can also
be present, contributing to the swelling and
a feeling of stiffness. And what about the wrist
movement? Does that get affected? Yes, range
of motion becomes increasingly limited as the
disease advances. You'll typically see a measurable
decrease in both wrist flexion, bending down,
and extension, bending back. Grip strength also
diminishes, which makes sense given the lunate's
role in load transmission during gripping. Okay,
so pain, swelling, tenderness, stiffness, reduced
grip. And in later stages, as the lunate bone
begins to collapse and fragment and the overall
carpal alignment changes, patients might start
to notice mechanical symptoms, things like clicking,
popping, or perhaps clunking sensations within
the wrist during movement. Ah, that sounds like
things are really starting to degenerate. It's
often a sign of instability and advancing joint
degeneration, yes. So it starts deceptively simply.
but can progress to significant pain, stiffness,
weakness, and even those mechanical noses. You
mentioned earlier, though, that symptom severity
doesn't always line up perfectly with the stage
seen on imaging. That's a crucial point emphasized
in the sources and one that makes managing expectations
well. quite challenging. Yes, you can have someone
experiencing severe debilitating pain early on,
even when imaging only shows stage one or perhaps
stage two changes. Really? Yes. Conversely, some
individuals with radiographic evidence of more
advanced stages might report surprisingly manageable
pain levels for a period of time. This variability
highlights the complex nature of pain perception
and the disease's sometimes unpredictable clinical
presentation. Given the subtle onset and that
potential symptom stage mismatch, how do doctors
go about diagnosing Keenbox disease? What's the
investigative process? Diagnosis is fundamentally
a clinical and imaging diagnosis. It starts with
a detailed patient history, understanding when
the symptoms began, what makes them worse, any
history of trauma or repetitive activities, and
reviewing any associated systemic conditions
we talked about. The detective work. Exactly.
Followed by a thorough physical examination to
assess that tenderness, swelling, range of motion,
and grip strength. But imaging is absolutely
essential to confirm the diagnosis and, importantly,
to stage the disease. Right, staging is key.
How does the imaging usually proceed? The imaging
process often follows a progression. Standard
radiography x -rays are usually the first step.
However, and this is a critical limitation, x
-rays are often completely normal in the very
early stages stage I. So a clear x -ray doesn't
mean you're in the clear. Not at all, especially
early on. The classic radiographic signs only
appear later. What doctors look for in x -rays
as the disease progresses are things like increased
density of the lunate bone, sclerosis, which
makes it appear whiter on the image due to hardening
and attempted repair. Also cystic changes, small
fluid -filled areas within the bone, obvious
collapse or fragmentation of the lunate, changes
in the alignment of the other carpal bones, what
we call carpal collapse, and signs of secondary
arthritis or arthrosis in the joints around the
lunate. Do they need special x -ray views? Yes.
X -rays are also needed in specific views, like
a zero -rotation PA view, to accurately measure
that ulnar variance we discussed earlier, as
well as the radial inclination. They can also
pick up coronal fractures within the lunate in
later stages. So a normal X -ray definitely doesn't
rule it out, especially early on. What's the
next step in imaging, then, if the X -ray is
normal but kin box is still suspected? Because
X -rays are often normal initially, MRI magnetic
resonance imaging, is considered the most sensitive
diagnostic tool, particularly for detecting early
-stage disease that isn't visible on x -rays,
what we call radiographically occult cases. An
MRI can directly visualize the changes in the
bone marrow associated with loss of blood supply.
What specifically does an MRI show in early -kin
box? What's the giveaway? The hallmark finding
on MRI, especially on T1 -weighted images, is
a diffuse decrease in the signal intensity of
the lunate bone marrow. This darkening of the
bone marrow is indicative of disrupted blood
flow and fat necrosis within the bone. Right,
so the MRI sees the blood supply problem directly.
Essentially, yes. As the disease progresses,
the signal characteristics on other types of
MRI sequences, like T2 -weighted or S -stora
images, can change, reflecting things like edema,
swelling, fragmentation, or those cystic changes.
MRI is also invaluable for assessing the health
of the surrounding cartilage and ligaments, helping
to identify complications like scaffolding, ligament
injury, or maybe ulnar impassioned syndrome,
which can sometimes mimic or coexist with Keenbox.
So MRI is key for catching it early by assessing
blood supply and soft tissues. While x -rays
are more useful for visualizing structural changes
and overall alignment in later stages, what about
CT scans? Where do they fit in? CTE computer
tomography is particularly useful once structural
damage is suspected or confirmed on x -ray, especially
when surgical planning is being considered. CTE
provides exquisite bony detail. Better than x
-ray for bone detail. Oh, yes. It's more sensitive
than x -ray for detecting subtle subchondral
fractures. That's fractures just below the cartilage
surface, any coronal lunate fractures, the precise
degree of fragmentation of the lunate, and the
extent of carpal instability patterns. The source
has mentioned that patients are actually frequently
restaged after getting a CT scan because it often
reveals more extensive bony damage or instability
than was apparent on the initial x -rays. Okay,
so x -ray for general overview and alignment,
MRI for early blood supply issues and soft tissue,
and CT for detailed bone structure and fragmentation,
especially important for surgery planning. Was
there an older imaging technique used? Something
else mentioned. Yes, nuclear scintigraphy. or
a bone scan, was used historically as an adjunct
tool, particularly for suspected early cases
when MRI wasn't perhaps as widely available or
sophisticated as it is today. It could show increased
uptake in areas of bone injury or decreased uptake
in areas of significant necrosis. But less common
now. Much less common now. Given the superior
sensitivity and the detailed anatomical information
provided by MRI, bone scans have largely fallen
out of favor for diagnosing Keenbox disease specifically.
It sounds like Piecing together the diagnosis,
especially in those crucial early stages, really
requires a high index of suspicion and using
the right imaging tools at the right time. It's
easy to see how delays could happen. They are,
unfortunately, very common. As the sources note,
the challenge of early diagnosis is significant
precisely because those initial symptoms are
vague and x -rays are often normal, necessitating
the use of MRI. Patients frequently experience
diagnostic delays, sometimes for months or even
years, which sadly allows the disease to progress
further before any intervention. Once the diagnosis
is made, how do doctors classify how severe the
disease is? This is where staging comes in, right?
You mentioned that's crucial. Correct. Staging
is absolutely fundamental. It provides a framework
for understanding the disease's progression,
and most importantly, it guides treatment decisions.
The most widely used system is morphologic staging
based on the Lichtman classification. Lichtman
classification. OK. This classification relies
primarily on radiographic findings, mainly x
-rays, often refined by CT. And it's known for
its relatively low interobserver variability,
meaning different clinicians tend to agree on
the stage when looking at the images. What are
the stages? The Lickman classification breaks
down the progression of the lunates' deterioration
and its effect on the surrounding wrist structure.
Stage one. This is the earliest stage. Crucially,
standard x -rays appear normal. The disease is
only detectable at this point on MRI, which shows
those characteristic signal changes indicating
compromised blood supply, ischemia, and edema.
So MRI positive, x -ray negative. Exactly. Stage
two. Now, changes become visible on x -ray. The
lunate shows increased density, or sclerosis.
It looks whiter and more otake than normal bone.
The overall shape and size of the lunand are
still preserved at this stage, but subtle fraction
lines might start to appear within the bone.
Okay, density changes on x -ray? Yes. Stage 3.
This is defined by collapse of the lunate's articular
surface that smooths surface that connects with
other bones. It's subdivided further. Stage 3
-3. The lunate has collapsed, but the overall
alignment and height of the carpal bones in the
wrist are still preserved. No major structural
shift yet. Stage 3 -4. The lunate collapse is
more significant, and it starts leading to changes
in carpal alignment. The scaphoid bone typically
starts to flex forward, and there is a measurable
loss of overall carpal height. This often results
in a specific pattern of instability called the
Dissy deformity, dorsal -interfilated segmental
instability. Stage I. This is similar to I .B.
with collapse and loss of carpal height, but
specifically includes an associated coronal fracture
of the fractal line visible on imaging running
vertically through the bone. So stage III is
all about collapse and its effect on alignment.
Precisely. Then finally, stage four. This is
the end stage. It includes the significant collapse
and carpal height loss seen in stage IB, plus
the development of secondary degenerative arthrosis,
basically arthritis in the radiocarpal joint
between the radius and the proximal carpal row,
and or the mid -carpal joint between the two
rows of carpal bones. So the lignum classification
is essentially mapping the physical destruction
of the bone and the cascade of effects on the
rest of the wrist structure. Is there another
way to stage the disease? You mentioned imaging
blood flow earlier. Yes, there's also functional
staging. This is typically assessed using contrast
-enhanced MRI. While morphologic staging tells
you about the structural damage, functional staging
tells you about the actual blood flow and the
extent of viable living bone tissue within the
lunet. And that's important for treatment planning.
Very much so. It's particularly valuable for
guiding treatment decisions regarding revascularization
procedures, which really only have a good chance
of working if there's enough viable bone remaining.
typically considered useful in stages first,
two, and perhaps early stage theia. How does
functional staging work with the contrast dye?
Functional staging, based on how the lunate enhances
after injecting contrast dye, looks something
like this. Stage one. After the contrast injection,
the lunate shows intense homogenous enhancement.
This indicates good blood flow and viable bone,
corresponding usually to morphologic stage I,
where there's ischemia and edema. but not yet
established necrosis. Stage 2. The enhancement
is patchy and inhomogeneous. This suggests partial
necrosis has occurred, but there are still areas
of viable bone, often in the distal part of the
lunate. This typically corresponds to morphologic
stage 2, stage 3. There is a complete absence
of contrast enhancement within the lunate. This
indicates full -blown, complete avascular necrosis
with no significant blood flow remaining, usually
seen in morphologic stages 3a and beyond. So
doctors use both morphologic staging to understand
the structural damage and functional staging
to understand the biological viability of the
bone itself. That combined picture must be absolutely
essential for deciding on the best course of
action for each patient. It's precisely that
comprehensive assessment that allows for tailoring
treatment. Keenvox is definitely not a one -size
-fits -all condition when it comes to management.
Which leads us perfectly into the final piece
of this puzzle. Navigating the treatment options
and what the road ahead looks like for someone
diagnosed with Keenbox disease. Yes, the management
strategies. So we've mapped the disease's progression
through staging. What are the main goals when
doctors and patients discuss treatment for Keenbox?
What are they trying to achieve? The fundamental
goals of treatment, as outlined pretty consistently
in the sources, are threefold. Alleviating pain,
preserving as much wrist motion as possible,
and maintaining or restoring grip strength. Pain,
motion, strength. Makes sense. However, the strategy
for achieving these goals is highly dependent
on several factors. The specific stage of the
disease, of course, based on Lickman and functional
staging, the patient's symptoms and their functional
demands, what they need their wrist to do, and
crucially, the presence of those contributing
biomechanical factors like ulnar negative variants.
So treatment is very much tailored to the individual
and their specific wrist anatomy and disease
state. Absolutely. highly personalized. Let's
start with the less invasive options. What happens
in the earlier stages or perhaps for patients
with milder symptoms? For early stage disease,
typically stage one and potentially some cases
of stage two where there's incomplete necrosis,
non -operative approaches are usually considered
initially. The most common method is immobilization
of the wrist. usually with a cast or rigid splint.
Immobilization. How long might someone need to
be immobilized for? Does it vary? That duration
varies quite significantly, as the sources highlight.
While some studies report average immobilization
periods around, say, 8 .6 months, historical
accounts in the literature mention extremes of
up to 20 years of casting, though that would
be highly unusual in modern practice. Twenty
years? Goodness. Yes. Immobilization is often
the preferred initial treatment for specific
demographics, such as adolescents, where bone
healing potential might be different, and perhaps
older adults over the age of 70, where surgical
risks might be higher. Does embolization often
lead to healing in adults? Does it fix the problem?
Unfortunately, the sources are quite clear on
this. In adults, spontaneous revascularization
and healing of the lunate with non -operative
treatment alone is rare. The disease is likely
to progress to later stages despite prolonged
casting in most adult cases. So it doesn't really
stop it? Not usually in adults, no. A majority
of adult patients initially treated nonoperatively
will eventually require surgical intervention
if they remain symptomatic, or the disease clearly
advances on imaging. So, while immobilization
might provide temporary pain relief by resting
the wrist, it typically doesn't alter the underlying
progressive course of the disease in adults.
Okay, so it's more about symptom control, maybe?
In many cases, yes. Other non -operative measures
include pain management with simple analgesics
like paracetamol or NSAIDs to reduce pain and
swelling, and sometimes just observation combined
with activity modification, advising patients
to avoid activities that aggravate their pain.
Again, while these can help manage symptoms,
the sources indicate that most adult patients
treated solely with observation or activity modification
will eventually need more definitive management
due to symptom progression or functional decline.
Okay, so non -operative is mainly for symptom
management, specific patient groups, or maybe
as a holding measure. More often than not, it
seems surgery becomes necessary. What are the
main categories of surgical intervention, then?
Operative treatment strategies broadly fall into
two main categories, or sometimes a combination
of both. One aims to restore blood supply to
the lunate. These are the revascularization procedures.
The other aims to reduce the mechanical load
or stress on the lunate and stabilize the wrist.
These are often called joint leveling or salvage
procedures. Okay, let's talk about relieving
the pressure first, the joint leveling ones.
Right, these are the joint leveling procedures
designed to offload the lunate. They're particularly
relevant when that contributing factor of ulnar
negative variance is present, but variations
are also used for neutral or even positive variance
situations. How does he do that? The most common
procedure for significant ulna minus is a radial
shortening osteotomy. This involves surgically
removing a small segment of the radius bone to
make it shorter, thus equalizing the lengths
of the radius and ulna at the wrist joint and
shifting load away from the lunate onto the ulnar
side. Does she shorten the longer bone? Exactly.
Alternatively, the less common and ulnar lengthening
osteotomy can be performed to achieve the same
relative length. For risks with neutral or positive
ulnar variants, where the ulna is already the
same length or longer, a radial wedge osteotomy
can be used. This involves cutting a wedge shape
out of the radius to alter the angle of the radial
joint surface, again aiming to shift load off
the lunate. So you're literally changing the
bones alignment to create a better biomechanical
environment for the struggling lunate. Do these
procedures make a significant difference in how
much stress the lunette actually bears? They
can have a really dramatic effect. The sources
cite some compelling data. A radial shortening
or ulnar lengthening of just four millimeters
can result in a substantial 45 percent decrease
in the contact stress on the radial lunette joint.
45%. That's huge. It is. This reduction in load
provides a much better environment for potential
healing, or at least slowing down progression,
particularly useful in the earlier stages, typically
stages 2 and higher IA. That's a massive reduction
from a relatively small adjustment. Okay, what
about the other approach, trying to bring blood
flow back to the lunate, the revascularization
you mentioned? Yes, these are the revascularization
procedures. They are most appropriate in earlier
stages, stages 5 and potentially early IDREA,
when there is still a significant amount of viable
bone remaining, which as we said can be assessed
with that functional contrast MRI. The primary
technique here is using vascularized bone grafts,
VBG. Vascularized bone graft? What does that
actually involve? Sounds complex. It is a complex
microsurgical technique. It involves taking a
bicep bone from another location in the body.
Common donor sites include the distal radius
itself, near the wrist, the iliac crest, which
is part of the hip bone, or even using small
bone pieces supplied by branches of the dorsal
metacarpal arteries in the hand. Like the 4 plus
5. Exactly. The 4 plus 5 extensor compartment
artery pedicle is mentioned as being favored
sometimes for its good mobility. Crucially, this
bone piece is transferred with its attached blood
vessels still intact and functioning. These kidney
vessels are then surgically connected and astimosed
to blood vessels near the lunate, effectively
aiming to give the lunate a new, living blood
supply and also some structural support. Bringing
in reinforcements with their own supply lines?
That's a good way to think of it. Another revascularization
technique mentioned, often used in earlier stages,
I5CDSE, is distal radius core decompression.
This involves drilling small holes into the distal
radius near the lunate attachment. Why drill
holes? Well, the thinking is it might potentially
reduce the pressure within the bone, the intraosseous
pressure, and perhaps stimulate a local healing
response and encourage the in -growth of new
blood vessels from the radius towards the lunate.
Sometimes, temporary pinning across the wrist
or external fixation is used alongside revascularization
to temporarily hold the wrist bones in a position
that minimizes stress on the lunate, allowing
the graft or decompression effect to establish.
How successful are these? VBGs are certainly
promising, especially in younger patients with
early stage disease. However, the sources do
note that long -term outcomes can be variable.
And success really depends on the graft properly
integrating and that new blood supply being sufficient
and sustained. Okay, so leveling the bones to
reduce stress or bringing in new blood supply
with bone grafts. What happens when the lunate
is already significantly collapsed or the wrist
has become unstable or arthritic those later
stages, IIB and IV? In these more advanced stages,
the focus often shifts away from trying to save
the lunated self towards salvage procedures.
These aim to eliminate pain and stabilize the
wrist, acknowledging that restoring full, normal
motion may not be achievable. One category here
is partial wrist fusions, arthrodesis. Partial
fusion. What does that mean exactly? Fusing only
some bones. Precisely. It means surgically fusing
specific carpal bones together while leaving
others free to move. The goal is usually to create
stability. offload the damaged lunate area, or
correct instability patterns like that dizzy
deformity we mentioned, while hopefully preserving
movement in the unfused portions of the wrist.
Which bones might they fuse? Common partial fusions
include STT fusion, which fuses the scaphoid,
trapezium, and trapezoid bones together, or perhaps
scaphocapitate fusion, or caponohamid fusion.
These are typically considered in stages 2, LEIA,
and IIB. What's the outcome of a partial fusion?
Well, a partial fusion can certainly reduce pain
and provide stability, but it necessarily limits
the overall range of motion compared to a healthy
wrist because the fused bones no longer move
independently. The choice of which bones to fuse
depends very much on the exact pattern of collapse
and instability present. The sources do mention
differing opinions and evidence regarding which
specific partial fusion is optimal for, say,
stage IB, with some studies suggesting STT fusion
might be preferred over other options like proximal
row carbectomy in certain cases. OK, so partial
fusion limits motion but helps pain and stability.
What if the lunate is severely fragmented, collapsed,
or there's already significant arthritis involving
that? whole first row of carpal bones. That's
where proximal row carpectomy, PRC, becomes a
very viable option. This involves surgically
removing the entire proximal row of carpal bones,
the scaphoid, the lunate, and the trichotrum.
Removing all three. Yes. This procedure is typically
indicated for stages I, IV, and IV, especially
when the lunate is really beyond repair or the
joints involving that proximal row are severely
affected by arthritis. Removing three bones from
the wrist sounds quite drastic. What's the outcome
like after a PRC? While it sounds significant,
PRC is actually a well -established procedure
that can be very effective at relieving pain.
It sacrifices that first row, but it preserves
a surprising amount of wrist motion, usually
around 50 -60 % of the normal range, by allowing
the distal carpal row, the second row of bones,
to articulate directly with the end of the radius
bone. So you still get decent movement. You get
functional movement, yes, and often good grip
strength returns, too. This makes it a favorite
option for individuals who need reasonable pain
relief and still require a degree of wrist flexibility,
perhaps for certain professions or activities
like playing musical instruments. And if the
arthritis is even more extensive, involving the
radius itself or the entire wrist joint in stage
4. When there is diffuse, severe arthritis throughout
the radiocarpal and mid -carpal joints, often
resulting from the end -stage collapse of Keenbach's
disease, then a total wrist fusion orthodesis
might be necessary. This is considered a definitive
salvage procedure. Total fusion, what does that
involve? Total wrist fusion involves surgically
joining all the carpal bones together and then
fusing this block of bones to the end of the
radius bone in the forearm. So everything is
locked solid? Essentially, yes. This procedure
is extremely effective at eliminating pain because
all the painful arthritic joints are immobilized.
However, the trade -off is significant. You lose
all notion at the wrist joint itself. No flexion,
extension, or side -to -side deviation is possible.
The hand is essentially fixed in a functional
position relative to the forearm. Right, so you
trade all wrist movement for complete pain relief
and maximum stability. Who is that typically
recommended for? Total wrist fusion is often
recommended for individuals in stage 3 who require
maximal strength and stability over flexibility,
perhaps those performing heavy manual labor.
It's important to note, though, that while you
lose wrist motion, you retain full forearm rotation,
turning your palm up and down, pronation and
supination, which is crucial for many daily tasks.
What about just taking the lunate out? Is that
ever done? A more traditional and perhaps less
commonly performed procedure now for advanced
stages is simple lunate excision. just removing
the lunate bone. However, this method on its
own is associated with a high risk of subsequent
carpal collapse and instability because of the
void it leaves behind. Right, things could just
fall into the gap. Exactly. So sometimes it's
combined with interposition techniques. For example,
using a harvested tendon, like the pulmaris longus
tendon from the forearm, fashioned into a ball
to try and fill the space and maintain some carpal
height and stability. That's known as tendon
ball arthroplasty. It aims to mitigate some of
the complications of just removing the bone.
Are there options for replacing the joint like
a prosthetic wrist? Yes. Total wrist arthroplasty
using an artificial joint replacement is also
an option for stage 4 disease, similar in concept
to hip or knee replacements. It aims to preserve
more motion than a total fusion while still relieving
pain. But how reliable are they? Well, the sources
indicate that the long -term results and durability
of total wrist arthroplasty are not as well established
or predictable. compared to total wrist fusion,
particularly if the wrist is subjected to heavy
loads. It's typically considered more for patients
with lower functional demands or perhaps those
who absolutely cannot tolerate the stiffness
of the fusion, maybe due to bilateral issues.
Any other techniques worth mentioning? The sources
also briefly mention a couple of other techniques
used in specific circumstances. Temporary scaphotripeziotropazoidal
STT pinning can sometimes be used in adolescents
with progressive pain to stabilize the scaphoid
and unload the lunate while they're still growing.
And a capitate -shortening osteotomy, sometimes
combined with a capital hamit fusion known as
the Omquist procedure, is another approach designed
to decompress the lunate, particularly in cases
with neutral or positive ulnar variants. Does
shortening the capitate help the lunate? It can.
The sources give interesting data here too. Capitate
shortening combined with Capito -Hammett fusion
can decrease radiolunate stress significantly
by about 66 percent. However, it does transfer
load elsewhere, increasing the stress on the
radioscapoid joint by around 26 percent, which
could potentially increase the risk of future
osteoarthritis developing there. So there are
always trade -offs. It's clear there are so many
surgical paths, each with its own specific goals,
indications based on stage and anatomy and very
distinct trade -offs in terms of pain relief
versus motion versus stability. Choosing the
right approach must be a really complex decision
for both the patient and the surgical team. It
absolutely is. It requires very careful consideration
of the disease state, the patient's individual
functional needs and expectations, and a thorough
discussion of the potential risks, benefits,
and long -term consequences of each procedure.
After any of these treatments, whether it's non
-operative immobilization or one of the surgical
procedures, what does the recovery process typically
involve? It can't be quick. No, recovery is a
critical and often lengthy phase that definitely
demands patients and dedicated rehabilitation.
Following a period of immobilization in a cast
or splint, which as we said can range from several
weeks to several months, depending on the procedure
or the non -operative plan, patients then transition
into rehabilitation. And that involves therapy?
Yes. The core of recovery involves working closely
with a specialized physical therapist, or occupational
therapist, often referred to as a hand therapist.
Their role is absolutely crucial in guiding the
patient through a structured program designed
to regain function. What does that structured
rehab program typically look like? What are the
stages? It's typically staged, yes. The initial
focus is usually on managing any post -treatment
pain and swelling, and then restore a basic,
gentle range of motion to prevent stiffness setting
in. As healing progresses, the program advances
to include strengthening exercises to rebuild
muscle power in the forearm and hand, including
grip strength, which is often significantly weakened
by the disease and the period of inactivity.
Finally, it moves towards improving fine motor
control and dexterity through specific exercises,
helping the patient regain the ability to perform
more complex tasks needed for daily living or
work. Hand therapists also provide essential
guidance on activity modification and ergonomic
strategies to help protect the wrist from excessive
load or stress in the future, trying to prevent
recurrence or further issues. How important is
that rehab? It's vital for patients to understand
that while rehabilitation is essential for maximizing
their functional outcome, regaining as much strength
and motion as possible within the limitations
imposed by the disease or the chosen treatment,
it doesn't cure the underlying disease process
itself. The goal of rehab is really to help the
patient adapt to their post -treatment risk mechanics
and maximize their ability to use their hand
as effectively as possible. Given the unpredictable
nature of Keenbox that we've discussed and the
range of interventions, what does the long -term
prognosis look like for someone diagnosed with
this condition? What does the future hold? Well,
the sources highlight a somewhat sobering reality.
Keenbox disease, if left completely untreated,
is considered invariably progressive. Without
intervention, the loss of blood supply inevitably
leads to bone death, fragmentation, collapse,
and ultimately significant degenerative arthritis
throughout the wrist. This progression can often
lead to severe joint destruction and considerable
loss of function within, say, three to five years
of symptom onset in many cases. That sounds quite
serious if it's just left. It is. It's ignored.
However, and this is the unpredictable aspect
we keep coming back to, the rate and extent of
that progression can vary significantly between
individuals. As the sources note, not every case
marches predictably through all four stages from
I to biv. So it's not always a straight line.
Not always. Some individuals, particularly those
diagnosed in earlier stages or perhaps with less
severe underlying risk factors, might experience
much slower progression or have relatively mild
symptoms for a longer period, despite radiographic
changes being visible. And in very rare instances,
spontaneous improvement or even cessation of
progression has been reported, though this is
definitely uncommon, especially in adults. You
can't rely on that happening. So it's progressive
generally, but the path isn't set in stone for
everyone. What factors do influence the prognosis?
What makes it more likely to be worse? Several
factors are associated with a less favorable
prognosis and a higher likelihood of faster progression
or worse outcomes. The functional stage we discussed
is key. the greater the extent of viable bones
seen on functional MRI. Generally, the better
the potential for success with revascularization
and perhaps a more favorable outlook overall.
Makes sense. The degree of negative ulnar variance
is also strongly correlated. The more ulna minus
the patient has, the more severe the biomechanical
stress and the more likely the disease is to
progress to advanced stages. Age at diagnosis
is also a factor. Patients diagnosed at an older
age are more likely to already have more advanced
stage disease when they present, and may experience
more rapid progression subsequently. And treatment,
does that change the prognosis? While treatment
can significantly improve pain and function,
the sources acknowledge that outcomes can still
vary, often categorized in studies as excellent,
good, fair, or poor. Treatment aims to manage
symptoms, improve function, and potentially slow
down the progression, even if the imaging findings
in later stages still show considerable structural
damage has occurred. Are there long -term problems
even after treatment? Unfortunately, yes. Even
after successful initial treatment, there are
potential long -term complications to be aware
of. These can include persistent or recurrent
pain, stiffness, and residual limitations in
motion or strength. Specific complications related
to the altered wrist mechanics or the surgical
interventions themselves can include things like
scapholunate dissociation, that's instability
developing between the scaphoid and the lunates
remaining portions or its neighbors. Also, secondary
degenerative arthrosis, or arthritis, developing
over time in joints that now take on increased
load because of the surgery, like the radioscapoid
joint after a capitate shortening or certain
partial fusions. And malignment of other carpal
bones, like the trichotrum, can occur. That increased
stress on the radial side of the wrist post -treatment
is a persistent risk factor for developing future
osteoarthritis. And given the progressive nature
and these potential complications, is it common
for someone with Kinbox to require more than
one procedure over their lifetime? Yes, that
is a distinct possibility, particularly perhaps
in younger patients or those with more aggressive
disease patterns or who develop significant complications.
The sources acknowledge that Keenbox disease
can really be a lifelong condition requiring
ongoing management, and some patients may unfortunately
need multiple surgical procedures over time as
the disease progresses or complications arise
from previous interventions. It truly sounds
like a condition that requires a comprehensive,
long -term approach involving very careful decision
making every step of the way and relying heavily
on an experienced healthcare team. Absolutely.
The sources really emphasize the value of an
interprofessional team approach involving hand
surgeons, radiologists, and specialist hand therapists
all working together for optimal diagnosis, planning,
and management throughout the patient's journey
with this condition. So we've taken a deep dive
today into Keenbok's disease, exploring that
delicate lunete bone, the complex interplay of
factors from subtle anatomical variations to
vascular patterns and repetitive stress that
contribute to its mysterious failure. We have.
And we've seen how challenging diagnosis can
be, often mimicking simpler issues initially,
and how advanced imaging like MRI and CT is absolutely
essential to truly see what's happening inside
the bone. and to stage the disease accurately
using classifications like Lickman. And we've
mapped out the wide spectrum of treatment options,
haven't we? Ranging from fairly limited non -operative
measures to quite complex surgical procedures
aimed at leveling bones, revascularizing the
lunet in early stages, or performing salvage
procedures like partial or total fusions or proximal
rocarpectomy in later stages, each, as we've
stressed, with its own benefits and inherent
trade -offs. And we've discussed the long view
that while it's invariably progressive if left
untreated, the disease course itself is unpredictable.
And even with timely interventions and dedicated
rehabilitation, it can lead to long -term complications
and potentially require multiple procedures,
making it a condition requiring ongoing care
and adaptation from the patient. If you found
this discussion helpful, perhaps consider sharing
it with colleagues who might also benefit. What
stands out to you most about the complexity of
Keenbox disease? Especially considering those
really difficult trade -offs, patients and doctors
must weigh balancing pain relief against preserving
precious wrist motion, or accepting the risks
and limitations of potentially multiple interventions
over a lifetime. It's a condition that really
highlights the intricate mechanics of the human
body and the profound challenges of intervening
when a fundamental supply line to a critical
structure fails, isn't it? It really does. It
underscores the importance of early diagnosis,
tailored treatment, and realistic expectations.
A fascinating and challenging condition.